PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 2809257-4 1989 CSF TNF activity peaked 2 h after initiation of antibiotic therapy (24.4 +/- 2 ng/ml), was significantly higher than that in untreated controls (1.4 +/- 1.1 ng/ml; P less than .05), and was associated with a substantially increased inflammatory response as reflected by higher CSF white blood cell count (24,500 +/- 8,151 vs. 1,920 +/- 644 in untreated controls; P less than .05), lower glucose, and higher protein and lactate concentrations. Glucose 387-394 tumor necrosis factor Homo sapiens 4-7 33924887-7 2021 In particular, TNFalpha levels negatively correlated with FEV1% decrease/year and FEV1% decrease (p = 0.023 and p = 0.02, respectively), and positively correlated with serum fasting glucose (p = 0.019) in PA CF patients. Glucose 182-189 tumor necrosis factor Homo sapiens 15-23 3055785-0 1988 Interleukin-1 induced impairment in pancreatic islet oxidative metabolism of glucose is potentiated by tumor necrosis factor. Glucose 77-84 tumor necrosis factor Homo sapiens 103-124 3259727-0 1988 Cachectin/TNF and IL-1 induced by glucose-modified proteins: role in normal tissue remodeling. Glucose 34-41 tumor necrosis factor Homo sapiens 0-9 3259727-0 1988 Cachectin/TNF and IL-1 induced by glucose-modified proteins: role in normal tissue remodeling. Glucose 34-41 tumor necrosis factor Homo sapiens 10-13 3370760-1 1988 This study was conducted to determine if macrophage elaborated monokines in general, and human recombinant tumor necrosis factor (hrTNF alpha) in particular alter glucose metabolism in a manner analogous to that observed in endotoxin-treated animals. Glucose 163-170 tumor necrosis factor Homo sapiens 107-128 3689407-0 1987 Tumor necrosis factor increases in vivo glucose utilization of macrophage-rich tissues. Glucose 40-47 tumor necrosis factor Homo sapiens 0-21 3689407-2 1987 After infusion of a non-lethal dose of recombinant human TNF-alpha (150 micrograms/kg) to rats, glucose utilization was increased by 80-100% in spleen, liver, kidney, by 60% in skin and by 30-40% in lung and ileum. Glucose 96-103 tumor necrosis factor Homo sapiens 57-66 34048666-2 2021 Physiological/pathological changes mediated by high glucose are the main factors causing injury of DN, including the enhancement of polyol pathway, the accumulation of advanced glycation products (AGEs), and the activation of protein kinase C (PKC) and transforming growth factor-beta (TGF-beta) signals. Glucose 52-59 tumor necrosis factor Homo sapiens 253-284 33989405-7 2021 TNFalpha measurably increased secretion of IL-8 and IL-1beta, which was enhanced at 60 mM glucose. Glucose 90-97 tumor necrosis factor Homo sapiens 0-8 33989405-10 2021 When TNFalpha hyperglycemia and <=30 mM glucose and were combined, MUC2 and ALP activity remained similar to that of TNFalpha alone, although synergistic effects were seen at 60 mM glucose. Glucose 181-188 tumor necrosis factor Homo sapiens 5-13 33544449-7 2021 Islets exposed to acute hypoxia (1-2% O2 ) or to inflammatory cytokines (including IFN-gamma, TNF-alpha, IL-B) in vitro undergo apoptosis and a rapid decline in glucose-stimulated insulin secretion. Glucose 161-168 tumor necrosis factor Homo sapiens 94-103 33333081-8 2021 TNFalpha-induced apoptosis under different glucose concentrations caused selective impoverishment of cell clusters and differentially influenced gene expression profiles of surviving hypox-subASCs. Glucose 43-50 tumor necrosis factor Homo sapiens 0-8 33707603-0 2021 Pentagalloyl glucose inhibits TNF-alpha-activated CXCL1/GRO-alpha expression and induces apoptosis-related genes in triple-negative breast cancer cells. Glucose 13-20 tumor necrosis factor Homo sapiens 30-39 33707603-2 2021 The current investigation was designed to examine the natural compound pentagalloyl glucose (PGG) effects on TNF-alpha activated TNBC cell lines, MDA-MB-231 and MDA-MB-468. Glucose 84-91 tumor necrosis factor Homo sapiens 109-118 33655586-9 2021 After high glucose induction, the expression of TNF-alpha, IL-1beta, and IL-6 was increased and the expression of MCP-1, NLPR3, and ASC proteins was also increased (p < .001). Glucose 11-18 tumor necrosis factor Homo sapiens 48-57 33124207-6 2020 Furthermore, HPDLCs under glucose-induced oxidative stress showed induction of inflammatory molecules (intercellular adhesion molecule-1, vascular cell adhesion protein-1, tumor necrosis factor-alpha, interleukin-1-beta) and disturbances of osteogenic differentiation (bone morphogenetic protein-2, and -7, runt-related transcription factor-2), cementogenesis (cementum protein-1), and autophagy-related molecules (autophagy related 5, light chain 3 I/II, beclin-1). Glucose 26-33 tumor necrosis factor Homo sapiens 172-199 33206345-2 2021 The present study aimed to characterize the ability of MaR1 to prevent the alterations induced by TNF-alpha on insulin actions in glucose uptake and Akt phosphorylation in cultured human adipocytes from overweight/obese subjects, as well as to investigate the effects of MaR1 acute and chronic administration on Akt phosphorylation in absence/presence of insulin in white adipose tissue (WAT) and skeletal muscle from lean and diet-induced obese (DIO) mice. Glucose 130-137 tumor necrosis factor Homo sapiens 98-107 33206345-3 2021 MaR1 (0.1 nM) prevented the inhibitory effect of TNF-alpha on insulin-stimulated 2-Deoxy-D-glucose uptake and Akt phosphorylation in human adipocytes. Glucose 91-98 tumor necrosis factor Homo sapiens 49-58 33252072-9 2021 RESULTS: reatment of HBMVECs with 30 mM glucose increased thrombin activity and expression of inflammatory proteins TNFalpha, IL-6, and MMPs 2 and 9; this elevation was reduced by the thrombin inhibitor dabigatran. Glucose 40-47 tumor necrosis factor Homo sapiens 116-124 32633001-7 2020 Moreover, has_circ_CCNB1 was positively correlated with glucose (GLU), glycosylated hemoglobin (GHb), interleukin 6 (IL-6), and tumor necrosis factor-alpha (TNF-alpha) while has_circ_0009024 was negatively correlated with them. Glucose 56-63 tumor necrosis factor Homo sapiens 128-155 32633001-7 2020 Moreover, has_circ_CCNB1 was positively correlated with glucose (GLU), glycosylated hemoglobin (GHb), interleukin 6 (IL-6), and tumor necrosis factor-alpha (TNF-alpha) while has_circ_0009024 was negatively correlated with them. Glucose 56-63 tumor necrosis factor Homo sapiens 157-166 32633001-7 2020 Moreover, has_circ_CCNB1 was positively correlated with glucose (GLU), glycosylated hemoglobin (GHb), interleukin 6 (IL-6), and tumor necrosis factor-alpha (TNF-alpha) while has_circ_0009024 was negatively correlated with them. Glucose 65-68 tumor necrosis factor Homo sapiens 157-166 32808710-3 2020 The present study aimed to explore the mechanisms by which high-glucose concentrations aggravate cell viability reduction in human CD146-positive periodontal ligament cells (CD146+ PDLCs) under TNF-alpha induction. Glucose 64-71 tumor necrosis factor Homo sapiens 194-203 32808710-12 2020 In conclusion, the present findings suggest that high glucose-induced CpG island hypomethylation within the TNFR-1 gene plays an essential role in TNFR-1 up-regulation, and this further enhances the cell viability reduction of CD146+ PDLCs caused by TNF-alpha. Glucose 54-61 tumor necrosis factor Homo sapiens 250-259 33136275-8 2022 HBMVECs injured by glucose and hypoxia induced increases in microglial production of NO, tumor necrosis factor-alpha (TNFalpha) and matrix metalloproteinase (MMP)-9. Glucose 19-26 tumor necrosis factor Homo sapiens 89-116 33136275-8 2022 HBMVECs injured by glucose and hypoxia induced increases in microglial production of NO, tumor necrosis factor-alpha (TNFalpha) and matrix metalloproteinase (MMP)-9. Glucose 19-26 tumor necrosis factor Homo sapiens 118-126 32830548-9 2020 Salsalate administration suppressed lipid- and glucose-stimulated reactive oxygen species generation, activated nuclear factor-kappaB and circulating tumor necrosis factor-alpha, normalized basal androgen levels, and lowered HCG-stimulated androgen secretion without altering EGP or GDR. Glucose 47-54 tumor necrosis factor Homo sapiens 150-177 32580157-9 2020 Butyrate and propionate were found to reverse TNF-induced increases in IRS-1 serine phosphorylation and decreases in glucose uptake. Glucose 117-124 tumor necrosis factor Homo sapiens 46-49 32806763-12 2020 RIH/glucose fluctuations also induced M1 polarization and an inflammatory profile (CD11c, IL-1beta, TNF-alpha, IL-6, and monocyte chemoattractant protein (MCP)-1) in macrophages. Glucose 4-11 tumor necrosis factor Homo sapiens 100-109 32684830-11 2020 Also, there was a significant positive correlation between serum levels of TNF-alpha with FBG (fasting blood glucose), creatinine, total cholesterol, LDL-C, HbA1c, and microalbumin/creatinine ratio (ACR) among the DN group (p = 0.042, <0.001, <0.001, <0.001, 0.027, and 0.043, respectively). Glucose 109-116 tumor necrosis factor Homo sapiens 75-84 32801814-7 2020 TNF-alpha level and expression of it showed agonistic behavior, ie no change at low concentration while enhances with the increase of glucose. Glucose 134-141 tumor necrosis factor Homo sapiens 0-9 32801814-12 2020 However, anti-diabetic drugs including insulin up-regulate the TNF-alpha gene expression in mild or severe glucose load. Glucose 107-114 tumor necrosis factor Homo sapiens 63-72 32319517-7 2020 An increasing trend for TNF-alpha and NO production was observed with higher concentration of glucose (R2 = 0.358; P = 0.019; R2 = 0.307; P = 0.027) and fructose (R2 = 0.669; P = 0.001; R2 = 0.339; P = 0.006). Glucose 94-101 tumor necrosis factor Homo sapiens 24-33 32606862-9 2020 In vitro, the mRNA expression of MCP-1 and TNF-alpha was significantly decreased when the generation of alpha1-AT in tubular epithelial cells was inhibited under high glucose stimulation. Glucose 167-174 tumor necrosis factor Homo sapiens 43-52 32587797-11 2020 Moreover, the highest ROS and the lowest insulin secretion were found in FAC combined with IL-1beta and TNF-alpha in the high-glucose condition of human pancreatic beta cell, which could be involved in the mechanism of DM development in beta-thalassemia patients. Glucose 126-133 tumor necrosis factor Homo sapiens 104-113 32587790-15 2020 TNF-alpha progressively increased the apoptotic cells at 48 and 72 h. Conclusion: At 0.008 microM of TNF-alpha, an IR condition was induced in hTeno, supported with the significant reduction in glucose uptake, as well as significantly reduced total collagen, specifically COL-I expression levels, downregulation of candidate tenogenic markers genes (SCX and MKX), and upregulation of ECM catabolic genes (MMP-9 and MMP-13). Glucose 194-201 tumor necrosis factor Homo sapiens 0-9 32587790-15 2020 TNF-alpha progressively increased the apoptotic cells at 48 and 72 h. Conclusion: At 0.008 microM of TNF-alpha, an IR condition was induced in hTeno, supported with the significant reduction in glucose uptake, as well as significantly reduced total collagen, specifically COL-I expression levels, downregulation of candidate tenogenic markers genes (SCX and MKX), and upregulation of ECM catabolic genes (MMP-9 and MMP-13). Glucose 194-201 tumor necrosis factor Homo sapiens 101-110 32550560-0 2020 Glucose and TNF enhance expression of TNF and IL1B, and histone H3 acetylation and K4/K36 methylation, in juvenile macrophage cells. Glucose 0-7 tumor necrosis factor Homo sapiens 38-41 32018221-5 2020 In addition, high-glucose (50 mM) significantly decreased the levels of miR-130a and superoxide dismutase (SOD) 1, and promoted tumor necrosis factor (TNF)-alpha expressions in ARPE-19 cells. Glucose 18-25 tumor necrosis factor Homo sapiens 128-161 32018221-7 2020 Furthermore, overexpression of miR-130a abrogated the effects of high-glucose (50 mM) on the above cell functions, which were all reversed by either upregulating TNF-alpha or knocking down SOD1 in ARPE-19 cells. Glucose 70-77 tumor necrosis factor Homo sapiens 162-171 32018221-8 2020 Taken together, upregulation of miR-130a alleviated the cytotoxic effects of high-glucose (50 mM) on ARPE-19 cells by regulating TNF-alpha/SOD1/ROS axis mediated pyroptotic cell death. Glucose 82-89 tumor necrosis factor Homo sapiens 129-138 32028854-2 2020 Biological function experiments showed that miR-218 and inflammatory factors TNF-alpha and IL-1beta were highly expressed in renal proximal tubule under high-glucose conditions. Glucose 158-165 tumor necrosis factor Homo sapiens 77-86 32306243-7 2020 Elevated serum levels of adipokines, including TNF-alpha, which inhibits the autophosphorylation of the insulin receptor and suppresses the expression of glucose transporter 4, favor insulin resistance and could partially explain the association between PsA and DM. Glucose 154-161 tumor necrosis factor Homo sapiens 47-56 32429534-9 2020 Finally, NTS and MSM inhibited the high glucose-induced expression of interleukin (IL)-1beta, IL-6, and tumor necrosis factor-alpha and binding of NF-kappaB protein to the DNA of proinflammatory cytokines. Glucose 40-47 tumor necrosis factor Homo sapiens 104-131 32509152-3 2020 The inverse correlations between non-alpha-tocopherols and tumor necrosis factor-alpha (TNF-alpha) varied substantially across different glucose tolerance status, with the strongest observed in prediabetes (r = -0.33 for beta-/gamma-tocopherol, r = -0.37 for delta-tocopherol, p < 0.01), followed by normal glucose tolerance (NGT). Glucose 137-144 tumor necrosis factor Homo sapiens 59-86 32509152-3 2020 The inverse correlations between non-alpha-tocopherols and tumor necrosis factor-alpha (TNF-alpha) varied substantially across different glucose tolerance status, with the strongest observed in prediabetes (r = -0.33 for beta-/gamma-tocopherol, r = -0.37 for delta-tocopherol, p < 0.01), followed by normal glucose tolerance (NGT). Glucose 137-144 tumor necrosis factor Homo sapiens 88-97 32509152-3 2020 The inverse correlations between non-alpha-tocopherols and tumor necrosis factor-alpha (TNF-alpha) varied substantially across different glucose tolerance status, with the strongest observed in prediabetes (r = -0.33 for beta-/gamma-tocopherol, r = -0.37 for delta-tocopherol, p < 0.01), followed by normal glucose tolerance (NGT). Glucose 307-314 tumor necrosis factor Homo sapiens 88-97 32018221-0 2020 MiR-130a alleviated high-glucose induced retinal pigment epithelium (RPE) death by modulating TNF-alpha/SOD1/ROS cascade mediated pyroptosis. Glucose 25-32 tumor necrosis factor Homo sapiens 94-103 32550560-2 2020 In this study, we investigated whether high glucose and/or tumor necrosis factor (TNF) would enhance pro-inflammatory cytokine expression of tumor necrosis factor (TNF) and interleukin (IL)-1beta (IL1B) by altering histone modifications in U937, a juvenile macrophage cell line. Glucose 44-51 tumor necrosis factor Homo sapiens 141-162 32550560-2 2020 In this study, we investigated whether high glucose and/or tumor necrosis factor (TNF) would enhance pro-inflammatory cytokine expression of tumor necrosis factor (TNF) and interleukin (IL)-1beta (IL1B) by altering histone modifications in U937, a juvenile macrophage cell line. Glucose 44-51 tumor necrosis factor Homo sapiens 164-167 32550560-3 2020 The mRNA levels of TNF and IL1B in U937 cells were significantly affected by glucose concentration and TNF treatment. Glucose 77-84 tumor necrosis factor Homo sapiens 19-22 32550560-4 2020 Mono-methylated histone H3K4 signals around TNF and IL1B were lower in cells treated with high glucose compared with low glucose. Glucose 95-102 tumor necrosis factor Homo sapiens 44-47 32550560-4 2020 Mono-methylated histone H3K4 signals around TNF and IL1B were lower in cells treated with high glucose compared with low glucose. Glucose 121-128 tumor necrosis factor Homo sapiens 44-47 32550560-6 2020 TNF treatment of U937 cells cultured in high glucose enhanced histone H3K36 tri-methylation, particularly around the gene regions of TNF and IL1B. Glucose 45-52 tumor necrosis factor Homo sapiens 0-3 32550560-6 2020 TNF treatment of U937 cells cultured in high glucose enhanced histone H3K36 tri-methylation, particularly around the gene regions of TNF and IL1B. Glucose 45-52 tumor necrosis factor Homo sapiens 133-136 32550560-7 2020 Histone acetylation was induced by treatment with TNF in high-glucose medium. Glucose 62-69 tumor necrosis factor Homo sapiens 50-53 32550560-8 2020 The induction of acetylation and tri-methylation of K4 and K36 of histone H3 around TNF and IL1B by treatment with high glucose and/or TNF was positively associated with the induction of these genes in juvenile macrophage U937 cells. Glucose 120-127 tumor necrosis factor Homo sapiens 84-87 32005665-8 2020 In hypoxia mimicked by treating MDM with oligomycin (a mitochondrial ATP synthase inhibitor), both 2-DG and glucose starvation strongly suppress TNF and interleukin-6 production, and compromise cell viability. Glucose 108-115 tumor necrosis factor Homo sapiens 145-148 32280713-4 2020 Results: We found that, with the elevation of glucose, the level of H2S was decreased in GDM pregnant women and newborns and the concentrations of IL-6 and TNF-alpha were upregulated. Glucose 46-53 tumor necrosis factor Homo sapiens 156-165 32280713-5 2020 With regression, IL-6 and TNF-alpha concentrations were positively correlated with the level of blood glucose and negatively correlated with H2S concentration. Glucose 102-109 tumor necrosis factor Homo sapiens 26-35 32056981-7 2020 Our results demonstrated that glucose modulated the macrophage cytokine production, including decreased LPS-induced pro-inflammatory cytokines (i.e., tumor necrosis factor [TNF]alpha and interleukin [IL]-6) and increased anti-inflammatory cytokine (i.e., IL-10), at resting state. Glucose 30-37 tumor necrosis factor Homo sapiens 150-171 32089705-0 2020 High Glucose Exacerbates TNF-alpha-Induced Proliferative Inhibition in Human Periodontal Ligament Stem Cells through Upregulation and Activation of TNF Receptor 1. Glucose 5-12 tumor necrosis factor Homo sapiens 25-34 32089705-1 2020 Objective: This research is aimed at investigating how high glucose affects the proliferation and apoptosis in periodontal ligament stem cells (PDLSCs) in the presence of TNF-alpha. Glucose 60-67 tumor necrosis factor Homo sapiens 171-180 32089705-5 2020 Results: CCK-8 assay showed that high glucose exacerbated TNF-alpha. Glucose 38-45 tumor necrosis factor Homo sapiens 58-67 32089705-11 2020 Conclusion: High glucose exacerbates TNF-alpha-induced proliferative inhibition in human periodontal ligament stem cells through the upregulation and activation of TNF receptor 1. Glucose 17-24 tumor necrosis factor Homo sapiens 37-46 31760230-5 2020 DHA blocked TNF-alpha-induced inhibition of alpha-methyl-D-glucose (alphaMG) uptake and SGLT1 expression in the apical membrane of Caco-2 cells, through a pathway independent of GPR120. Glucose 44-66 tumor necrosis factor Homo sapiens 12-21 31760230-5 2020 DHA blocked TNF-alpha-induced inhibition of alpha-methyl-D-glucose (alphaMG) uptake and SGLT1 expression in the apical membrane of Caco-2 cells, through a pathway independent of GPR120. Glucose 68-75 tumor necrosis factor Homo sapiens 12-21 32364405-7 2020 Importantly, CORM-2 pretreatment prevented the impairment caused by TNF-alpha, evidenced by the improved glucose-stimulated index and transplantation outcomes. Glucose 105-112 tumor necrosis factor Homo sapiens 68-77 32056981-7 2020 Our results demonstrated that glucose modulated the macrophage cytokine production, including decreased LPS-induced pro-inflammatory cytokines (i.e., tumor necrosis factor [TNF]alpha and interleukin [IL]-6) and increased anti-inflammatory cytokine (i.e., IL-10), at resting state. Glucose 30-37 tumor necrosis factor Homo sapiens 173-182 32056981-8 2020 Moreover, glucose-containing CM reduced the macrophage secretion of TNFalpha and IL-8 but elevated the IL-12 and IL-23 levels, showing an opposite pattern of distinct pro-inflammatory cytokines modulated by cancer glucose metabolites. Glucose 10-17 tumor necrosis factor Homo sapiens 68-76 32056981-11 2020 The downregulation of death-inducing TNFalpha and upregulation of Th1/17-polarizing IL-12/IL-23 axis in macrophages caused by exposure to cancer-derived glucose metabolites may contribute to tumor progression. Glucose 153-160 tumor necrosis factor Homo sapiens 37-45 31638409-3 2019 A high glucose concentration induced HRVEC inflammation metabolic memory by decreasing SIRT1 and increasing Ac-NF-kappaB, NLRP3, caspase 1, interleukin-1beta, inducible nitric oxide synthase, and tumor necrosis factor alpha, whereas exposure of HRVECs to a high glucose medium for 4 days, followed by a normal glucose concentration for an additional 4 days, failed to reverse these changes. Glucose 7-14 tumor necrosis factor Homo sapiens 196-223 31912702-6 2019 Oxygen-glucose deprivation up-regulated the expression of regulator of reprogramming, and regulator of reprogramming promoted ASK-1/STRAP/14-3-3 complex formation to inhibit the activation of TNF-alpha/ASK-1-mediated apoptosis of human brain microvascular endothelial cells, while small interfering ribonucleic acid (RNA) targeting regulator of reprogramming amplified these effects. Glucose 7-14 tumor necrosis factor Homo sapiens 192-201 30368556-4 2019 RESULTS: Both high glucose and high fructose resulted in intracellular lipid accumulation after 48 h, and this was further augmented (up to twofold, as compared to basal levels) by co-treatment with the lipogenesis-stimulating hormone insulin and the pro-inflammatory cytokine tumour necrosis factor alpha (TNF-alpha), respectively. Glucose 19-26 tumor necrosis factor Homo sapiens 307-316 31723203-6 2019 TNF-induced TXNIP down-regulation correlated with increased glucose uptake. Glucose 60-67 tumor necrosis factor Homo sapiens 0-3 31819571-3 2019 Genetic polymorphism of cytokines like tumor necrosis factor-alpha (TNF-alpha) is suggestive of interference with insulin-sensitive glucose uptake and induces insulin resistance that ultimately could lead to T2DM. Glucose 132-139 tumor necrosis factor Homo sapiens 39-66 31397188-10 2019 Conclusion: Anti-TNF-alpha agents could have a crucial role in modifying the impact of lipid profile and glucose levels dysregulation in RA patients. Glucose 105-112 tumor necrosis factor Homo sapiens 17-26 31819571-3 2019 Genetic polymorphism of cytokines like tumor necrosis factor-alpha (TNF-alpha) is suggestive of interference with insulin-sensitive glucose uptake and induces insulin resistance that ultimately could lead to T2DM. Glucose 132-139 tumor necrosis factor Homo sapiens 68-77 31665127-4 2019 MATERIAL AND METHODS Expression of miR-34b, IL-6R, and other key factors of inflammation, apoptosis (TNF-alpha, IL-1ss, IL-6, caspase-3) in high glucose (HG)-induced HK-2 cells were measured by real-time PCR, Western blot, and flow cytometric cell apoptosis assays. Glucose 145-152 tumor necrosis factor Homo sapiens 101-110 31627295-4 2019 At real-time PCR, HT significantly inhibited TNF-alpha-induced mRNA levels, of monocyte chemoattractant protein-1, C-X-C Motif Ligand-10, interleukin (IL)-1beta, IL-6, vascular endothelial growth factor, plasminogen activator inhibitor-1, cyclooxygenase-2, macrophage colony-stimulating factor, matrix metalloproteinase-2, Cu/Zn superoxide dismutase-1, and glutathione peroxidase, as well as surface expression of intercellular adhesion molecule-1, and reverted the TNF-alpha-mediated inhibition of endothelial nitric oxide synthase, peroxisome proliferator-activated receptor coactivator-1alpha, and glucose transporter-4. Glucose 601-608 tumor necrosis factor Homo sapiens 45-54 31229280-10 2019 Co-incubation of high-glucose-treated endothelial cells with milk extracts from group S15 improved cell viability compared with cells treated with high glucose only; it also reduced intracellular lipid peroxidation (144.3 +- 0.4 vs. 177.5 +- 1.9%), reactive oxygen species (141.3 +- 0.9 vs. 189.3 +- 4.7 optical density units), and cytokine release (tumor necrosis factor-alpha, IL-1beta, IL-6). Glucose 22-29 tumor necrosis factor Homo sapiens 332-377 31455007-8 2019 The obtained data implies that glucose-induced insulin secretion (GIS) in pancreatic beta cells is significantly attenuated by IH, and that IH increases selenoprotein P, which is one of the hepatokines, as well as TNF-alpha, CCL-2, and resistin, members of adipokines, to induce insulin resistance via direct cellular mechanisms. Glucose 31-38 tumor necrosis factor Homo sapiens 214-223 29687969-9 2019 CONCLUSIONS: Levels of serum hs-CRP, TNF-alpha and IL-6 are significantly elevated in patients with type 2 DM combined with essential hypertension, which are important factors affecting changes in blood glucose. Glucose 203-210 tumor necrosis factor Homo sapiens 37-46 31462987-10 2019 Besides, high-glucose (25 mM) inhibited HRECs viability and induced oxidative stress, inflammation associated cytokines (TNF-alpha, IL-6 and IL-1beta) secretion and cell apoptosis, which were all reversed by synergistically overexpressing CKIP-1 and aggravated by knocking down CKIP-1. Glucose 14-21 tumor necrosis factor Homo sapiens 121-130 31485188-5 2019 Moreover, we found that the level of glucose in serum was positively correlated with the APACHE II scores, TNF-alpha and CRP. Glucose 37-44 tumor necrosis factor Homo sapiens 107-116 31298304-11 2019 RESULTS: In the presence of high glucose, hRECs cells proliferation was significantly reduced, Caspase-3 activity was enhanced, LDH and ROS levels were increased, SOD activity was declined with increased expression of HMGB-1, NF-kappaB, VEGF, as well as secretion of TNF-alpha and IL-1beta compared with control group (p < 0.05). Glucose 33-40 tumor necrosis factor Homo sapiens 267-276 30512227-8 2019 Finally, lycopene isomers restore the TNF-alpha-blunted uptake of glucose by adipocytes via a modulation of AKT phosphorylation. Glucose 66-73 tumor necrosis factor Homo sapiens 38-47 31061619-1 2019 The aim of this study is to discuss the non-catechin flavonoids (NCF) from Camellia sinensis (L.) O. Kuntze seed improving TNF-alpha impaired insulin stimulated glucose uptake and insulin signaling. Glucose 161-168 tumor necrosis factor Homo sapiens 123-132 31061619-5 2019 Detecting the glucose concentration of medium, insulin decreased the glucose levels of medium meant that insulin promoted glucose uptake into cells, but TNF-alpha inhibited the glucose uptake effect of insulin. Glucose 14-21 tumor necrosis factor Homo sapiens 153-162 30352123-7 2019 In Caco-2 cells, GLUT12 translocation to the apical membrane and alpha-methyl- d-glucose uptake by the transporter are stimulated by protons, glucose, insulin, tumor necrosis factor-alpha (TNF-alpha), protein kinase C, and AMP-activated protein kinase. Glucose 81-88 tumor necrosis factor Homo sapiens 160-187 30352123-7 2019 In Caco-2 cells, GLUT12 translocation to the apical membrane and alpha-methyl- d-glucose uptake by the transporter are stimulated by protons, glucose, insulin, tumor necrosis factor-alpha (TNF-alpha), protein kinase C, and AMP-activated protein kinase. Glucose 81-88 tumor necrosis factor Homo sapiens 189-198 30871567-12 2019 The levels of TNF-a, IL-6, and IL-8 were positively correlated with increases in BMI, serum glucose and cholesterol levels. Glucose 92-99 tumor necrosis factor Homo sapiens 14-19 30569107-7 2019 The present data indicated that, compared with mannitol treatment, high glucose treatment reduced RPEC viability, increased TNF-alpha, IL-6 and IL-1beta secretion, increased ROS formation and promoted phosphorylation of AKT and mTOR. Glucose 72-79 tumor necrosis factor Homo sapiens 124-133 30516514-11 2018 Based on the latest research studies the main component in the big picture of DN formation is hyperglycemia.The list of mechanisms are associated with high glucose level leading inflammation, oxidative stress, hypoxia and apoptosis through the activation of several pathogenic pathways induced by Tumor Necrosis Factor alfa (TNFa), AgII, (pro)renin, Protein Kinase C (PKC), glycolysis intermediated products, Cyclooxygenase 2 (COX2) and reactive nitrogen species (RNS). Glucose 156-163 tumor necrosis factor Homo sapiens 325-329 30260514-7 2018 TNF-alpha-treated adipocytes showed a significant 64% decrease in insulin-stimulated glucose uptake as compared with control cells, whereas infliximab reversed TNF-alpha actions by significantly improving glucose incorporation. Glucose 85-92 tumor necrosis factor Homo sapiens 0-9 30260514-7 2018 TNF-alpha-treated adipocytes showed a significant 64% decrease in insulin-stimulated glucose uptake as compared with control cells, whereas infliximab reversed TNF-alpha actions by significantly improving glucose incorporation. Glucose 205-212 tumor necrosis factor Homo sapiens 160-169 30696869-5 2019 Biochemical parameters were assayed and showed that the shift from normal glucose (NG; 5.5 mM) to high glucose (HG; 25 mM) promoted cell growth and induced oxidative/inflammatory stress and microglial activation, as evidenced by increased MTT reduction, elevated pro-inflammatory factor secretion (i.e., TNF-alpha and oxygen free radicals), and upregulated expression of stress/inflammatory proteins (i.e., HSP70, HO-1, iNOS, and COX-2). Glucose 103-110 tumor necrosis factor Homo sapiens 304-313 29749036-6 2018 Moreover, mRNA expression levels of IL-1beta, TNFalpha, TLR1, and TLR2 in the SDH were positively correlated with plasma glucose concentrations in all monkeys. Glucose 121-128 tumor necrosis factor Homo sapiens 46-54 29752628-7 2018 Moreover, TNF-alpha and Hsp90 in T2DM patients correlated positively with fasting blood glucose (FBG). Glucose 88-95 tumor necrosis factor Homo sapiens 10-19 30143256-7 2018 Furthermore, telmisartan treatment restored the decrease of cellular glucose uptake due to TNFalpha stimulation. Glucose 69-76 tumor necrosis factor Homo sapiens 91-99 30237731-6 2018 After stimulation with LPS, we observed an exacerbated increase in TNF-alpha, IL-6, and MCP-1 concentration in the high glucose condition compared to the normal glucose environment. Glucose 120-127 tumor necrosis factor Homo sapiens 67-76 30237731-7 2018 THP-1 macrophages in high glucose conditions developed tolerance to IL-10 anti-inflammatory effects (TNF-alpha production) when challenged with LPS. Glucose 26-33 tumor necrosis factor Homo sapiens 101-110 30158937-6 2018 High glucose concentration was found to elevate dye uptake, a response that was enhanced by IL-1beta/TNF-alpha. Glucose 5-12 tumor necrosis factor Homo sapiens 101-110 30029058-11 2018 Lastly, we report that humanin treatment inhibited high glucose-induced secretion of tumor necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta). Glucose 56-63 tumor necrosis factor Homo sapiens 85-112 30029058-11 2018 Lastly, we report that humanin treatment inhibited high glucose-induced secretion of tumor necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta). Glucose 56-63 tumor necrosis factor Homo sapiens 114-123 29576769-1 2018 Background: The aim of this study was to investigate the effect of anti-TNF therapy on glucose and lipid metabolism in nondiabetic, nonobese patients with inflammatory bowel disease (IBD). Glucose 87-94 tumor necrosis factor Homo sapiens 72-75 29896271-5 2018 Inhibition of miRNA27a expression also increased the expression of interleukin (IL)-6, IL-1beta, tumor necrosis factor (TNF)-alpha and Toll-like receptor 4 (TLR4) in RPE cells treated with high glucose. Glucose 194-201 tumor necrosis factor Homo sapiens 97-130 29739054-9 2018 The results demonstrated that high-glucose could increase the proinflammatory cytokines, such as tumor necrosis factor alpha (TNF-alpha), interferon-gamma (INF-gamma), and transforming growth factor-beta (TGF-beta), while these effects were reduced when treated with dioscin (p < 0.05). Glucose 35-42 tumor necrosis factor Homo sapiens 97-124 29739054-9 2018 The results demonstrated that high-glucose could increase the proinflammatory cytokines, such as tumor necrosis factor alpha (TNF-alpha), interferon-gamma (INF-gamma), and transforming growth factor-beta (TGF-beta), while these effects were reduced when treated with dioscin (p < 0.05). Glucose 35-42 tumor necrosis factor Homo sapiens 126-135 29587203-4 2018 We found that high glucose induced phosphorylation of Btk, MAPKs and NF-kappaB, and the expression of downstream inflammation cytokines monocyte chemo-attractant protein-1 (MCP-1), tumor necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta). Glucose 19-26 tumor necrosis factor Homo sapiens 181-208 29587203-4 2018 We found that high glucose induced phosphorylation of Btk, MAPKs and NF-kappaB, and the expression of downstream inflammation cytokines monocyte chemo-attractant protein-1 (MCP-1), tumor necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta). Glucose 19-26 tumor necrosis factor Homo sapiens 210-219 29850615-6 2018 Accordingly, the expression of A-FABP and the release of the proinflammatory cytokines TNF-alpha and IL-1beta also increased in response to constant high glucose, an effect that also was more evident in intermittent high glucose. Glucose 154-161 tumor necrosis factor Homo sapiens 87-96 29850615-6 2018 Accordingly, the expression of A-FABP and the release of the proinflammatory cytokines TNF-alpha and IL-1beta also increased in response to constant high glucose, an effect that also was more evident in intermittent high glucose. Glucose 221-228 tumor necrosis factor Homo sapiens 87-96 29996768-10 2018 Long-term high glucose increased the expression of IL-1beta and TNFalpha but reduced the expression of IL-12p40 and nitric oxide production in M1 macrophage. Glucose 15-22 tumor necrosis factor Homo sapiens 64-72 29134442-9 2018 Interestingly, the conditioned media obtained from THP-1 cells grown in the presence of 25 mM glucose was able to induce the secretion of TNF-alpha in human vascular endothelium cell line (HUVEC). Glucose 94-101 tumor necrosis factor Homo sapiens 138-147 30010177-7 2018 A correlation was also noted between the increase in TNF-alpha and DHEA-SO4, FSH, glucose level and total cholesterol. Glucose 82-89 tumor necrosis factor Homo sapiens 53-62 29402837-16 2018 In addition, the results revealed that the expression of CCL5, IL-1beta and TNF-alpha was increased in the high-glucose group, and that the NO produced by HUVECs decreased due to hyperglycemia; however, co-culture with OMT or A2B siRNA abolished these effects. Glucose 112-119 tumor necrosis factor Homo sapiens 76-85 29310812-5 2018 However, TNF-alpha inhibited glucose uptake into cells treated with insulin. Glucose 29-36 tumor necrosis factor Homo sapiens 9-18 29310812-10 2018 In conclusion, this study found that TNF-alpha inhibited insulin stimulated glucose uptake and aggravated related proteins expressions, suggesting that it might cause insulin resistance. Glucose 76-83 tumor necrosis factor Homo sapiens 37-46 29240802-8 2017 Among the inflammatory molecules correlated with s(P)RR in the plasma, TNF-alpha, but not CFD or LRG1, application to retinal endothelial cells upregulated the mRNA expression of (P)RR but not prorenin, while stimulation with high glucose enhanced both (P)RR and prorenin expression. Glucose 231-238 tumor necrosis factor Homo sapiens 71-80 28958848-4 2017 As predicted based on SIRT6 biological roles, the new leads increase histone 3 lysine 9 acetylation and glucose uptake in cultured cells, while blocking TNF-alpha production and T lymphocyte proliferation. Glucose 104-111 tumor necrosis factor Homo sapiens 153-162 28598282-9 2017 Also, high glucose increased TRAF6, interleukin (IL)-6, TNF-alpha, and chemical chemokine ligand (CCL) 2 levels, whereas it decreased IL-10 level. Glucose 11-18 tumor necrosis factor Homo sapiens 56-65 28598282-12 2017 Overexpression of miR-126 significantly abrogated high glucose-induced secretion of proinflammatory cytokines such as IL-6, TNF-alpha, and CCL2 and promoted production of IL-10. Glucose 55-62 tumor necrosis factor Homo sapiens 124-133 28976943-9 2017 High glucose-induced secretion of IL-8, TNF-alpha, ICAM-1, and VCAM-1 was reduced, and translocation of the p65 subunit of NF-kappaB to the endothelial cell nucleus was inhibited by EOFAZ. Glucose 5-12 tumor necrosis factor Homo sapiens 40-49 28304381-5 2017 In the present study, we discovered that TNF-alpha might stimulate PA transcytosis across cardiac microvascular endothelial cells, which further impaired the insulin-stimulated glucose uptake by cardiomyocytes and promoted insulin resistance. Glucose 177-184 tumor necrosis factor Homo sapiens 41-50 27900559-11 2017 Elastic net regression analysis showed that fasting glucose levels and CASP3 predicted increased TNF expression in the post-obese group. Glucose 52-59 tumor necrosis factor Homo sapiens 97-100 28320859-9 2017 Additionally, in human embryonic stem cell-derived cardiomyocytes challenged with TNFalpha or FFA, we demonstrate that 2-AG improves insulin sensitivity and glucose uptake. Glucose 157-164 tumor necrosis factor Homo sapiens 82-90 28535046-4 2017 Piceatannol also partially improved the malfunction of insulin-stimulated glucose uptake, which was reduced by TNF-alpha in 3T3-L1 adipocytes. Glucose 74-81 tumor necrosis factor Homo sapiens 111-120 28278187-7 2017 Resveratrol also significantly restored the defects in the insulin signalling pathway and glucose uptake induced by TNF-alpha, LPS and poly(I:C). Glucose 90-97 tumor necrosis factor Homo sapiens 116-125 28251164-7 2017 TNF-alpha and IL-6 could aggregate peripheral neuropathy in impaired glucose regulation patients; TNF-alpha might be independent risk factor for peripheral neuropathy in glucose regulation impaired patients. Glucose 69-76 tumor necrosis factor Homo sapiens 0-9 28848152-0 2017 Effect of the Diabetic Environment On the Expression of MiRNAs in Endothelial Cells: Mir-149-5p Restoration Ameliorates the High Glucose-Induced Expression of TNF-alpha and ER Stress Markers. Glucose 129-136 tumor necrosis factor Homo sapiens 159-168 28848152-14 2017 The over-expression of miR-149-5p ameliorates the high glucose-induced injury in the HUVECs by regulating the expression of TNF-alpha and ERS markers. Glucose 55-62 tumor necrosis factor Homo sapiens 124-133 28553653-6 2017 Our study revealed several unexpected correlations which are indicative of a much more complex relationship between glucose and lipid factors (namely, glycosylated haemoglobin Hb1Ac, the presence of one but not multiple chronic diabetic complications, and atherogenic indexes) and proinflammatory cytokines (IL-1alpha and TNF-alpha). Glucose 116-123 tumor necrosis factor Homo sapiens 322-331 27931833-4 2016 In addition, poorly regulated glucose metabolism in diabetic patients is often found with increased levels of chronic inflammatory markers, e.g., interleukin (IL)-1beta, IL-6, and tumor necrosis factor (TNF)-alpha, and emerging evidence has highlighted activation of the immune response in the progression and development of cancer cells. Glucose 30-37 tumor necrosis factor Homo sapiens 180-213 27456841-11 2016 CONCLUSIONS: Our findings suggest that TNFA -308G A polymorphism may be an important candidate for BMI, fasting glucose and postprandial TAG response. Glucose 114-121 tumor necrosis factor Homo sapiens 39-43 27569685-7 2016 Finally, we evaluated TNF-alpha effect on glucose uptake in cultured human endometrial stromal cells (T-HESC) treated or not with testosterone/insulin resembling partially the PCOS condition. Glucose 42-49 tumor necrosis factor Homo sapiens 22-31 27569685-11 2016 Finally, TNF-alpha treatment of T-HESC cultures exhibited a decrease of glucose uptake (P<0.05), although similar to cells treated with testosterone or testosterone/insulin/TNF-alpha. Glucose 72-79 tumor necrosis factor Homo sapiens 9-18 27569685-12 2016 CONCLUSIONS: These results suggest that the PCOS condition induces an inflammatory state exacerbated when obesity is present, where a higher TNF-alpha signaling is observed, all of which could affect glucose uptake in the tissue and may cause fertility failures in these women. Glucose 200-207 tumor necrosis factor Homo sapiens 141-150 27664897-2 2016 However, in high-glucose microenvironment, the original inflammation-inhibiting function of MSCs leads to turns into secreting large amounts of inflammatory mediators, such as tumor necrosis factor alpha, for example, which decreases their capacity and becomes poor quality stem cells over inflammation cells for diabetic foot ulcers repair in the healing of diabetic foot ulcers. Glucose 17-24 tumor necrosis factor Homo sapiens 176-203 27664897-7 2016 More importantly, EPO could reduce the damage to MSCs by high-glucose microenvironment, promote their proliferation and migration functions, and inhibit the high-glucose-induced MSCs from secreting the inflammatory mediator tumor necrosis factor alpha. Glucose 162-169 tumor necrosis factor Homo sapiens 224-251 27648010-14 2016 Concomitant TNFalpha and adiponectin exposure blunted adiponectin-induced glucose uptake (11% reduction; p < 0.001). Glucose 74-81 tumor necrosis factor Homo sapiens 12-20 28572933-5 2017 Moreover, ABE exerted anti-insulin resistance activity as it significantly improved the glucose uptake in tumor necrosis factor (TNF)-alpha treated 3T3-L1 adipocytes. Glucose 88-95 tumor necrosis factor Homo sapiens 106-139 27207546-8 2016 Our investigation concludes that vascular smooth muscle cell TNF augments resistance artery myogenic vasoconstriction in a diabetes model that induces a small elevation of blood glucose. Glucose 178-185 tumor necrosis factor Homo sapiens 61-64 27379180-7 2016 By allowing rapid exchange fluxes around the pyruvate node, (13)C-MFA revealed that PANC-1 cells cultured in [U-(13)C6]-glucose doubled the conversion of unlabelled substrates to pyruvate when treated with TNF-alpha. Glucose 120-127 tumor necrosis factor Homo sapiens 206-215 26945994-0 2016 TNF-alpha is upregulated in T2DM patients with fracture and promotes the apoptosis of osteoblast cells in vitro in the presence of high glucose. Glucose 136-143 tumor necrosis factor Homo sapiens 0-9 26976796-7 2016 Under the same conditions, aleglitazar also reversed the TNF-alpha-mediated suppression of insulin-stimulated ser473 Akt phosphorylation and decreased the TNF-alpha-induced ser312 IRS1 phosphorylation, two major switches in insulin-mediated metabolic activities, restoring glucose uptake in insulin-resistant adipocytes. Glucose 273-280 tumor necrosis factor Homo sapiens 57-66 27173229-7 2016 In a high-glucose environment, TLR-2/4 expression was significantly upregulated in RGCs (while their viability decreased); additionally, NF-kappaB expression and secretion of TNF-alpha and IL-8 were significantly increased. Glucose 10-17 tumor necrosis factor Homo sapiens 175-184 26902174-5 2016 Furthermore, LPS-, poly(I:C)- or TNF-alpha-induced insulin resistance was improved following suppression of ER stress, by increasing insulin-stimulated phosphorylation of IR-beta, IRS-1, GLUT-4 expression and glucose uptake. Glucose 209-216 tumor necrosis factor Homo sapiens 33-42 26945994-3 2016 In the present study, we examined the promotion to proinflammatory cytokines and chemokines in type 2 diabetes mellitus (T2DM) patients with bone fractures, and then evaluated the promotion to TNF-alpha by the high glucose treatment in human osteoblast-like MG-63 cells and the regulatory role of the promoted TNF-alpha on the MG-63 cell apoptosis. Glucose 215-222 tumor necrosis factor Homo sapiens 193-202 26945994-5 2016 And the promotion to TNF-alpha and IL-1beta was confirmed in vitro in both mRNA and protein levels in high glucose-treated MG-63 cells. Glucose 107-114 tumor necrosis factor Homo sapiens 21-30 26969461-4 2016 TNF-alpha regulates the secretion of certain peptides which play a crucial role in glucose and lipid homeostasis. Glucose 83-90 tumor necrosis factor Homo sapiens 0-9 27162237-6 2016 When cells were stimulated with tumor necrosis factor-alpha (or high glucose), C242T p22(phox) significantly inhibited tumor necrosis factor-alpha-induced Nox2 maturation, O2 (.-) production, mitogen-activated protein kinases and nuclear factor kappaB activation, and inflammation (all P<0.05). Glucose 69-76 tumor necrosis factor Homo sapiens 119-146 27082844-7 2016 Additionally, T0901317 treatment inhibited nuclear factor-kappaB (NF-kappaB) signaling and the secretion of high glucose-induced proinflammatory mediators, including tumor necrosis factor-alpha and interleukin-1beta in GECs. Glucose 113-120 tumor necrosis factor Homo sapiens 166-193 27026343-0 2016 VIP protects human retinal microvascular endothelial cells against high glucose-induced increases in TNF-alpha and enhances RvD1. Glucose 72-79 tumor necrosis factor Homo sapiens 101-110 27026343-8 2016 RESULTS: High glucose-induced changes in TNF-alpha and RvD1 were restored to control levels with VIP treatment. Glucose 14-21 tumor necrosis factor Homo sapiens 41-50 27156321-7 2016 CONCLUSIONS: Due to the influence of such factors as high glucose levels, hypertension and obesity, schizophrenic patients at risk of MS exhibited elevated levels of TNF-alpha and Hs-CRP, enhanced ventricular myocardial fibrosis, and reduced HRV, which might have resulted from structural changes and autonomic nervous dysfunction in cardiac tissues. Glucose 58-65 tumor necrosis factor Homo sapiens 166-175 26095630-3 2015 In this paper, we evaluated the production of IL-1 beta and TNF, in peripheral blood MO of patients affected by RA or T2D or both diseases, in order to understand if an alteration of the glucose metabolism may influence their proinflammatory status. Glucose 187-194 tumor necrosis factor Homo sapiens 60-63 26997759-8 2016 Overexpression of miR-146a using mimics reduced the levels of TLR4/NF-kappaB and TNFalpha in REC cultured in high glucose. Glucose 114-121 tumor necrosis factor Homo sapiens 81-89 26453924-5 2015 Under high glucose/high lipids (HG/HL), APN-stimulated nitric oxide production by HUVEC was decreased, phosphorylation of eNOS, AMPK, and Akt was attenuated (P<0.01), and APN"s anti-TNFalpha effect was blunted (P<0.01). Glucose 11-18 tumor necrosis factor Homo sapiens 185-193 25427620-4 2015 Even if TNF-alpha is a single player in the great molecular cauldron of inflammation, the use of TNF-alpha inhibitors may be an important approach for not only treating articular and cutaneous symptoms but also for ameliorating glucose and lipid metabolism. Glucose 228-235 tumor necrosis factor Homo sapiens 97-106 27025058-0 2015 INHIBITION OF IRE1 MODIFIES EFFECT OF GLUCOSE DEPRIVATION ON THE EXPRESSION OF TNFalpha-RELATED GENES IN U87 GLIOMA CELLS. Glucose 38-45 tumor necrosis factor Homo sapiens 79-87 26705025-5 2016 High glucose also elevated IL-6 (1.8-fold), IL-1beta (1.9-fold), and TNF-alpha (1.6-fold) level, as well as induced cell apoptosis and NF-kappaB (6.1-fold) activation. Glucose 5-12 tumor necrosis factor Homo sapiens 69-78 26095630-4 2015 Our data showed, after 24 h of incubation with different glucose concentrations, a significantly increased production of IL-1beta and TNF in all evaluated groups when compared with healthy controls. Glucose 57-64 tumor necrosis factor Homo sapiens 134-137 26722449-11 2015 Under high glucose environment, hRECs proliferation increased, TNF-alpha and IL-1beta expression elevated, and NF-kappaB protein level upregulated significantly. Glucose 11-18 tumor necrosis factor Homo sapiens 63-72 26100037-10 2015 In addition, DHE-Glc suppressed TNF-alpha/IFN-gamma-induced expression of the Th2 chemokines CCL17 and CCL22 by inhibiting NF-kappaB and STAT activation in TNF-alpha/IFN-gamma-induced HaCaT cells. Glucose 17-20 tumor necrosis factor Homo sapiens 32-41 26100037-10 2015 In addition, DHE-Glc suppressed TNF-alpha/IFN-gamma-induced expression of the Th2 chemokines CCL17 and CCL22 by inhibiting NF-kappaB and STAT activation in TNF-alpha/IFN-gamma-induced HaCaT cells. Glucose 17-20 tumor necrosis factor Homo sapiens 156-165 26305534-7 2015 The addition of NAC markedly reduced the high glucose-induced ROS activation, Annexin-PI-positive cells, and levels of cleaved caspase-3, BAX, IL-6, and TNF-alpha. Glucose 46-53 tumor necrosis factor Homo sapiens 153-162 25816073-6 2015 Lactate dehydrogenase activity and tumor necrosis factor-alpha mRNA expression were significantly reduced in Muller cells exposed to a high glucose concentration, following agmatine treatment, compared with cells not treated with agmatine. Glucose 140-147 tumor necrosis factor Homo sapiens 35-62 25787249-7 2015 Results of this study indicate that LncRNA MALAT1 regulates glucose-induced up-regulation of inflammatory mediators IL-6 and TNF-alpha through activation of SAA3. Glucose 60-67 tumor necrosis factor Homo sapiens 125-134 26261550-5 2015 Results demonstrated that high glucose promoted the pre-inflammatory cytokines, such as TNF-alpha, IL-1beta and IL-6 in patients with T2DM or in SV40 MES 13 cells. Glucose 31-38 tumor necrosis factor Homo sapiens 88-97 28531388-10 2015 Resistin mRNA expression significantly correlated with changes in HbA1c and TNF-alpha and IL-6 levels, all of which are strongly associated with glucose metabolism and/or inflammation. Glucose 145-152 tumor necrosis factor Homo sapiens 76-85 25675385-2 2015 OBJECTIVE: The objective of the study was to determine whether the infusion of TNF-alpha at high physiological levels impairs GLP-1"s effects on glucose metabolism. Glucose 145-152 tumor necrosis factor Homo sapiens 79-88 26131370-13 2015 High glucose increased reactive oxygen species production and TNFalpha expression levels. Glucose 5-12 tumor necrosis factor Homo sapiens 62-70 26131370-15 2015 In addition, N-acetylcysteine treatment or knockdown of TNFalpha attenuated high glucose-induced sclerostin expression. Glucose 81-88 tumor necrosis factor Homo sapiens 56-64 25725372-3 2015 Here, we demonstrated that high glucose-induced impairment of insulin-stimulated glucose uptake by 3T3-L1 adipocytes was concomitant with decreased tmTNF-alpha expression and increased soluble TNF-alpha (sTNF-alpha) secretion. Glucose 32-39 tumor necrosis factor Homo sapiens 150-159 25714674-3 2015 We determined the relationship between beta-cell function and MNC-derived nuclear factor-kappaB (NF-kappaB) activation and tumor necrosis factor-alpha (TNF-alpha) secretion in response to a 2-h 75-g oral glucose tolerance test (OGTT) in normoglycemic women with PCOS (15 lean, 15 obese) and controls (16 lean, 14 obese). Glucose 204-211 tumor necrosis factor Homo sapiens 123-150 25714674-5 2015 Glucose-stimulated NF-kappaB activation and TNF-alpha secretion from MNC, and fasting plasma thiobarbituric acid-reactive substances (TBARS) and high-sensitivity C-reactive protein (hs-CRP) were also assessed. Glucose 0-7 tumor necrosis factor Homo sapiens 44-53 25651160-7 2015 Moreover, our results showed that tumor necrosis factor-alpha (TNF-alpha) expression in keratinocytes was dose-dependently upregulated by glucose, and TNF-alpha treatment downregulated the expression of TM and TLR4. Glucose 138-145 tumor necrosis factor Homo sapiens 34-61 25651160-7 2015 Moreover, our results showed that tumor necrosis factor-alpha (TNF-alpha) expression in keratinocytes was dose-dependently upregulated by glucose, and TNF-alpha treatment downregulated the expression of TM and TLR4. Glucose 138-145 tumor necrosis factor Homo sapiens 63-72 25651160-8 2015 Taken together, high-glucose environment reduces the expression of TM and TLR4 in keratinocytes possibly through the action of TNF-alpha, and recombinant sTM can increase the TLR4 expression and promote wound healing under diabetic condition. Glucose 21-28 tumor necrosis factor Homo sapiens 127-136 25796348-0 2015 Locally controlled delivery of TNFalpha antibody from a novel glucose-sensitive scaffold enhances alveolar bone healing in diabetic conditions. Glucose 62-69 tumor necrosis factor Homo sapiens 31-39 25796348-3 2015 Herein, we report a glucose-sensitive TNFalpha-antibody-delivery system based on quaternized chitosan and collagen for local long-term control of inflammation and improving osteogenesis in diabetes. Glucose 20-27 tumor necrosis factor Homo sapiens 38-46 25710281-8 2015 TNF-alpha increased myotube glucose uptake and lactate production and enhanced the activity and expression levels of multiple effectors of muscle glycolytic metabolism in a NF-kappaB-dependent manner. Glucose 28-35 tumor necrosis factor Homo sapiens 0-9 25922828-9 2015 RESULTS: Serum glucose was positively correlated with beta2M and TNF-alpha (r = 0.320, p = 0.002 and r = 0.215, p = 0.03 respectively).We observed significant association between the patients with higher serum glucose concentrations and the patients with greater beta2Mu concentrations (x(2) = 4.44, p = 0.03). Glucose 15-22 tumor necrosis factor Homo sapiens 65-74 25922828-9 2015 RESULTS: Serum glucose was positively correlated with beta2M and TNF-alpha (r = 0.320, p = 0.002 and r = 0.215, p = 0.03 respectively).We observed significant association between the patients with higher serum glucose concentrations and the patients with greater beta2Mu concentrations (x(2) = 4.44, p = 0.03). Glucose 210-217 tumor necrosis factor Homo sapiens 65-74 24512496-0 2014 Hyperandrogenism induces a proinflammatory TNFalpha response to glucose ingestion in a receptor-dependent fashion. Glucose 64-71 tumor necrosis factor Homo sapiens 43-51 25222109-10 2015 TNF-alpha may be involved in high glucose-induced renal tubular damage in HK2 cells possibly via AT1 receptor signaling. Glucose 34-41 tumor necrosis factor Homo sapiens 0-9 25078146-12 2014 In response to glucose ingestion, MNC-derived TNFalpha, IL-6, and IL-1beta release decreased in both normal-weight control groups but failed to suppress in either normal-weight PCOS group and in obese women regardless of PCOS status. Glucose 15-22 tumor necrosis factor Homo sapiens 46-54 25320679-8 2014 The glycolytic inhibitor iodoacetate prevented both butyrate- and tumor necrosis factor-alpha-(TNF-alpha) mediated increases in rates of lipolysis indicating glucose metabolism is required. Glucose 158-165 tumor necrosis factor Homo sapiens 95-104 25180167-1 2014 AIMS: Sphingolipid and oxidant signaling affect glucose uptake, atrophy, and force production of skeletal muscle similarly and both are stimulated by tumor necrosis factor (TNF), suggesting a connection between systems. Glucose 48-55 tumor necrosis factor Homo sapiens 173-176 25375979-3 2015 OBJECTIVE: To define differential effects of TNF-alpha on glucose, protein, and lipid metabolism in hypopituitary patients (without intact hypothalamo-pituitary axis) and healthy controls. Glucose 58-65 tumor necrosis factor Homo sapiens 45-54 25375979-8 2015 Endogenous glucose production (EGP) was elevated in CTR compared to HP after TNF-alpha administration, whereas insulin sensitivity remained similarly unaffected in both groups. Glucose 11-18 tumor necrosis factor Homo sapiens 77-86 25111421-6 2015 But, TNF-alpha levels increased significantly in the GDM (p < 0.0001) and in glucose intolerance (p = 0.0062) groups as compared with the control group. Glucose 80-87 tumor necrosis factor Homo sapiens 5-14 25222109-0 2015 Possible roles of tumor necrosis factor-alpha and angiotensin II type 1 receptor on high glucose-induced damage in renal proximal tubular cells. Glucose 89-96 tumor necrosis factor Homo sapiens 18-45 25222109-6 2015 High glucose treatment (30 mM) significantly increased NAG release, TNF-alpha/angiotensin II concentrations in cell media and p22(phox) protein levels compared with those in regular glucose medium (5.6 mM). Glucose 5-12 tumor necrosis factor Homo sapiens 68-77 25222109-8 2015 In addition, significant decreases of NAG release, TNF-alpha concentrations and p22(phox) protein levels in HK2 cells were observed in high glucose-treated group with thalidomide. Glucose 140-147 tumor necrosis factor Homo sapiens 51-60 25765663-4 2015 RESULTS: Inflammatory cytokines (TNF-alpha and interferon-gamma) cooperate with bioincompatible PD fluids containing high glucose degradation product (GDP) concentrations to promote mesothelial cell death. Glucose 122-129 tumor necrosis factor Homo sapiens 33-42 25150534-4 2014 RESULTS: High concentrations of glucose increased the production of pro-inflammatory cytokines interleukin-1 beta (IL-1beta), tumour necrosis factor alpha (TNF-alpha), Interleukin-6 (IL-6) at both mRNA and protein levels, and receptor activator of NF-kB ligand (RANKL) at mRNA levels in hPDL cells. Glucose 32-39 tumor necrosis factor Homo sapiens 156-165 25247624-8 2014 Of particular interest is that the glucose unit promotes the generation of TNF-alpha. Glucose 35-42 tumor necrosis factor Homo sapiens 75-84 25182190-7 2014 In vitro, high glucose induced the over-expression of miR-155 and miR-146a in the HRGECs, which, in turn, increased the TNF-alpha, TGF-beta1, and NF-kappaB expression. Glucose 15-22 tumor necrosis factor Homo sapiens 120-129 25109718-10 2014 sE-selectin correlated with BMI, triglycerides and VLDL cholesterol, whereas TNF-alpha correlated with fasting plasma glucose. Glucose 118-125 tumor necrosis factor Homo sapiens 77-86 24517151-0 2014 TNFalpha dynamics during the oral glucose tolerance test vary according to the level of insulin resistance in pregnant women. Glucose 34-41 tumor necrosis factor Homo sapiens 0-8 23835341-6 2013 During the clamp, TNF-alpha perfusion increased glucose arteriovenous differences (0.91 +- 0.17 vs. 0.74 +- 0.15 mmol/L, P = 0.012) and leg glucose uptake rates. Glucose 48-55 tumor necrosis factor Homo sapiens 18-27 25605194-11 2014 CONCLUSIONS: The glucose fluctuation of patients undergoing intracranial excision is related to postoperative IL-6, TNF-alpha and CRP levels and those with small range of glucose fluctuation have better prognosis. Glucose 17-24 tumor necrosis factor Homo sapiens 116-125 24420848-7 2014 After 12 h-incubation, MET significantly inhibited the increase of MDA, TNF-alpha, LDH and CK levels induced by high glucose, especially at the 5 x 10(-5) to 10(-4 )mol/L concentrations while inhibiting the decrease of SOD level. Glucose 117-124 tumor necrosis factor Homo sapiens 72-81 24692847-0 2014 The acute effects of low-dose TNF-alpha on glucose metabolism and beta-cell function in humans. Glucose 43-50 tumor necrosis factor Homo sapiens 30-39 23625043-6 2013 RESULTS: Periodic high glucose caused a more intense inflammatory response than normal glucose and constant high glucose in HCAECs, with a marked increase in IL-6, TNF-alpha and ICAM-1 in supernatants of cell culture (P < 0.05). Glucose 23-30 tumor necrosis factor Homo sapiens 164-173 23651848-6 2013 Our data reveal that sTWEAK ameliorates TNF-alpha-induced insulin resistance on glucose uptake, GLUT4 translocation and insulin signaling without affecting other metabolic effects of TNF-alpha such as lipolysis or apoptotis. Glucose 80-87 tumor necrosis factor Homo sapiens 40-49 24114113-8 2013 The 12 week fall in fasting glucose was significantly related to baseline lymphocyte and T lymphocyte numbers, and to granulocyte activation, but also to the magnitude of the 12 week reduction in lymphocyte and T lymphocyte numbers and TNF-alpha levels. Glucose 28-35 tumor necrosis factor Homo sapiens 236-245 23661584-6 2013 Upon glucose starvation, MCF7 cells treated with TNF-alpha demonstrated significantly lower viability than nontreated cells. Glucose 5-12 tumor necrosis factor Homo sapiens 49-58 23831394-5 2013 Troglitazone (10 muM) and L-165,041 (1 muM) significantly inhibited high glucose (25mM)-induced interleukin-6 and TNF-alpha production, RAGE expression and NF-kappaB translocation in HEK cells. Glucose 73-80 tumor necrosis factor Homo sapiens 114-123 23080424-5 2013 We found that treatment of 3T3-L1 adipocytes with TNF-alpha leads to deficiency in insulin-stimulated glucose consumption and uptake and increase in endogenous H2 S generation. Glucose 102-109 tumor necrosis factor Homo sapiens 50-59 23866118-0 2013 TNFalpha and IL-17 cooperatively stimulate glucose metabolism and growth factor production in human colorectal cancer cells. Glucose 43-50 tumor necrosis factor Homo sapiens 0-8 23369747-6 2013 KEY FINDINGS: Compared with the normal glucose group, exposure of HUVECs to 50 mmol/L of glucose or 1000 mug/L of LPS significantly increased the concentrations of TNF-alpha and IL-6 in the culture supernatants. Glucose 89-96 tumor necrosis factor Homo sapiens 164-173 23780308-4 2013 EGCG inhibited high glucose(HG)-induced TNF-alpha and IL-6 production in human embryonic kidney (HEK) cells. Glucose 20-27 tumor necrosis factor Homo sapiens 40-49 24426199-6 2013 TNF-alpha levels were significantly higher in NAFLD patients compared to control subjects with a significant positive correlation with body mass index and fasting blood glucose (FBG) but with negative correlation with IL-10. Glucose 169-176 tumor necrosis factor Homo sapiens 0-9 23480316-3 2013 We sought to determine whether first trimester adiponectin and tumor necrosis factor-alpha (TNF)-alpha concentrations were independently associated and predictive of maternal glucose tolerance, as measured by the 1-hour glucose challenge test (GCT), after adjustment for maternal lifestyle behaviors and body mass index (BMI). Glucose 175-182 tumor necrosis factor Homo sapiens 63-90 23480316-3 2013 We sought to determine whether first trimester adiponectin and tumor necrosis factor-alpha (TNF)-alpha concentrations were independently associated and predictive of maternal glucose tolerance, as measured by the 1-hour glucose challenge test (GCT), after adjustment for maternal lifestyle behaviors and body mass index (BMI). Glucose 175-182 tumor necrosis factor Homo sapiens 92-102 22409372-7 2013 RESULTS: IL-6, TNF-alpha and hs-CRP were significantly and positively correlated with fasting plasma glucose (FPG), insulin and HOMA-IR. Glucose 101-108 tumor necrosis factor Homo sapiens 15-24 21212994-8 2013 TNF-alpha (10 ng/ml) increased ERK1/2 levels 1.76 +- 0.23-fold (P < 0.01) after 25 mmol/l glucose pretreatment, but added glucose did not enhance ERK1/2 activation when given subsequent to TNF-alpha treatment. Glucose 93-100 tumor necrosis factor Homo sapiens 0-9 23383064-5 2013 In human adipocytes, we show that IGFBP-3 inhibits TNF-alpha-induced NF-kappaB activity in an IGF-independent manner, thereby restoring the deregulated insulin signaling and negating TNF-alpha-induced inhibition of glucose uptake. Glucose 215-222 tumor necrosis factor Homo sapiens 51-60 22884000-5 2013 After the preparation of the immunosensor based on the traditional sandwich protocol, the response of the immunosensor towards glucose was used as a signal to differentiate various concentrations of TNF-alpha. Glucose 127-134 tumor necrosis factor Homo sapiens 199-208 22566008-5 2013 Tocotrienols are well known for their apoptotic effect on tumor cells; nevertheless, an attempt was made to study glucose uptake in HEP-G2 cells, which needs to induce an insulin-resistant state by TNF-alpha. Glucose 114-121 tumor necrosis factor Homo sapiens 198-207 23484124-5 2013 The subsequent addition of high glucose significantly upregulated resistin and TNF- alpha mRNA and protein secretion, while it did not have any effect on IL-6 or IL-1 beta production. Glucose 32-39 tumor necrosis factor Homo sapiens 79-89 23383064-5 2013 In human adipocytes, we show that IGFBP-3 inhibits TNF-alpha-induced NF-kappaB activity in an IGF-independent manner, thereby restoring the deregulated insulin signaling and negating TNF-alpha-induced inhibition of glucose uptake. Glucose 215-222 tumor necrosis factor Homo sapiens 183-192 20449757-8 2012 A significant interaction (P = 0.011) was observed between the effects of plasma glucose and group for intracellular expression of TNF-alpha in stimulated pDCs. Glucose 81-88 tumor necrosis factor Homo sapiens 131-140 23176569-8 2012 After intervention, only variant allele carriers of the TNF-alpha -308 G/A decreased plasma glucose, after adjusting for age and gender (OR 2.96, p = 0.025). Glucose 92-99 tumor necrosis factor Homo sapiens 56-65 23176569-11 2012 CONCLUSION: The TNFalpha -308 G/A SNP may predispose a better response of glucose metabolism to lifestyle intervention. Glucose 74-81 tumor necrosis factor Homo sapiens 16-24 23026048-5 2012 Also, high glucose increased nuclear factor kappa B (NF-kappaB) p65 nuclear activity, tumor necrosis factor-alpha (TNF-alpha) and interleukin-lbeta (IL-1beta) levels. Glucose 11-18 tumor necrosis factor Homo sapiens 86-113 23026048-5 2012 Also, high glucose increased nuclear factor kappa B (NF-kappaB) p65 nuclear activity, tumor necrosis factor-alpha (TNF-alpha) and interleukin-lbeta (IL-1beta) levels. Glucose 11-18 tumor necrosis factor Homo sapiens 115-124 23026048-8 2012 Collectively, these data suggest that high glucose stimulates TNF-alpha and IL-1beta secretion via inducing TLR2 through PKC-alpha and PKC-delta in human gingival fibroblasts. Glucose 43-50 tumor necrosis factor Homo sapiens 62-71 22943853-3 2012 In present study, we investigated the effect of spinasterol-Glc on production of TARC/CCL17 induced by TNF-alpha and IFN-gamma in human HaCaT keratinocytes. Glucose 60-63 tumor necrosis factor Homo sapiens 103-112 22943853-4 2012 Spinasterol-Glc inhibited the mRNA and protein expression of TARC/CCL17 induced by TNF-alpha/IFN-gamma in a dose-dependent manner. Glucose 12-15 tumor necrosis factor Homo sapiens 83-92 22575517-0 2012 High glucose increases the expression of proinflammatory cytokines and secretion of TNFalpha and beta-hexosaminidase in human mast cells. Glucose 5-12 tumor necrosis factor Homo sapiens 84-92 23027940-2 2012 Using nuclear factor-kappaB (NF-kappaB) as a glucose-responsive transcription factor, we show that cells use the hexosamine biosynthesis pathway and O-linked beta-N-acetylglucosamine (O-GlcNAc) transferase (OGT) to potentiate gene expression in response to tumor necrosis factor (TNF) or etoposide. Glucose 45-52 tumor necrosis factor Homo sapiens 257-278 23027940-2 2012 Using nuclear factor-kappaB (NF-kappaB) as a glucose-responsive transcription factor, we show that cells use the hexosamine biosynthesis pathway and O-linked beta-N-acetylglucosamine (O-GlcNAc) transferase (OGT) to potentiate gene expression in response to tumor necrosis factor (TNF) or etoposide. Glucose 45-52 tumor necrosis factor Homo sapiens 280-283 22476617-9 2012 HepG2 cells incubated with 40 muM Fe alone or Fe/glucose and challenged with IL-6 and/or CoCl(2) showed increased IL-6, NF-kappaB, and TNF-alpha mRNA expression and decreased mRNA expression of Mfn-2 in all experimental conditions. Glucose 49-56 tumor necrosis factor Homo sapiens 135-144 22780915-8 2012 The profiles of cytokine gene expression in peripheral blood were set: a positive correlation between glucose and MCSF, HMOX1 or TNFalpha were found. Glucose 102-109 tumor necrosis factor Homo sapiens 129-137 22575517-6 2012 High glucose increased the secretion of TNFalpha by unstimulated HMC-1 cells and IgE crosslinking-stimulated LAD2 cells. Glucose 5-12 tumor necrosis factor Homo sapiens 40-48 22575517-7 2012 High glucose increased the phosphorylation of extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), and p38 mitogen-activated protein kinases (MAPKs), which regulate the expression of TNFalpha and other inflammatory cytokines, in both HMC-1 and LAD2 cells. Glucose 5-12 tumor necrosis factor Homo sapiens 206-214 22575517-8 2012 Thus, high glucose increased the expression of proinflammatory and proallergic cytokines, the secretion of TNFalpha, and beta-hexosaminidase activity in human mast cells. Glucose 11-18 tumor necrosis factor Homo sapiens 107-115 23156724-0 2012 [Research of the mechanism for high glucose induced glomerular mesangial cell express TNF-alpha]. Glucose 36-43 tumor necrosis factor Homo sapiens 86-95 22397368-0 2012 Postchallenge responses of nitrotyrosine and TNF-alpha during 75-g oral glucose tolerance test are associated with the presence of coronary artery diseases in patients with prediabetes. Glucose 72-79 tumor necrosis factor Homo sapiens 45-54 22522145-0 2012 Contribution of TNF receptor 1 to retinal neural cell death induced by elevated glucose. Glucose 80-87 tumor necrosis factor Homo sapiens 16-19 22522145-3 2012 Since tumor necrosis factor-alpha (TNF-alpha) has been shown to trigger the death of perycites and endothelial cells as well as the breakdown of the blood-retinal barrier, we set out to investigate whether TNF-alpha acting through tumor necrosis factor receptor 1 (TNFR1), the major receptor responsible for mediating TNF-induced cell death, could also be responsible for the early neuronal cell death observed in DR. We used retinal neural cell cultures exposed to high glucose conditions, to mimic hyperglycaemia, and evaluated the contribution of TNFR1 in neural cell death. Glucose 471-478 tumor necrosis factor Homo sapiens 35-44 22522145-8 2012 In conclusion, our data indicate that TNF-alpha acting through TNFR1 is responsible for the high glucose-induced cell death and that blocking the activity of this receptor is an adequate strategy to avoid cell loss in such conditions. Glucose 97-104 tumor necrosis factor Homo sapiens 38-47 22536561-5 2012 TNF-alpha and IL-6 levels were also correlated with fasting plasma glucose of obese and nonobese diabetic patients after insulin therapy. Glucose 67-74 tumor necrosis factor Homo sapiens 0-9 22266116-8 2012 Data indicate that high glucose culturing conditions significantly increase TNFalpha and SOCS3 protein levels. Glucose 24-31 tumor necrosis factor Homo sapiens 76-84 22500980-0 2012 High glucose concentrations induce TNF-alpha production through the down-regulation of CD33 in primary human monocytes. Glucose 5-12 tumor necrosis factor Homo sapiens 35-44 22500980-9 2012 Furthermore, the down-regulation of CD33 and increase in TNF-alpha production were prevented when monocytes were treated with the antioxidant alpha-tocopherol and cultured under high glucose conditions. Glucose 183-190 tumor necrosis factor Homo sapiens 57-66 22178787-5 2012 Glucose-stimulated TNFalpha release from MNC along with molecular markers of inflammation are associated with insulin resistance in PCOS. Glucose 0-7 tumor necrosis factor Homo sapiens 19-27 22045316-6 2012 Compared with placebo, DHEA administration raised levels of testosterone, androstenedione, and DHEA-S, increased the percent change in fasting and glucose-challenged activated NF-kappaB, p65, p105, TNFalpha, and IL-1beta RNA and p65 protein, and decreased the percent change in fasting and glucose-challenged IkappaB protein. Glucose 147-154 tumor necrosis factor Homo sapiens 198-206 22238388-5 2012 RESULTS: Compared with those with normal glucose tolerance, circulating levels of TNF-alpha were elevated in individuals with impaired glucose tolerance (IGT) and type 2 diabetes mellitus (T2D) after adjusting for age, gender, ethnicity, clinic site, and body mass index (3.3, 3.5, and 3.7 pg/ml in subjects with normal glucose tolerance, IGT, and T2D, respectively; P<0.05). Glucose 41-48 tumor necrosis factor Homo sapiens 82-91 22238388-5 2012 RESULTS: Compared with those with normal glucose tolerance, circulating levels of TNF-alpha were elevated in individuals with impaired glucose tolerance (IGT) and type 2 diabetes mellitus (T2D) after adjusting for age, gender, ethnicity, clinic site, and body mass index (3.3, 3.5, and 3.7 pg/ml in subjects with normal glucose tolerance, IGT, and T2D, respectively; P<0.05). Glucose 135-142 tumor necrosis factor Homo sapiens 82-91 21234613-0 2012 Relationships between serum adiponectin and soluble TNF-alpha receptors and glucose and lipid oxidation in lean and obese subjects. Glucose 76-83 tumor necrosis factor Homo sapiens 52-61 21234613-11 2012 Our data suggest that soluble TNF-alpha receptors and adiponectin have multiple effects on glucose and lipid metabolism in obesity. Glucose 91-98 tumor necrosis factor Homo sapiens 30-39 21637955-9 2012 Taken together, these data demonstrate the role of AR in regulating iNOS expression induced by TNF-alpha in cultured HMC, indicating the novel function of AR in glomerulonephritis besides glucose metabolism. Glucose 188-195 tumor necrosis factor Homo sapiens 95-104 21928330-8 2012 Similarly, glycation of HDL in vitro impaired its ability to inhibit TNF-alpha and IL-1beta release in a glucose dose-dependent manner. Glucose 105-112 tumor necrosis factor Homo sapiens 69-78 21902468-9 2012 Importantly, TNF-alpha inhibited glucose uptake, an indication of the metabolic activity of the tissue. Glucose 33-40 tumor necrosis factor Homo sapiens 13-22 22234148-3 2012 CASE PRESENTATION: We report nine cases of non-diabetic Caucasian women who were between 29 and 68 years of age and who developed low glucose readings after treatment with tumor necrosis factor-alpha inhibitors. Glucose 134-141 tumor necrosis factor Homo sapiens 172-199 22035595-7 2012 The association between TNF-alpha, however, was attenuated when comparisons were performed based on glucose control. Glucose 100-107 tumor necrosis factor Homo sapiens 24-33 21366510-7 2012 RESULTS: In-vitro hyperglycemia induced a dose-dependent increase of IL-8 in all age groups while TNF-alpha was demonstrated to be stimulated by glucose in cord blood samples of preterm infants <=32 weeks of gestational age and term infants. Glucose 145-152 tumor necrosis factor Homo sapiens 98-107 22110065-6 2011 RESULTS: TNF-alpha-only treatments of Muller cells resulted in significant decreases of tyrosine phosphorylation of the insulin receptor and Akt in high-glucose conditions. Glucose 153-160 tumor necrosis factor Homo sapiens 9-18 22012292-4 2011 Prevalence ratios for glucose intolerance and diabetes across allelic variants of IL-6 and TNF-alpha did not associate IL-6 with unbalanced glucose levels, despite adjustment for BMI, age, and conicity index. Glucose 22-29 tumor necrosis factor Homo sapiens 91-100 21905824-8 2011 The regulatory effects of BTM-0512 on high glucose-induced changes in vascular endothelial growth factor mRNA expression and tumor necrosis factor-alpha release were also abolished by splitomicin. Glucose 43-50 tumor necrosis factor Homo sapiens 125-152 21905824-9 2011 The results suggest that BTM-0512 exerts beneficial effects on high glucose-induced endothelial cell dysfunction through regulation of the SIRT1 - reactive oxygen species - vascular endothelial growth factor - tumor necrosis factor-alpha pathway. Glucose 68-75 tumor necrosis factor Homo sapiens 210-237 21813649-10 2011 Together, these data demonstrate that TNF-alpha-mediated insulin resistance of glucose uptake can occur through a MEK/Erk-dependent activation of CDK5. Glucose 79-86 tumor necrosis factor Homo sapiens 38-47 21905824-5 2011 We found that high glucose significantly impaired the function of endothelial cells as shown by reduced tube formation, cell migration, and cell adhesion concomitantly with downregulation of mRNA expression of SIRT1 and vascular endothelial growth factor as well as increased tumor necrosis factor-alpha release and reactive oxygen species production. Glucose 19-26 tumor necrosis factor Homo sapiens 276-303 21461612-4 2011 After 10 ng/ml TNF-alpha treatment for 24 h, insulin-stimulated glucose uptake was reduced by 47% in 3T3-L1 adipocytes. Glucose 64-71 tumor necrosis factor Homo sapiens 15-24 21816064-8 2011 High glucose increased TNF-alpha production by HCAECs and exogenous TNF-alpha up-regulated TNF-R1 and Fas expression in HCAECs. Glucose 5-12 tumor necrosis factor Homo sapiens 23-32 21816064-9 2011 High glucose-induced up-regulation of TNF-R1 and Fas expression was undetectable in the presence of TNF-alpha. Glucose 5-12 tumor necrosis factor Homo sapiens 100-109 21816064-12 2011 CONCLUSIONS: In association with increased TNF-alpha levels, the death receptors, TNF-R1 and Fas, are up-regulated in HCAECs under high glucose conditions, which could in turn play a role in high glucose-induced endothelial cell apoptosis. Glucose 136-143 tumor necrosis factor Homo sapiens 43-52 21816064-12 2011 CONCLUSIONS: In association with increased TNF-alpha levels, the death receptors, TNF-R1 and Fas, are up-regulated in HCAECs under high glucose conditions, which could in turn play a role in high glucose-induced endothelial cell apoptosis. Glucose 196-203 tumor necrosis factor Homo sapiens 43-52 21709287-0 2011 Does therapy with anti-TNF-alpha improve glucose tolerance and control in patients with type 2 diabetes? Glucose 41-48 tumor necrosis factor Homo sapiens 23-32 21567299-9 2011 TNF-alpha alone did not induce beta cell death, but did abrogate preproinsulin precursor mRNA synthesis in response to high glucose stimulation, which was inversely associated with upregulation of BBC3 mRNA expression by TNF-alpha. Glucose 124-131 tumor necrosis factor Homo sapiens 0-9 21886908-6 2011 In addition, plasma glucose level showed significant positive correlation with hydrogen peroxide, malondialdehyde, tumor necrosis factor-alpha and interleukin-6. Glucose 20-27 tumor necrosis factor Homo sapiens 115-142 20034685-8 2011 In addition, combined treatment with atorvastatin and metformin reduces the post-glucose loading levels of TNF-alpha compared to metformin monotherapy. Glucose 81-88 tumor necrosis factor Homo sapiens 107-116 22041269-7 2011 (3) High glucose increased the FN, CTGF, TNFalpha protein secretion of HMCs in a time-dependent manner, but normal glucose and mannitol had no such effect. Glucose 9-16 tumor necrosis factor Homo sapiens 41-49 21756816-9 2011 CONCLUSION: The levels of FN, CTGF and TNF-alpha in high glucose-induced HMC may be lowered by inhibiting RhoA through RNA interference and reducing the accumulation of extracellular matrix, glomerular fibrosis and inflammation. Glucose 57-64 tumor necrosis factor Homo sapiens 39-48 21393240-7 2011 Strikingly, S-nitrosylation of Syntaxin 4 could be induced by acute treatment with inflammatory cytokines (TNFalpha, IL-1beta, and IFNgamma), coordinate with inappropriate Syntaxin 4 activation and insulin release in the absence of the glucose stimulus, consistent with nitrosative stress and dysfunctional exocytosis, preceding the cell dysfunction and death associated with more chronic stimulation (24 h). Glucose 236-243 tumor necrosis factor Homo sapiens 107-115 21238462-2 2011 DIF derivatives exhibit antiproliferative activities and promote glucose consumption in mammalian cells in vitro. Glucose 65-72 tumor necrosis factor Homo sapiens 0-3 21063745-5 2011 RESULTS: Activation of monocytes was most pronounced in the fluctuating glucose conditions, as measured by concentrations of IL-6 and TNF-alpha in cultured supernatants and surface expression of CD11b in monocytes (P < 0.05). Glucose 72-79 tumor necrosis factor Homo sapiens 134-143 21542902-13 2011 HBO increased glucose uptake in human CAECs as HBO and visfatin siRNA and TNF-alpha antibody attenuated the glucose uptake induced by HBO. Glucose 108-115 tumor necrosis factor Homo sapiens 74-83 21355310-0 2011 [Influence of high glucose and mannose binding lectin complement pathway activation to IL-6 and TNF-alpha"s expression by human renal glomerular endothelial cells]. Glucose 19-26 tumor necrosis factor Homo sapiens 96-105 20382011-7 2011 Finally, GPE prevented TNFalpha-induced expression of protein tyrosine phosphatase (PTP)-1B and phosphorylation of serine residue 307 of insulin receptor substrate-1 (IRS-1), which are negative regulators of insulin sensitivity, and suppression of insulin-stimulated glucose uptake. Glucose 267-274 tumor necrosis factor Homo sapiens 23-31 21047923-0 2011 TNF-alpha antagonism with etanercept decreases glucose and increases the proportion of high molecular weight adiponectin in obese subjects with features of the metabolic syndrome. Glucose 47-54 tumor necrosis factor Homo sapiens 0-9 21355310-1 2011 OBJECTIVE: To investigate the effect of high glucose and mannose binding lectin (MBL) complement pathway activation"s effect on expression of Interleukin-6 (IL-6) and Tumor necrosis factor-alpha (TNF-alpha) from human renal glomerular endothelial cells (HRGEC), to explore unknown pathogenesy of diabetic nephropathy. Glucose 45-52 tumor necrosis factor Homo sapiens 167-194 21355310-1 2011 OBJECTIVE: To investigate the effect of high glucose and mannose binding lectin (MBL) complement pathway activation"s effect on expression of Interleukin-6 (IL-6) and Tumor necrosis factor-alpha (TNF-alpha) from human renal glomerular endothelial cells (HRGEC), to explore unknown pathogenesy of diabetic nephropathy. Glucose 45-52 tumor necrosis factor Homo sapiens 196-205 21355310-8 2011 RESULTS: Compared with normal glucose group and manicol group, the mRNA and protein expression of IL-6 and TNF-alpha in high glucose group were increased (P < 0.05). Glucose 30-37 tumor necrosis factor Homo sapiens 107-116 21355310-8 2011 RESULTS: Compared with normal glucose group and manicol group, the mRNA and protein expression of IL-6 and TNF-alpha in high glucose group were increased (P < 0.05). Glucose 125-132 tumor necrosis factor Homo sapiens 107-116 21355310-10 2011 Compared with single high glucose group, the mRNA and protein expression of IL-6 and TNF-alpha in high glucose+ MBL group were significantly higher (P < 0.05). Glucose 26-33 tumor necrosis factor Homo sapiens 85-94 21355310-10 2011 Compared with single high glucose group, the mRNA and protein expression of IL-6 and TNF-alpha in high glucose+ MBL group were significantly higher (P < 0.05). Glucose 103-110 tumor necrosis factor Homo sapiens 85-94 21197110-4 2010 Age-related factors contributing to glucose intolerance, which may be improved with RT, include improvements in insulin signaling defects, reductions in tumor necrosis factor-alpha, increases in adiponectin and insulin-like growth factor-1 concentrations, and reductions in total and abdominal visceral fat. Glucose 36-43 tumor necrosis factor Homo sapiens 153-180 20943792-12 2010 Quercetin prevented the TNF-alpha-mediated serine phosphorylation of insulin receptor substrate-1 and protein tyrosine phosphatase-1B gene expression and the suppression of insulin-stimulated glucose uptake, whereas trans-RSV prevented only the TNF-alpha-mediated serine phosphorylation of insulin receptor substrate-1. Glucose 192-199 tumor necrosis factor Homo sapiens 24-33 21151899-4 2010 METHODOLOGY/PRINCIPAL FINDINGS: High glucose and hyperglycemia reduced upregulation of the NF-kappaB inhibitory and atheroprotective protein A20 in human coronary endothelial (EC) and smooth muscle cell (SMC) cultures challenged with Tumor Necrosis Factor alpha (TNF), aortae of diabetic mice following Lipopolysaccharide (LPS) injection used as an inflammatory insult and in failed vein-grafts of diabetic patients. Glucose 37-44 tumor necrosis factor Homo sapiens 234-261 21151899-4 2010 METHODOLOGY/PRINCIPAL FINDINGS: High glucose and hyperglycemia reduced upregulation of the NF-kappaB inhibitory and atheroprotective protein A20 in human coronary endothelial (EC) and smooth muscle cell (SMC) cultures challenged with Tumor Necrosis Factor alpha (TNF), aortae of diabetic mice following Lipopolysaccharide (LPS) injection used as an inflammatory insult and in failed vein-grafts of diabetic patients. Glucose 37-44 tumor necrosis factor Homo sapiens 263-266 20582713-5 2010 RESULTS: Treatment with 50 mmol/L glucose markedly increased the level of IL-1beta, IL-18, TNF-alpha, PGE2, NO, TGF-beta1, MCP-1, MIP-1alpha, and RANTES. Glucose 34-41 tumor necrosis factor Homo sapiens 91-100 20638299-0 2010 Effects of anti-TNF therapy on glucose metabolism in patients with ankylosing spondylitis, psoriatic arthritis or juvenile idiopathic arthritis. Glucose 31-38 tumor necrosis factor Homo sapiens 16-19 20510806-8 2010 Tumor necrosis factor-alpha concentrations were significantly lower for samples incubated at higher glucose concentrations (179 +/- 50 pg/mL, 125 +/- 30 pg/mL, and 107 +/- 29 pg/mL; p < 0.05). Glucose 100-107 tumor necrosis factor Homo sapiens 0-27 20208423-4 2010 We investigated the effects of SAM on the glucose transport and insulin signaling impaired by the tumor necrosis factor alpha (TNFalpha) in 3T3-L1 adipocytes. Glucose 42-49 tumor necrosis factor Homo sapiens 98-125 20208423-4 2010 We investigated the effects of SAM on the glucose transport and insulin signaling impaired by the tumor necrosis factor alpha (TNFalpha) in 3T3-L1 adipocytes. Glucose 42-49 tumor necrosis factor Homo sapiens 127-135 20208423-5 2010 SAM partially reversed the basal and insulin stimulated glucose transport, which was impaired by TNFalpha. Glucose 56-63 tumor necrosis factor Homo sapiens 97-105 20067961-7 2010 CONCLUSIONS: Although both glucose and cream induce NF-kappaB binding and an increase in the expression of SOCS3, TNF-alpha, and IL-1beta in MNCs, only cream caused an increase in LPS concentration and TLR-4 expression. Glucose 27-34 tumor necrosis factor Homo sapiens 114-123 20646597-10 2010 In vitro system, RBP4 gene expression in visceral adipose tissue of normal weight normal glucose subjects was regulated by insulin, dexamethasone, pioglitazone, palmitic acid and TNF-alpha, such factors were also participated in the pathophysiological process of insulin resistance and type 2 diabetes. Glucose 89-96 tumor necrosis factor Homo sapiens 179-188 20200188-1 2010 The objective of this study was to investigate the effects of glucose-based peritoneal dialysis (PD) fluids and icodextrin-based PD fluids on the expression of Toll-like receptor 2 (TLR2)/TLR4 and subsequent ligand-induced mitogen-activated protein kinase (MAPK) and NF-kappaB signaling and tumor necrosis factor alpha (TNF-alpha) and interleukin-1beta (IL-1beta) mRNA expression in human peritoneal mesothelial cells (HPMCs). Glucose 62-69 tumor necrosis factor Homo sapiens 291-318 20200188-1 2010 The objective of this study was to investigate the effects of glucose-based peritoneal dialysis (PD) fluids and icodextrin-based PD fluids on the expression of Toll-like receptor 2 (TLR2)/TLR4 and subsequent ligand-induced mitogen-activated protein kinase (MAPK) and NF-kappaB signaling and tumor necrosis factor alpha (TNF-alpha) and interleukin-1beta (IL-1beta) mRNA expression in human peritoneal mesothelial cells (HPMCs). Glucose 62-69 tumor necrosis factor Homo sapiens 320-329 20019678-7 2010 Fasting glucose related to VAT expression of TNFalpha, MIP, serum amyloid A (SAA), IL-1alpha, IL-1beta, IL-8, and IL-8 receptor. Glucose 8-15 tumor necrosis factor Homo sapiens 45-53 19854062-2 2010 For example, treatment of adipocytes with either tumor-necrosis factor-alpha or dexamethasone increases ROS before impairing glucose uptake. Glucose 125-132 tumor necrosis factor Homo sapiens 49-76 20110094-8 2010 Predictors of elevated brain interstitial TNF-alpha included higher brain interstitial fluid glucose levels (beta=0.066, p<0.02), intraventricular hemorrhage (beta=0.085, p<0.021), and aneurysm size >6mm (beta=0.14, p<0.001). Glucose 93-100 tumor necrosis factor Homo sapiens 42-51 20110094-10 2010 INTERPRETATION: Brain interstitial TNF-alpha levels are elevated after SAH, and are associated with large aneurysm size, the burden of intraventricular blood, and elevation brain interstitial glucose levels. Glucose 192-199 tumor necrosis factor Homo sapiens 35-44 20459024-5 2010 RESULTS: With no insulin stimulation, the glucose remained in culture medium in TNF-alpha group was equal to that in the control group (P > 0.05). Glucose 42-49 tumor necrosis factor Homo sapiens 80-89 19741020-8 2009 High glucose (25 mM) increased TNF-alpha, IL-6, and monocyte chemoattractant protein-1 in mesangial cell conditioned medium. Glucose 5-12 tumor necrosis factor Homo sapiens 31-40 19769745-2 2009 The liver is critical in maintaining circulating glucose levels and, in a preliminary investigation using the human hepatoma (HepG2) cell line in this study, we demonstrated the role of TNFalpha in the regulation of this phenomenon and determined the underlying molecular mechanisms. Glucose 49-56 tumor necrosis factor Homo sapiens 186-194 19721200-7 2009 Recently, many researches demonstrated that periodontitis affected diabetic condition, in which periodontal pathogen like P-LPS and TNF-alpha possibly elevated insulin resistance by inhibiting glucose incorporation into smooth muscle cells. Glucose 193-200 tumor necrosis factor Homo sapiens 132-141 19690174-0 2009 Silencing mitogen-activated protein 4 kinase 4 (MAP4K4) protects beta cells from tumor necrosis factor-alpha-induced decrease of IRS-2 and inhibition of glucose-stimulated insulin secretion. Glucose 153-160 tumor necrosis factor Homo sapiens 81-108 19690174-5 2009 Prior exposure to TNF-alpha for 24 h inhibits glucose-stimulated insulin secretion from primary beta cells. Glucose 46-53 tumor necrosis factor Homo sapiens 18-27 19632244-2 2009 DIF derivatives exhibit antiproliferative activities and promote glucose consumption in mammalian cells in vitro. Glucose 65-72 tumor necrosis factor Homo sapiens 0-3 19567513-4 2009 METHODS: We analyzed the impact of TNF-alpha on glucose uptake and insulin action in human visceral and sc adipocytes. Glucose 48-55 tumor necrosis factor Homo sapiens 35-44 19567513-6 2009 RESULTS: TNF-alpha per se increased glucose transporter-4 translocation to the plasma membrane and glucose uptake by activating the AMP-activated protein kinase/AS160 pathway in both visceral and sc adipocytes. Glucose 36-43 tumor necrosis factor Homo sapiens 9-18 19567513-12 2009 CONCLUSIONS: TNF-alpha induces insulin resistance on glucose uptake in human visceral but not sc adipocytes, suggesting depot-specific effects of TNF-alpha on glucose uptake. Glucose 53-60 tumor necrosis factor Homo sapiens 13-22 19567513-12 2009 CONCLUSIONS: TNF-alpha induces insulin resistance on glucose uptake in human visceral but not sc adipocytes, suggesting depot-specific effects of TNF-alpha on glucose uptake. Glucose 159-166 tumor necrosis factor Homo sapiens 13-22 19567513-12 2009 CONCLUSIONS: TNF-alpha induces insulin resistance on glucose uptake in human visceral but not sc adipocytes, suggesting depot-specific effects of TNF-alpha on glucose uptake. Glucose 159-166 tumor necrosis factor Homo sapiens 146-155 19769745-7 2009 TNFalpha preincubation also significantly attenuated insulin-induced inhibition of the expression of gluconeogenic enzymes and hepatic glucose production. Glucose 135-142 tumor necrosis factor Homo sapiens 0-8 19769745-10 2009 Our results indicate that another transcription factor, Foxa2, is at least partly responsible for the attenuating effect of TNFalpha on insulin action on PEPCK expression and glucose production in HepG2 cells. Glucose 175-182 tumor necrosis factor Homo sapiens 124-132 18952604-9 2008 RNAi knockdown demonstrated an important role for S6K1 in mediating TNF-alpha-induced IRS-1 inhibition that led to impaired insulin-stimulated glucose uptake in adipocytes. Glucose 143-150 tumor necrosis factor Homo sapiens 68-77 19386985-3 2009 We hypothesized that human mesenchymal stem cells (hMSCs) cultured in high glucose-containing media would exhibit diminished proliferation and attenuated production of VEGF, hepatocyte growth factor (HGF), and FGF2 in response to treatment with TNF-alpha, LPS, or hypoxia. Glucose 75-82 tumor necrosis factor Homo sapiens 245-254 19002565-6 2009 Transduced islets were viable after incubation with the cocktail of TNF-alpha, IL-1beta and IFN-gamma, as evidenced by insulin release in response to glucose concentration. Glucose 150-157 tumor necrosis factor Homo sapiens 68-77 19473519-11 2009 Recombinant resistin and TNF-alpha significantly reduced glucose uptake in cultured macrophages, while atorvastatin reversed the reduced glucose uptake by TNF-alpha. Glucose 57-64 tumor necrosis factor Homo sapiens 25-34 19473519-11 2009 Recombinant resistin and TNF-alpha significantly reduced glucose uptake in cultured macrophages, while atorvastatin reversed the reduced glucose uptake by TNF-alpha. Glucose 137-144 tumor necrosis factor Homo sapiens 155-164 19038972-4 2009 METHODS AND RESULTS: Exposure of AC16 cells to TNF-alpha inhibited the expression of peroxisome proliferator-activated receptor coactivator 1alpha (PGC-1alpha), an upstream regulator of lipid and glucose oxidative metabolism. Glucose 196-203 tumor necrosis factor Homo sapiens 47-56 18443205-8 2008 TNF-alpha exposure fully impaired insulin-mediated glucose uptake and metabolism. Glucose 51-58 tumor necrosis factor Homo sapiens 0-9 17698217-8 2008 In obese male population, correlations between omental TNF-alpha protein levels and fasting glucose (r=0.762, P<0.01); fasting insulin (r=0.622, P<0.05); triglycerides (r=0.650, P<0.05); HDL-cholesterol (r=-0.880, P<0.01) were found. Glucose 92-99 tumor necrosis factor Homo sapiens 55-64 18980683-1 2008 BACKGROUND: Toxicity to glucose is not a normal state, however, it has been reported that after certain individuals ingest sugar, they produce excess tumor necrosis factor. Glucose 24-31 tumor necrosis factor Homo sapiens 150-171 18980683-5 2008 In a controlled challenge with glucose, tumor necrosis factor was found to be elevated in his serum. Glucose 31-38 tumor necrosis factor Homo sapiens 40-61 18446810-0 2008 Elevated fibroblast growth factor-2 increases tumor necrosis factor-alpha induced endothelial cell death in high glucose. Glucose 113-120 tumor necrosis factor Homo sapiens 46-73 18446810-7 2008 TNFalpha-induced endothelial cell death increased for cells in high glucose, and cell death was enhanced with increasing FGF-2 exposure and negated by a neutralizing FGF-2 antibody. Glucose 68-75 tumor necrosis factor Homo sapiens 0-8 18446810-10 2008 Endothelial cell release of FGF-2 in high glucose leads to cell cycle progression, which makes cells more susceptible to TNFalpha-induced cell death. Glucose 42-49 tumor necrosis factor Homo sapiens 121-129 18443205-9 2008 IKKbeta siRNA protected against TNF-alpha-induced impairments in glucose metabolism, since insulin-induced increases in glucose uptake (1.5-fold; P < 0.05) and glycogen synthesis (3.5-fold; P < 0.05) were restored. Glucose 65-72 tumor necrosis factor Homo sapiens 32-41 18443205-14 2008 CONCLUSIONS: IKKbeta silencing prevents TNF-alpha-induced impairments in insulin action on Akt phosphorylation and glucose uptake and metabolism in human skeletal muscle. Glucose 115-122 tumor necrosis factor Homo sapiens 40-49 18162526-9 2008 The results indicate that TNFalpha can stimulate glucose uptake in L6 muscle cells by inducing GLUT4 translocation to the plasma membrane, possibly through activation of the nuclear factor-kappaB and p38MAPK signaling pathways and independently of the production of IL-6. Glucose 49-56 tumor necrosis factor Homo sapiens 26-34 18629684-3 2008 The activation of proinflammatory pathways after exposure to TNF-alpha induces a state of insulin resistance in terms of glucose uptake in myocytes and adipocytes that impair insulin signalling at the level of the insulin receptor substrate (IRS) proteins. Glucose 121-128 tumor necrosis factor Homo sapiens 61-70 18420487-7 2008 In marked contrast, exposure of HRECs to proinflammatory cytokines IL-1beta or TNF-alpha increased glucose consumption, mitochondrial superoxide production, ERK and JNK phosphorylation, tyrosine phosphorylation, NF-kappaB activation, and caspase activation. Glucose 99-106 tumor necrosis factor Homo sapiens 79-88 18328265-10 2008 Levels of hsCRP and TNF-alpha increase with increasing severity of glucose intolerance 2. Glucose 67-74 tumor necrosis factor Homo sapiens 20-29 18162526-5 2008 Here we show that TNFalpha increased the amount of glucose transporter (GLUT)-4 at the plasma membrane and also glucose uptake in the L6 muscle cell line stably expressing GLUT4 tagged with the c-myc epitope. Glucose 51-58 tumor necrosis factor Homo sapiens 18-26 18162526-7 2008 The stimulatory effects of TNFalpha on cell surface GLUT4 and glucose uptake were blocked by nuclear factor-kappaB and p38MAPK pathway specific inhibitors (Bay 11-7082 and SB220025), and these two pathways were stimulated by TNFalpha. Glucose 62-69 tumor necrosis factor Homo sapiens 27-35 18162526-7 2008 The stimulatory effects of TNFalpha on cell surface GLUT4 and glucose uptake were blocked by nuclear factor-kappaB and p38MAPK pathway specific inhibitors (Bay 11-7082 and SB220025), and these two pathways were stimulated by TNFalpha. Glucose 62-69 tumor necrosis factor Homo sapiens 225-233 18436850-8 2008 In pericytes undergoing apoptosis induced by either TNF-alpha or high glucose Ang-1 increased survival (P < 0.05 for TNF-alpha; P < 0.01 for high glucose), whereas Ang-2 increased apoptosis. Glucose 152-159 tumor necrosis factor Homo sapiens 52-61 17940160-3 2008 Direct exposure to TNF-alpha induces a state of insulin resistance in terms of glucose uptake in myocytes and brown adipocytes because of the activation of proinflammatory pathways that impair insulin signaling at the level of the insulin receptor substrate (IRS) proteins. Glucose 79-86 tumor necrosis factor Homo sapiens 19-28 18060802-7 2008 Basal glucose uptake, lipolysis and IL-6 mRNA were induced by exogenous TNFalpha (10 ng/mL) but not by IL-6 (10 ng/mL), IL-8 (100 ng/mL) and IL-10 (20 ng/mL). Glucose 6-13 tumor necrosis factor Homo sapiens 72-80 17707405-7 2008 Moreover, the hyperglycemia associated with elevated TNF-alpha was found to enhance the level of IL-8 production by the HUVECs cultured at all glucose concentrations and over both time courses, compared to the control (P < 0.05). Glucose 143-150 tumor necrosis factor Homo sapiens 53-62 17936398-10 2008 Treatments with insulin and TNFalpha as well as stearic acid, a saturated free fatty acid, upregulated RELMbeta expression, while d-glucose downregulated RELMbeta. Glucose 130-139 tumor necrosis factor Homo sapiens 28-36 19378424-0 2008 C-reactive protein and tumor necrosis factor-alpha in relation to insulin-mediated glucose uptake, smoking and atherosclerosis. Glucose 83-90 tumor necrosis factor Homo sapiens 23-50 17934698-1 2008 Culturing hepatocytes with a combination of LPS, TNF-alpha, IL-1beta and IFN-gamma resulted in an inhibition of glucose output from glycogen and prevented the repletion of glycogen in freshly cultured cells. Glucose 112-119 tumor necrosis factor Homo sapiens 49-58 18487876-7 2008 The plasma levels of TNF-alpha were positively correlated with SpO(2) <90%, BMI and fasting plasma glucose levels. Glucose 102-109 tumor necrosis factor Homo sapiens 21-30 17476613-1 2007 OBJECTIVES: We undertook this study to test the hypotheses that patients with active rheumatoid arthritis (RA) are insulin resistant and that anti-tumour necrosis factor-alpha (TNFalpha) therapy improves not only the clinical state of these patients but also their glucose metabolism. Glucose 265-272 tumor necrosis factor Homo sapiens 177-185 17928988-1 2007 AIMS/HYPOTHESIS: Clear evidence exists that TNF-alpha inhibits insulin signalling and thereby glucose uptake in myocytes and adipocytes. Glucose 94-101 tumor necrosis factor Homo sapiens 44-53 17584970-4 2007 High glucose (HG)-induced TNF-alpha release was specifically inhibited by protein kinase C (PKC)-delta inhibitor (Rottlerin; EMD Biosciences, San Diego, CA), but not PKC-beta2 inhibitor (CGP53353; Tocris Cookson Inc., Ellisville, MO), indicating the possible involvement of PKC-delta in HG signaling. Glucose 5-12 tumor necrosis factor Homo sapiens 26-35 17284447-6 2007 In adipocytes rendered insulin-resistant by a long-lasting tumor necrosis factor alpha treatment, the protein level of Gab1 was strongly decreased, and HGF-stimulated PKB activation and glucose uptake were also altered. Glucose 186-193 tumor necrosis factor Homo sapiens 59-86 17284447-8 2007 These data provide the first evidence that in vitro HGF promotes glucose uptake through a Gab1/PI 3-kinase/PKB/AS160 pathway which was altered in tumor necrosis factor alpha-treated adipocytes. Glucose 65-72 tumor necrosis factor Homo sapiens 146-173 17031641-4 2007 NeuAc-TNFalpha reduced activities in the up-regulation of serum levels of IL-6 and NOx, but comparable activity as native TNFalpha in the down-regulation of the serum level of glucose. Glucose 176-183 tumor necrosis factor Homo sapiens 6-14 17031641-4 2007 NeuAc-TNFalpha reduced activities in the up-regulation of serum levels of IL-6 and NOx, but comparable activity as native TNFalpha in the down-regulation of the serum level of glucose. Glucose 176-183 tumor necrosis factor Homo sapiens 122-130 17371479-7 2007 Forearm glucose uptake incremental area significantly correlated with NO(x) incremental area, forearm c-GMP release incremental area, TNF-alpha levels and ET-1 incremental area. Glucose 8-15 tumor necrosis factor Homo sapiens 134-143 17227768-2 2007 We tested whether mitogenic-activated protein kinase kinase kinase kinase isoform 4 (MAP4K4) causes the TNF-alpha-induced negative regulation of extracellular signal-regulated kinase-1/2 (ERK-1/2), c-Jun NH2-terminal kinase (JNK), and the insulin receptor substrate-1 (IRS-1) on the insulin signaling pathway governing glucose metabolism. Glucose 319-326 tumor necrosis factor Homo sapiens 104-113 17227768-3 2007 Using small interfering RNA (siRNA) to suppress the expression of MAP4K4 protein 85% in primary human skeletal muscle cells, we provide evidence that TNF-alpha-induced insulin resistance on glucose uptake was completely prevented. Glucose 190-197 tumor necrosis factor Homo sapiens 150-159 17227768-5 2007 These results highlight the MAPK4K4/JNK/ERK/IRS module in the negative regulation of insulin signaling to glucose transport in response to TNF-alpha. Glucose 106-113 tumor necrosis factor Homo sapiens 139-148 17227768-6 2007 Depletion of MAP4K4 also prevented TNF-alpha-induced insulin resistance on Akt and the Akt substrate 160 (AS160), providing evidence that appropriate insulin signaling inputs for glucose metabolism were rescued. Glucose 179-186 tumor necrosis factor Homo sapiens 35-44 17227768-8 2007 Thus, strategies to inhibit MAP4K4 may be efficacious in the prevention of TNF-alpha-induced inhibitory signals that cause skeletal muscle insulin resistance on glucose metabolism in humans. Glucose 161-168 tumor necrosis factor Homo sapiens 75-84 16930761-9 2007 TNF-alpha had not only significant negative correlation with the changes of insulin secretion, but also significant positive correlation with the changes of HOMA-IR after adjustment of blood glucose. Glucose 191-198 tumor necrosis factor Homo sapiens 0-9 17244513-0 2007 Different TNFalpha expression elicited by glucose in monocytes from type 2 diabetes mellitus patients. Glucose 42-49 tumor necrosis factor Homo sapiens 10-18 16832663-6 2006 Finally, the observation that TNF-alpha levels are also linked to glycaemic values suggests that in patients, as well as in vitro, the glycosylation-mediated cell adhesion process that plays a role in diabetic retinopathy may involve glucose- and TNF-alpha-induced protein kinase beta2 activation, and subsequently raise activity of core 2 GlcNAc-T through increased enzyme phosphorylation. Glucose 234-241 tumor necrosis factor Homo sapiens 30-39 17189875-6 2007 Proinflammatory cytokines such as interleukin-1 and tumor necrosis factor-alpha (TNF-alpha) also stimulated NF-kappaB-dependent transcription and showed an additive effect with high glucose. Glucose 182-189 tumor necrosis factor Homo sapiens 81-90 16919536-3 2006 Glucose intake caused an increase in NF-kappaB binding to NF-kappaB2, NF-kappaB2a, and NF-kappaB3 sequences in the promoter site of tumor necrosis factor alpha (TNF-alpha) gene along with an increase in the expression of TNF-alpha messenger RNA in MNCs. Glucose 0-7 tumor necrosis factor Homo sapiens 132-159 16919536-3 2006 Glucose intake caused an increase in NF-kappaB binding to NF-kappaB2, NF-kappaB2a, and NF-kappaB3 sequences in the promoter site of tumor necrosis factor alpha (TNF-alpha) gene along with an increase in the expression of TNF-alpha messenger RNA in MNCs. Glucose 0-7 tumor necrosis factor Homo sapiens 161-170 16919536-3 2006 Glucose intake caused an increase in NF-kappaB binding to NF-kappaB2, NF-kappaB2a, and NF-kappaB3 sequences in the promoter site of tumor necrosis factor alpha (TNF-alpha) gene along with an increase in the expression of TNF-alpha messenger RNA in MNCs. Glucose 0-7 tumor necrosis factor Homo sapiens 221-230 16919536-5 2006 We conclude that glucose intake induces an immediate increase in intranuclear NF-kappaB binding, a fall in IkappaBalpha, an increase in IKKalpha, IKKbeta, IKK activity, and messenger RNA expression of TNF-alpha in MNCs in healthy subjects. Glucose 17-24 tumor necrosis factor Homo sapiens 201-210 16371367-1 2006 Inhibition of peroxisome proliferator-activated receptor gamma (PPARgamma) function by TNF-alpha contributes to glucose and fatty acid metabolic disorders in inflammation and cancer, although the molecular mechanism is not fully understood. Glucose 112-119 tumor necrosis factor Homo sapiens 87-96 16754954-7 2006 NEMO expression also enhanced TNF-alpha-induced Ser307-IRS-1 phosphorylation and inhibited glucose uptake. Glucose 91-98 tumor necrosis factor Homo sapiens 30-39 16784178-6 2006 TNF only suppressed glucose uptake in insulin-stimulated subcutaneous tissue and this suppression was only observed in tissue from lean subjects. Glucose 20-27 tumor necrosis factor Homo sapiens 0-3 16784178-7 2006 These data support a relationship between the TNF system and body mass index (BMI), but not fat distribution, and suggest depot specificity of the TNF effect on glucose uptake. Glucose 161-168 tumor necrosis factor Homo sapiens 147-150 16641887-1 2006 Pyruvic acid, an intermediate metabolite of glucose, an effective scavenger of reactive oxygen species (ROS), inhibits tumor necrosis factor-alpha production and NF-kappaB signaling pathways, reduces circulating levels of HMGB1 (high mobility group B1), decreases COX-2 (cyclo-oxygenase-2), iNOS (inducible nitric oxide synthase), and IL-6 (interleukin-6) mRNA expression in liver, ileal mucosa, and colonic mucosa in animal models with endotoxemia. Glucose 44-51 tumor necrosis factor Homo sapiens 119-146 16494630-0 2006 Glucose-stimulated prehepatic insulin secretion is associated with circulating alanine, triglyceride, glucagon, lactate and TNF-alpha in patients with HIV-lipodystrophy. Glucose 0-7 tumor necrosis factor Homo sapiens 124-133 16464907-1 2006 Inflammation is associated with insulin resistance, and both tumor necrosis factor (TNF)-alpha and interleukin (IL)-6 may affect glucose uptake. Glucose 129-136 tumor necrosis factor Homo sapiens 61-94 16464907-9 2006 Whole body insulin-mediated glucose uptake was significantly reduced during TNF infusion but remained unchanged during IL-6 infusion. Glucose 28-35 tumor necrosis factor Homo sapiens 76-79 16464907-11 2006 We conclude that TNF-induced insulin resistance of whole body glucose uptake is associated with increased IL-18 gene expression in muscle tissue, indicating that TNF and IL-18 interact, and both may have important regulatory roles in the pathogenesis of insulin resistance. Glucose 62-69 tumor necrosis factor Homo sapiens 17-20 16464907-11 2006 We conclude that TNF-induced insulin resistance of whole body glucose uptake is associated with increased IL-18 gene expression in muscle tissue, indicating that TNF and IL-18 interact, and both may have important regulatory roles in the pathogenesis of insulin resistance. Glucose 62-69 tumor necrosis factor Homo sapiens 162-165 16803616-4 2006 AIM: The purpose of the present study was to examine the associations of TNFalpha system with plasma lipids in lean and obese subjects with normal glucose metabolism. Glucose 147-154 tumor necrosis factor Homo sapiens 73-81 16627554-8 2006 After the intensive control of glucose level, FMD increased significantly (from 2.5+/-0.9 to 7.2+/-3.0%), accompanied by a significant (P<0.01) decrease in TNF-alpha (from 29+/-16 to 11+/-9 pg/dL) and ADMA (from 4.8+/-1.5 to 3.5+/-1.1 microM/L) levels. Glucose 31-38 tumor necrosis factor Homo sapiens 159-168 16516847-1 2006 The inflammatory cytokine TNF is known to affect glucose and lipid metabolism, where its action leads to a cachexic state. Glucose 49-56 tumor necrosis factor Homo sapiens 26-29 16494630-9 2006 CONCLUSION: Plasma triglyceride, alanine, glucagon, lactate and TNF-alpha may be associated with alterations in the first-phase prehepatic insulin secretion response to intravenous glucose in normoglycaemic lipodystrophic HIV-infected patients. Glucose 181-188 tumor necrosis factor Homo sapiens 64-73 16754199-5 2006 In consequence, TNF-alpha-induced insulin resistance on glucose uptake was completely alleviated. Glucose 56-63 tumor necrosis factor Homo sapiens 16-25 16423637-3 2006 Tumor necrosis factor alpha release was measured from MNCs cultured in the presence of LPS after isolation from blood samples drawn fasting and 2 hours after glucose ingestion. Glucose 158-165 tumor necrosis factor Homo sapiens 0-27 16430720-6 2006 In addition, there was a positive correlation between blood glucose and tissue levels of both TNF-alpha and ICAM-1. Glucose 60-67 tumor necrosis factor Homo sapiens 94-103 16497175-9 2006 The actual physiological roles of resistin and TNF-alpha in altering muscle lipid metabolism are more controversial, but each has been shown to directly impair insulin signalling and consequently, insulin stimulated glucose uptake in muscle. Glucose 216-223 tumor necrosis factor Homo sapiens 47-56 16376274-7 2006 There was correlation between tumor necrosis factor-alpha and cerebrospinal fluid leukocytes (P = 0.019), protein (P = 0.000), and glucose (P = 0.038). Glucose 131-138 tumor necrosis factor Homo sapiens 30-57 16477538-5 2006 Serum IL-6 and TNFalpha concentrations were elevated during glucose loading (for each comparison, p < 0.01). Glucose 60-67 tumor necrosis factor Homo sapiens 15-23 16477538-7 2006 Serum IL-6 and TNFalpha concentration significantly correlated with insulin and glucose in IGT group (for each comparison, p < 0.01). Glucose 80-87 tumor necrosis factor Homo sapiens 15-23 16186396-4 2005 TNF-alpha directly impairs glucose uptake and metabolism by altering insulin signal transduction. Glucose 27-34 tumor necrosis factor Homo sapiens 0-9 16186396-7 2005 Thus, excessive concentrations of TNF-alpha negatively regulate insulin signaling and whole-body glucose uptake in humans. Glucose 97-104 tumor necrosis factor Homo sapiens 34-43 16080843-12 2005 Serum TNFalpha was also positively correlated to fasting blood glucose. Glucose 63-70 tumor necrosis factor Homo sapiens 6-14 15985479-8 2005 TNFalpha release was measured from MNC cultured in the presence of LPS from blood samples drawn fasting and 2 h after glucose ingestion. Glucose 118-125 tumor necrosis factor Homo sapiens 0-8 15936753-9 2005 TNFalpha also significantly increased basal glucose transport rates (+44(14)%; P=0.006 versus +34(11)%; P=0.007) and GLUT1 localisation to the plasma membrane. Glucose 44-51 tumor necrosis factor Homo sapiens 0-8 15979544-8 2005 Further studies should disclose the source of increased TNF-alpha in these women, and to assess whether TNF-alpha is causally related to glucose intolerance during pregnancy. Glucose 137-144 tumor necrosis factor Homo sapiens 104-113 16081485-7 2005 Additional studies demonstrated that TNFalpha increased basal glucose transport via GLUT1, nitric oxide synthase and p38MAPK-dependent mechanisms. Glucose 62-69 tumor necrosis factor Homo sapiens 37-45 15625348-6 2005 A model of mice transgenic for the HCV core protein demonstrated insulin resistance, glucose intolerance, and elevated intrahepatic TNF-alpha mRNA; all of which were ameliorated by anti-TNF-alpha antibodies. Glucose 85-92 tumor necrosis factor Homo sapiens 186-195 16356228-2 2005 There is extensive evidence that glucose can stimulate the production of pro-inflammatory cytokines such as tumor necrosis factor (TNF)-alpha and IL-6, with no effect on the anti-inflammatory cytokine IL-10. Glucose 33-40 tumor necrosis factor Homo sapiens 108-141 15679072-0 2005 Serum levels of soluble tumor necrosis factor-alpha receptor 2 are linked to insulin resistance and glucose intolerance in children. Glucose 100-107 tumor necrosis factor Homo sapiens 24-51 15679072-2 2005 Tumor necrosis factor-alpha (TNF-alpha) has important effects on lipid and glucose metabolism. Glucose 75-82 tumor necrosis factor Homo sapiens 0-27 15679072-2 2005 Tumor necrosis factor-alpha (TNF-alpha) has important effects on lipid and glucose metabolism. Glucose 75-82 tumor necrosis factor Homo sapiens 29-38 15746249-9 2005 Adipocytes preexposed to TNF-alpha for 5 h and then stimulated with insulin for 30 min exhibited decreased levels of Akt, phosphorylated Akt, as well as phosphorylated Mdm2, which is a known direct substrate of Akt, and glucose uptake. Glucose 220-227 tumor necrosis factor Homo sapiens 25-34 15654920-8 2005 Tumour necrosis factor (TNF-alpha) caused insulin resistance on glucose uptake by impairing insulin signalling at the level of IRS-2. Glucose 64-71 tumor necrosis factor Homo sapiens 24-33 15381186-1 2004 Inflammatory cytokines such as interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha) may have a direct effect on glucose and lipid metabolism. Glucose 124-131 tumor necrosis factor Homo sapiens 56-83 15381186-1 2004 Inflammatory cytokines such as interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha) may have a direct effect on glucose and lipid metabolism. Glucose 124-131 tumor necrosis factor Homo sapiens 85-94 15248836-1 2004 OBJECTIVE: Adipocytes secrete a number of molecules such as tumor necrosis factor-alpha, leptin and free fatty acids that can influence the ability of the body to metabolize glucose. Glucose 174-181 tumor necrosis factor Homo sapiens 60-87 15646011-4 2004 Correlation analyses showed that the serum IL-18 and TNF-alpha concentration were positively correlated with each other and positively with fasting plasma glucose (FPG), 2h postprandial glucose, glycosylated hemoglobin (HbA1c), triglyceride, and urinary albumin levels and negative correlation between TNF-alpha and high density lipoprotein cholesterol (HDL-C) were also found in diabetic subjects. Glucose 186-193 tumor necrosis factor Homo sapiens 53-62 14757289-8 2004 Plasma glucose and insulin levels decreased after weight loss in all subjects and weak correlations were found with TNF-alpha concentrations (r=0.3, P<0.05). Glucose 7-14 tumor necrosis factor Homo sapiens 116-125 15646011-4 2004 Correlation analyses showed that the serum IL-18 and TNF-alpha concentration were positively correlated with each other and positively with fasting plasma glucose (FPG), 2h postprandial glucose, glycosylated hemoglobin (HbA1c), triglyceride, and urinary albumin levels and negative correlation between TNF-alpha and high density lipoprotein cholesterol (HDL-C) were also found in diabetic subjects. Glucose 155-162 tumor necrosis factor Homo sapiens 53-62 15283163-7 2004 Exposure of growth-arrested HRCs with hypoxia (1% O2) or TNF-alpha (10 ng/ml) for 24 hours increased the secretion rate of PAI-1 protein by about 2.0-fold, while 24-hour treatment with high glucose (450 mg/dl) did not increase PAI-1 secretion at all, compared with that of the control cells under normal glucose (100 mg/dl) and normoxia (18% O2). Glucose 190-197 tumor necrosis factor Homo sapiens 57-66 15283163-7 2004 Exposure of growth-arrested HRCs with hypoxia (1% O2) or TNF-alpha (10 ng/ml) for 24 hours increased the secretion rate of PAI-1 protein by about 2.0-fold, while 24-hour treatment with high glucose (450 mg/dl) did not increase PAI-1 secretion at all, compared with that of the control cells under normal glucose (100 mg/dl) and normoxia (18% O2). Glucose 304-311 tumor necrosis factor Homo sapiens 57-66 15203553-5 2004 RESULTS: TNF-alpha levels after 1.36% and 3.86% glucose used dwells were 23+/-14 pg/ml and 28+/-4 pg/ml, respectively (p=0.78). Glucose 48-55 tumor necrosis factor Homo sapiens 9-18 14757289-9 2004 CONCLUSIONS: We conclude that maximal production of TNF-alpha from mononuclear cells decreases with energy restriction and is weakly associated with plasma glucose and insulin concentrations in obese patients. Glucose 156-163 tumor necrosis factor Homo sapiens 52-61 14693700-0 2004 Stimulation of lipolysis by tumor necrosis factor-alpha in 3T3-L1 adipocytes is glucose dependent: implications for long-term regulation of lipolysis. Glucose 80-87 tumor necrosis factor Homo sapiens 28-55 14981209-4 2004 Through this activation, TNF alpha induces oxidative stress, which exacerbates pathological processes leading to oxidized low-density lipoprotein and dyslipidemia, glucose intolerance, insulin resistance, hypertension, endothelial dysfunction, and atherogenesis. Glucose 164-171 tumor necrosis factor Homo sapiens 25-34 14693700-10 2004 We conclude that the lipolytic action of TNF-alpha is influenced by glucose in 3T3-L1 adipocytes. Glucose 68-75 tumor necrosis factor Homo sapiens 41-50 14693700-11 2004 The findings suggest that glucose metabolism is required for the lipolytic response to TNF-alpha but not for early signaling events. Glucose 26-33 tumor necrosis factor Homo sapiens 87-96 15230146-8 2004 Furthermore TNF-alpha and IL-8 levels correlated with pleocytosis, and protein and glucose levels, whereas IL-1 beta correlated with pleocytosis and protein level in CSF. Glucose 83-90 tumor necrosis factor Homo sapiens 12-21 14984317-5 2004 The effect of high glucose concentration on TNF-alpha induced expression of ELAM-1, VCAM-1 and ICAM-1 was negligible, if at all. Glucose 19-26 tumor necrosis factor Homo sapiens 44-53 14530204-0 2003 Tumor necrosis factor-alpha inhibits insulin"s stimulating effect on glucose uptake and endothelium-dependent vasodilation in humans. Glucose 69-76 tumor necrosis factor Homo sapiens 0-27 14530204-2 2003 Therefore, we aimed at examining whether the proinflammatory cytokine tumor necrosis factor (TNF)-alpha inhibits insulin-stimulated glucose uptake and insulin-stimulated endothelial function in humans. Glucose 132-139 tumor necrosis factor Homo sapiens 70-103 14530204-7 2003 This increase was completely inhibited during coinfusion of TNF-alpha (started 10 min before insulin) with a more pronounced inhibition of glucose extraction than of blood flow. Glucose 139-146 tumor necrosis factor Homo sapiens 60-69 12855762-4 2003 RESULTS: The -308A allele of the TNF-alpha gene was associated with high rates of glucose oxidation (p = 0.008 adjusted for age, gender, and BMI) and lipid synthesis (p = 0.037) and suppression of FFA levels (p = 0.023) during hyperinsulinemia. Glucose 82-89 tumor necrosis factor Homo sapiens 33-42 12918129-3 2003 We assessed the role of glucose in the regulation of circulating levels of insulin, glucagon, cortisol, IL-6 and TNF-alpha in human sepsis with normal or impaired glucose tolerance. Glucose 24-31 tumor necrosis factor Homo sapiens 113-122 12773307-0 2003 Endothelin-1-stimulated glucose uptake is desensitized by tumor necrosis factor-alpha in 3T3-L1 adipocytes. Glucose 24-31 tumor necrosis factor Homo sapiens 58-85 12773307-3 2003 Here, we report that exposure of 3T3-L1 adipocytes to TNF-alpha for 48 h dose-dependently decreased endothelin-1-stimulated glucose uptake and translocation of GLUT4 to the plasma membrane. Glucose 124-131 tumor necrosis factor Homo sapiens 54-63 12773307-6 2003 Taken together, these results suggest that TNF-alpha-induced desensitization of endothelin-1-stimulated GLUT4 translocation and glucose uptake in 3T3-L1 adipocytes is due, at least in part, to a decreased expression of Galphaq/11, leading to a suppression in tyrosine phosphorylation of PYK2. Glucose 128-135 tumor necrosis factor Homo sapiens 43-52 12714600-12 2003 Finally, aspirin rescued insulin-induced glucose uptake in 3T3-L1 adipocytes pretreated with TNF-alpha. Glucose 41-48 tumor necrosis factor Homo sapiens 93-102 12855762-7 2003 DISCUSSION: The -308A allele of the promoter of the TNF-alpha gene is associated with high rates of glucose oxidation in normal weight subjects and with effective lipid storage in overweight subjects. Glucose 100-107 tumor necrosis factor Homo sapiens 52-61 12782301-0 2003 Early changes in glucose and phospholipid metabolism following apoptosis induction by IFN-gamma/TNF-alpha in HT-29 cells. Glucose 17-24 tumor necrosis factor Homo sapiens 96-105 12716761-3 2003 We have previously shown that high glucose (HG) treatment activates monocytes and induces the expression of tumor necrosis factor (TNF)-alpha via oxidant stress and nuclear factor-kB transcription factor. Glucose 35-42 tumor necrosis factor Homo sapiens 108-141 12388119-2 2002 We hypothesized that the skeletal muscle will release IL-6, but not TNF-alpha, during exercise because of previous observations that TNF-alpha negatively affects glucose uptake in skeletal muscle. Glucose 162-169 tumor necrosis factor Homo sapiens 133-142 12532151-1 2003 OBJECTIVE: To investigate mechanisms for the regulation of glucose incorporation into triacylgycerols in adipocytes by ceramides, which mediate some actions of tumour necrosis factor-alpha (TNFalpha). Glucose 59-66 tumor necrosis factor Homo sapiens 190-198 12556444-3 2003 We show that both substitution of glucose for pyruvate and treatment with 2-deoxyglucose enhanced apoptosis induced by tumor necrosis factor (TNF)-alpha, CD95 agonistic antibody, and TNF-related apoptosis-inducing ligand (TRAIL). Glucose 34-41 tumor necrosis factor Homo sapiens 119-152 12747594-9 2003 The A/G variation at position -308 in the promoter region of the TNF-alpha gene could be an important genetic factor predisposing to insulin resistance in obese women and increased levels of glucose, triglyceride, and free fatty acids in men. Glucose 191-198 tumor necrosis factor Homo sapiens 65-74 12532159-9 2003 These results suggest that: (i) an increase in circulating TNFalpha concentration is associated with peripheral insulin resistance and increased plasma glucose and insulin levels prior to the onset of type 2 diabetes; and (ii) the further deterioration in peripheral insulin resistance in T2DM (compared with NGT and IGT) is unrelated to the increase in serum TNFalpha concentration. Glucose 152-159 tumor necrosis factor Homo sapiens 59-67 12399623-13 2002 The 30 mM D-glucose induced downregulation of CCR2 mRNA expression was prevented in the presence of TNFalpha. Glucose 10-19 tumor necrosis factor Homo sapiens 100-108 12453902-8 2002 In the SGA group, fasting insulin-to-glucose ratios were significantly higher in the TNF/-308A (P = 0.03), the PPAR/Ala12 (P = 0.01), and the ADRB3/+250G (P = 0.02) carriers than in the noncarriers. Glucose 37-44 tumor necrosis factor Homo sapiens 85-88 11888514-2 2002 The purpose of this study was to investigate whether the TNF alpha/G-308A polymorphism was associated with responses to oral glucose and fat tolerance tests in a case--control study comparing male offspring with a paternal history of premature myocardial infarction (cases, n=335) to age-matched controls (n=340) recruited from 14 European university populations. Glucose 125-132 tumor necrosis factor Homo sapiens 57-66 12086962-8 2002 Third, exogenous addition of dibutyryl cAMP, endogenous stimulation of cAMP production by forskolin, and antioxidant N-acetylcysteine (NAC) prevented stimulation of TNF-alpha secretion caused by AA alone or with high glucose. Glucose 217-224 tumor necrosis factor Homo sapiens 165-174 12006357-4 2002 Infusion of glucose and insulin significantly amplified and/or prolonged the cardiovascular, plasma interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-alpha), and counterregulatory hormone responses to LPS, whereas the effects on fever, plasma norepinephrine concentrations, and oxygen consumption were unaffected. Glucose 12-19 tumor necrosis factor Homo sapiens 122-149 12006357-4 2002 Infusion of glucose and insulin significantly amplified and/or prolonged the cardiovascular, plasma interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-alpha), and counterregulatory hormone responses to LPS, whereas the effects on fever, plasma norepinephrine concentrations, and oxygen consumption were unaffected. Glucose 12-19 tumor necrosis factor Homo sapiens 151-160 12187392-6 2002 Increased glucose uptake (M) was accompanied by a significant decrease of TNF-alpha mRNA (76.67+/-12.59-14.01+/-5.21 AU, P<0.01) and an increase of GLUT4. Glucose 10-17 tumor necrosis factor Homo sapiens 74-83 12086956-6 2002 Pericytes exposed to high glucose showed increased expression of Bax and of tumor necrosis factor-alpha, which were prevented by the NF-kappaB inhibitors and mimicked by transfection with the p65 subunit of NF-kappaB, and failed to increase the levels of the NF-kappaB-dependent inhibitors of apoptosis. Glucose 26-33 tumor necrosis factor Homo sapiens 76-103 11944024-0 2002 Effects of TNF-alpha on glucose metabolism and lipolysis in adipose tissue and isolated fat-cell preparations. Glucose 24-31 tumor necrosis factor Homo sapiens 11-20 11944024-3 2002 We also studied the effects of this 24-hour TNF-alpha tissue exposure on subsequent glucose metabolism and lipolysis by isolated adipocytes. Glucose 84-91 tumor necrosis factor Homo sapiens 44-53 11944024-7 2002 Prior exposure to TNF-alpha resulted in a significant increase in adipocyte glycerol release (P =.044), total glucose metabolism (P =.019), and lactate production (P =.037). Glucose 110-117 tumor necrosis factor Homo sapiens 18-27 11944024-9 2002 The pattern of glucose metabolism elicited by TNF-alpha exposure differs from that usually attributed to a lipolytic hormone and suggests that the effects of TNF-alpha on glucose metabolism involve pathways separate from, or in addition to, its effects on lipolytic stimulation. Glucose 15-22 tumor necrosis factor Homo sapiens 46-55 11944024-9 2002 The pattern of glucose metabolism elicited by TNF-alpha exposure differs from that usually attributed to a lipolytic hormone and suggests that the effects of TNF-alpha on glucose metabolism involve pathways separate from, or in addition to, its effects on lipolytic stimulation. Glucose 15-22 tumor necrosis factor Homo sapiens 158-167 11944024-9 2002 The pattern of glucose metabolism elicited by TNF-alpha exposure differs from that usually attributed to a lipolytic hormone and suggests that the effects of TNF-alpha on glucose metabolism involve pathways separate from, or in addition to, its effects on lipolytic stimulation. Glucose 171-178 tumor necrosis factor Homo sapiens 46-55 11944024-9 2002 The pattern of glucose metabolism elicited by TNF-alpha exposure differs from that usually attributed to a lipolytic hormone and suggests that the effects of TNF-alpha on glucose metabolism involve pathways separate from, or in addition to, its effects on lipolytic stimulation. Glucose 171-178 tumor necrosis factor Homo sapiens 158-167 12715715-8 2002 RESULTS: Homozygous and heterozygous carriers of the A allele in position -308 of the TNF-alpha gene promoter showed higher plasma insulin levels at 120 min OGTT versus GG carriers (44.77 microliters/ml; SD 40.4 vs. 26.82; SD 19.9; p = 0.04) and a higher ratio of the 30 min increment in insulin to the 30 min increment in glucose (35.4; SD 21.5 vs. 22.6: SD 21.5; p = 0.03). Glucose 323-330 tumor necrosis factor Homo sapiens 86-95 11739520-4 2001 IL-1beta and TNF-alpha, and to a lesser degree IL-6, accelerate facilitated glucose transport as measured by [(3)H]2-deoxyglucose uptake. Glucose 76-83 tumor necrosis factor Homo sapiens 13-22 11726202-0 2001 Chromium chloride inhibits oxidative stress and TNF-alpha secretion caused by exposure to high glucose in cultured U937 monocytes. Glucose 95-102 tumor necrosis factor Homo sapiens 48-57 11726202-6 2001 This study demonstrates for the first time that chromium supplementation inhibits TNF-alpha secretion in U937 monocytes cultured in high-glucose medium, which appears to be mediated by its antioxidative effect. Glucose 137-144 tumor necrosis factor Homo sapiens 82-91 11679435-1 2001 Tumor necrosis factor (TNF)-alpha causes insulin resistance on glucose uptake in fetal brown adipocytes. Glucose 63-70 tumor necrosis factor Homo sapiens 0-33 11701426-10 2001 In conclusion, these findings suggest a possible mechanism by which TNF-alpha may modulate glucose metabolism in younger people. Glucose 91-98 tumor necrosis factor Homo sapiens 68-77 11681809-13 2001 TNF-alpha also down regulates insulin-stimulated glucose uptake via effects on glucose transporter 4, insulin receptor autophosphorylation and insulin receptor substrate-1. Glucose 49-56 tumor necrosis factor Homo sapiens 0-9 11703438-2 2001 We investigated the effect of exogenous glucose on the release of TNF-alpha from placental and adipose (omental and subcutaneous) tissue obtained from normal pregnant women, and women with GDM. Glucose 40-47 tumor necrosis factor Homo sapiens 66-75 11703438-4 2001 The effect of normal (5 mmol/l) and high (15 and 25 mmol/l) glucose concentrations on the release of TNF-alpha was assessed. Glucose 60-67 tumor necrosis factor Homo sapiens 101-110 11703438-5 2001 RESULTS: In placental and subcutaneous adipose tissues obtained from women with GDM (n = 6), TNF-alpha release was significantly greater under conditions of high glucose compared with normal glucose (placenta, 25 mmol/l 5915.7 +/- 2579.6 and 15 mmol/l 4547.1 +/- 2039.1 vs. 5 mmol/l 1897.1 +/- 545.5; subcutaneous adipose tissue, 25 mmol/l 423.5 +/- 207.0 and 15 mmol/l 278.5 +/- 138.7 vs. 5 mmol/l 65.3 +/- 28.5 pg/mg protein; P < 0.05). Glucose 162-169 tumor necrosis factor Homo sapiens 93-102 11703438-5 2001 RESULTS: In placental and subcutaneous adipose tissues obtained from women with GDM (n = 6), TNF-alpha release was significantly greater under conditions of high glucose compared with normal glucose (placenta, 25 mmol/l 5915.7 +/- 2579.6 and 15 mmol/l 4547.1 +/- 2039.1 vs. 5 mmol/l 1897.1 +/- 545.5; subcutaneous adipose tissue, 25 mmol/l 423.5 +/- 207.0 and 15 mmol/l 278.5 +/- 138.7 vs. 5 mmol/l 65.3 +/- 28.5 pg/mg protein; P < 0.05). Glucose 191-198 tumor necrosis factor Homo sapiens 93-102 11703438-7 2001 CONCLUSIONS: These observations suggest that tissues from patients with GDM release greater amounts of TNF-alpha in response to high glucose. Glucose 133-140 tumor necrosis factor Homo sapiens 103-112 11703438-8 2001 As TNF-alpha has been previously implicated in the regulation of glucose and lipid metabolism, and of insulin resistance, these data are consistent with the hypothesis that TNF-alpha may be involved in the pathogenesis and/or progression of GDM. Glucose 65-72 tumor necrosis factor Homo sapiens 3-12 11703438-8 2001 As TNF-alpha has been previously implicated in the regulation of glucose and lipid metabolism, and of insulin resistance, these data are consistent with the hypothesis that TNF-alpha may be involved in the pathogenesis and/or progression of GDM. Glucose 65-72 tumor necrosis factor Homo sapiens 173-182 11225716-2 2000 Inflammatory mediators such as tumor necrosis factor-alpha and interleukin-6 (IL-6) may have a direct effect on glucose and lipid metabolism. Glucose 112-119 tumor necrosis factor Homo sapiens 31-58 11279172-8 2001 Rather, p38 MAPK activation leads to a marked down-regulation of insulin-induced glucose uptake via GLUT4, which may underlie cellular stress-induced insulin resistance caused by tumor necrosis factor alpha and other factors. Glucose 81-88 tumor necrosis factor Homo sapiens 179-206 11207674-3 2001 Because TNF-alpha is also known to affect lipid and glucose metabolism, the association between the circulating concentration of TNF-alpha and atherogenic risk factors was examined in 82 apparently healthy Japanese women (aged 19-69 years; mean age 48.5 years). Glucose 52-59 tumor necrosis factor Homo sapiens 8-17 11145126-0 2000 Tumor necrosis factor alpha gene G-308A polymorphism, insulin resistance, and fasting plasma glucose in young, older, and diabetic Japanese men. Glucose 93-100 tumor necrosis factor Homo sapiens 0-27 11204450-8 2000 Transforming growth factor beta (TGFbeta), polyunsaturated fatty acids and the glucose-insulin-potassium regimen can antagonize the harmful actions of TNFalpha and protect the myocardium. Glucose 79-86 tumor necrosis factor Homo sapiens 151-159 11334414-12 2001 These studies demonstrate that TNF, if present during differentiation, decreases insulin-stimulated rates of storage of glucose as glycogen and total GS activity but does not downregulate the insulin-signaling system to GS. Glucose 120-127 tumor necrosis factor Homo sapiens 31-34 11377135-2 2001 Therefore, the glucose-insulin-potassium regimen might be beneficial in acute myocardial infarction and useful in the management of patients with septicemia, septic shock, and other inflammatory diseases in which tumor necrosis factor-alpha and macrophage migration-inhibitory factor have important roles. Glucose 15-22 tumor necrosis factor Homo sapiens 213-240 11900368-0 2001 Tumor necrosis factor-alpha, sphingomyelinase and ceramides activate tyrosine kinase, p21Ras and phosphatidylinositol 3-kinase: implications for glucose transport and insulin resistance. Glucose 145-152 tumor necrosis factor Homo sapiens 0-27 11227245-6 2000 Another factor is given by Tumor Necrosis Factor-alpha, which is overexpressed in animal and human obesity, producing insulin signaling and glucose uptake inhibition. Glucose 140-147 tumor necrosis factor Homo sapiens 27-54 11227245-9 2000 Adipose tissue also, increase TNF-alpha secretion impairing glucose utilization and insulin signaling. Glucose 60-67 tumor necrosis factor Homo sapiens 30-39 11033992-14 2000 CONCLUSION: Changes in serum TNF-alpha that occur with exercise may play an important role in improving glucose metabolism parameters. Glucose 104-111 tumor necrosis factor Homo sapiens 29-38 10995595-2 2000 TNF-alpha impairs insulin-mediated glucose uptake in adipocytes, but because of lipolytic effects the interpretation of clinical studies and the extent to which TNF-alpha affects muscle insulin sensitivity are unclear. Glucose 35-42 tumor necrosis factor Homo sapiens 0-9 10905474-0 2000 Secretion of tumor necrosis factor-alpha shows a strong relationship to insulin-stimulated glucose transport in human adipose tissue. Glucose 91-98 tumor necrosis factor Homo sapiens 13-40 10837498-4 2000 Here, we demonstrate that chronic high glucose (CHG) causes a dramatic increase in the release of the inflammatory cytokine tumor necrosis factor alpha (TNFalpha), at least in part through enhanced TNFalpha mRNA transcription, mediated by ROS via activation of transcription factors nuclear factor kappaB (NF-kappaB) and activating protein-1 (AP-1). Glucose 39-46 tumor necrosis factor Homo sapiens 124-151 10837498-4 2000 Here, we demonstrate that chronic high glucose (CHG) causes a dramatic increase in the release of the inflammatory cytokine tumor necrosis factor alpha (TNFalpha), at least in part through enhanced TNFalpha mRNA transcription, mediated by ROS via activation of transcription factors nuclear factor kappaB (NF-kappaB) and activating protein-1 (AP-1). Glucose 39-46 tumor necrosis factor Homo sapiens 153-161 10837498-4 2000 Here, we demonstrate that chronic high glucose (CHG) causes a dramatic increase in the release of the inflammatory cytokine tumor necrosis factor alpha (TNFalpha), at least in part through enhanced TNFalpha mRNA transcription, mediated by ROS via activation of transcription factors nuclear factor kappaB (NF-kappaB) and activating protein-1 (AP-1). Glucose 39-46 tumor necrosis factor Homo sapiens 198-206 10875261-8 2000 We conclude that p60-TNFR mediates the antiadipogenic effect as well as the down-regulation of GLUT4 by TNF, thereby leading to long-term inhibition of insulin-stimulated glucose transport. Glucose 171-178 tumor necrosis factor Homo sapiens 21-24 10905474-1 2000 Some animal models suggest that tumor necrosis factor (TNF)-alpha is a key component in obesity-linked insulin resistance because it inhibits insulin receptor signaling and glucose transport in insulin-sensitive tissues. Glucose 173-180 tumor necrosis factor Homo sapiens 32-65 10905474-4 2000 We found a strong inverse correlation between adipose TNF-alpha secretion and maximum insulin-stimulated glucose transport in adipocytes that was independent of fat cell volume, age, and BMI (P < 0.001, r = 0.58). Glucose 105-112 tumor necrosis factor Homo sapiens 54-63 10905474-5 2000 As much as one-third of the variation in insulin-stimulated glucose transport could be accounted for by variations in TNF-alpha secretion. Glucose 60-67 tumor necrosis factor Homo sapiens 118-127 10905474-7 2000 Furthermore, subcutaneous adipose tissue of 4 obese women (BMI 40+/-4) incubated with TNF-A for 24 h showed a one-third concentration-dependent inhibition of insulin-stimulated glucose transport (P < 0.01). Glucose 177-184 tumor necrosis factor Homo sapiens 86-91 10905474-8 2000 In conclusion, adipose TNF-alpha may be an important specific and local factor in adipose tissue that influences the ability of insulin to stimulate glucose transport in human fat cells, at least in obese women. Glucose 149-156 tumor necrosis factor Homo sapiens 23-32 10727667-9 2000 An antioxidant N-acetyl-L-cysteine and a selective protein kinase C (PKC) inhibitor GF109203X significantly suppressed the TNFalpha-induced NF-kappaB activation, and abrogated potentiation of TNFalpha-induced NF-kappaB activity caused by high glucose (27.5 mmol/l). Glucose 243-250 tumor necrosis factor Homo sapiens 123-131 10668912-5 1999 Recent studies demonstrated that TNF directly interferes with the insulin signaling cascade at early steps and, thus, impairs insulin-stimulated glucose transport. Glucose 145-152 tumor necrosis factor Homo sapiens 33-36 10727667-6 2000 High glucose or mannitol also enhanced TNFalpha-stimulated NF-kappaB activity. Glucose 5-12 tumor necrosis factor Homo sapiens 39-47 10727667-7 2000 Incubation with high glucose for 48 h followed by stimulation with TNFalpha led to a marked potentiation of NF-kappaB activation compared with normoglycemic (5.5 mmol/l) VSMCs exposed to TNFalpha, while mannitol attenuated this effect. Glucose 21-28 tumor necrosis factor Homo sapiens 187-195 10542046-6 1999 Palmitate also abrogated TNF-dependent enhancement of basal glucose uptake, suggesting that palmitate has the capacity to render muscle cells resistant not only to insulin but also to TNF with respect to glucose transport by GLUT4 and GLUT1, respectively. Glucose 60-67 tumor necrosis factor Homo sapiens 25-28 10542046-6 1999 Palmitate also abrogated TNF-dependent enhancement of basal glucose uptake, suggesting that palmitate has the capacity to render muscle cells resistant not only to insulin but also to TNF with respect to glucose transport by GLUT4 and GLUT1, respectively. Glucose 204-211 tumor necrosis factor Homo sapiens 184-187 10542046-0 1999 Cross-talk mechanisms in the development of insulin resistance of skeletal muscle cells palmitate rather than tumour necrosis factor inhibits insulin-dependent protein kinase B (PKB)/Akt stimulation and glucose uptake. Glucose 203-210 tumor necrosis factor Homo sapiens 110-132 10542046-3 1999 We here show that, although TNF downregulated insulin-induced insulin receptor (IR) and IR substrate (IRS)-1 phosphorylation as well as phosphoinositide 3-kinase (PI3-kinase) activity in pmi28 myotubes, this was, unlike in adipocytes, not sufficient to affect insulin-induced glucose transport. Glucose 276-283 tumor necrosis factor Homo sapiens 28-31 10469164-5 1999 Such changes are combined with a decline in plasma DHEAS and IGF-I concentration and a rise in plasma TNF-alpha concentrations and oxidative stress, which, in turn, may interact with the anthropometric changes determining the worsening in insulin-mediated glucose uptake. Glucose 256-263 tumor necrosis factor Homo sapiens 102-111 10542046-4 1999 Rather, TNF increased membrane expression of GLUT1 and glucose transport in these muscle cells. Glucose 55-62 tumor necrosis factor Homo sapiens 8-11 10535400-6 1999 However, TNFalpha levels were significantly elevated in obese subjects with a 2-hour glucose level more than 140 mg/dL (n = 8) compared with the other obese subjects (n = 18) and the non-obese controls (2.88 +/- 0.46 v 1.75 +/- 0.10 and 1.65 +/- 0.18 pg/mL, respectively, P < .01). Glucose 85-92 tumor necrosis factor Homo sapiens 9-17 10535400-7 1999 Furthermore, the TNFalpha level correlated significantly with the waist to hip ratio ([WHR] r = .53, P < .01) and fasting and post-oral glucose tolerance test (OGTT) insulin levels (r = .47, P < .02), but not with the BMI, and was higher in obese women with a WHR more than 0.90 (n = 14) in comparison to those with a WHR less than 0.90 (n = 12, 2.47 +/- 0.29 v 1.66 +/- 0.18 pg/mL, respectively, P < .03). Glucose 139-146 tumor necrosis factor Homo sapiens 17-25 9920095-10 1999 Individuals with normal glucose tolerance had lower log TNF alpha concentrations than those with impaired glucose tolerance or type 2 DM (both P = 0.03, adjusted for age and sex), although differences were not significant after adjustment for HOMA IR (both P > 0.25). Glucose 24-31 tumor necrosis factor Homo sapiens 56-65 10433158-7 1999 Combined stimulation by high glucose or spent dialysate, together with IL-1beta or TNFalpha, showed a greater increase in TGFbeta1 mRNA expression and protein secretion compared to stimulation by high glucose or spent dialysate alone. Glucose 201-208 tumor necrosis factor Homo sapiens 83-91 11715473-1 1999 OBJECTIVE: To investigate the relationship between the G to A variant at the--308 bp of the promoter region of tumor necrosis factor-alpha gene (TNF-alpha-P) and the body adiposity, the insulin secretion and action, and the glucose and lipid levels in Chinese population. Glucose 224-231 tumor necrosis factor Homo sapiens 111-138 11715473-1 1999 OBJECTIVE: To investigate the relationship between the G to A variant at the--308 bp of the promoter region of tumor necrosis factor-alpha gene (TNF-alpha-P) and the body adiposity, the insulin secretion and action, and the glucose and lipid levels in Chinese population. Glucose 224-231 tumor necrosis factor Homo sapiens 145-154 10355025-3 1999 In adipose tissue, in particular, TNF alpha has been demonstrated to regulate or interfere with adipocyte metabolism at numerous sites including transcriptional regulation, glucose and fatty acid metabolism and hormone receptor signaling. Glucose 173-180 tumor necrosis factor Homo sapiens 34-43 10373483-5 1999 TNFalpha inhibited p70(s6k) activation by glucose-stimulated beta-cells of the islets of Langerhans in a dose- and time-dependent manner, with maximal inhibition observed at approximately 20-50 ng/ml, detected after 24 and 48 h of exposure. Glucose 42-49 tumor necrosis factor Homo sapiens 0-8 10233023-1 1999 In L6 myotubes, glucose uptake stimulated by interferon (IFN)-gamma or lipopolysaccharides (LPS) and a combination of LPS, IFN-gamma, and tumor necrosis factor (TNF)-alpha was inhibited by the antioxidant pyrrolidinedithiocarbamate and potentiated in reduced glutathione (GSH)-deficient cells. Glucose 16-23 tumor necrosis factor Homo sapiens 138-171 10233023-2 1999 Also, the stimulatory effect of LPS and IFN-gamma individually, and of a combination of LPS, IFN-gamma, and TNF-alpha, on glucose uptake was associated with an increased level of intracellular oxidants (dichlorofluorescein assay) and loss of intracellular GSH. Glucose 122-129 tumor necrosis factor Homo sapiens 108-117 9920095-12 1999 We conclude that in this homogeneous Native Canadian population, circulating TNF alpha concentrations are positively correlated with insulin resistance across a spectrum of glucose tolerance. Glucose 173-180 tumor necrosis factor Homo sapiens 77-86 9832415-0 1998 Effects of tumor necrosis factor-alpha on glucose metabolism in cultured human muscle cells from nondiabetic and type 2 diabetic subjects. Glucose 42-49 tumor necrosis factor Homo sapiens 11-38 10419100-7 1999 This demonstrates the existence of a novel signaling pathway for TNF-alpha that could contribute to the effects of this cytokine in stimulating basal glucose uptake. Glucose 150-157 tumor necrosis factor Homo sapiens 65-74 10419100-10 1999 Our work provides further mechanisms whereby TNF-alpha and ceramides produce insulin resistance and decrease the effectiveness of insulin in stimulating glucose disposal from the blood. Glucose 153-160 tumor necrosis factor Homo sapiens 45-54 10419100-11 1999 Conversely, TNF-alpha and ceramides increase the ability of adipocytes to take up glucose and store triacylglycerol in the absence of insulin. Glucose 82-89 tumor necrosis factor Homo sapiens 12-21 9918825-4 1998 Decreased glucose uptake (M value) in peripheral tissues was accompanied by a significantly increased TNF-alpha mRNA in skeletal muscle (r=0.867, p=0.0025). Glucose 10-17 tumor necrosis factor Homo sapiens 102-111 9832415-1 1998 The effects of tumor necrosis factor-alpha (TNF alpha) on glucose uptake and glycogen synthase (GS) activity were studied in human skeletal muscle cell cultures from nondiabetic and type 2 diabetic subjects. Glucose 58-65 tumor necrosis factor Homo sapiens 44-53 9832415-2 1998 In nondiabetic muscle cells, acute (90-min) exposure to TNF alpha (5 ng/ml) stimulated glucose uptake (73 +/- 14% increase) to a greater extent than insulin (37 +/- 4%; P < 0.02). Glucose 87-94 tumor necrosis factor Homo sapiens 56-65 9832415-8 1998 In summary, both acute and prolonged treatment with TNF alpha up-regulate glucose uptake activity in cultured human muscle cells, but reduce GS activity. Glucose 74-81 tumor necrosis factor Homo sapiens 52-61 9832415-9 1998 Increased skeletal muscle glucose uptake in conditions of TNF alpha excess may serve as a compensatory mechanism in the insulin resistance of type 2 diabetes. Glucose 26-33 tumor necrosis factor Homo sapiens 58-67 9691088-3 1998 Treatment of human islets with a combination of tumor necrosis factor (TNF) + lipopolysaccharide (LPS) + interferon-gamma (IFN-gamma) stimulates inducible nitric oxide synthase (iNOS) expression, nitric oxide production, and inhibits glucose-stimulated insulin secretion. Glucose 234-241 tumor necrosis factor Homo sapiens 48-69 9714125-2 1998 TNF-alpha decreases insulin-dependent glucose uptake by inhibiting autophosphorylation of the insulin receptor, suggesting that TNF-alpha may play a role in insulin resistance. Glucose 38-45 tumor necrosis factor Homo sapiens 0-9 9714125-2 1998 TNF-alpha decreases insulin-dependent glucose uptake by inhibiting autophosphorylation of the insulin receptor, suggesting that TNF-alpha may play a role in insulin resistance. Glucose 38-45 tumor necrosis factor Homo sapiens 128-137 9714125-6 1998 TNF-alpha was significantly related to body mass index, fasting glucose levels, and serum triglyceride levels and inversely related to the high density lipoprotein cholesterol level. Glucose 64-71 tumor necrosis factor Homo sapiens 0-9 9697673-2 1998 Initial experiments demonstrated that tumor necrosis factor-alpha (TNFalpha) release (assessed by TNF-direct immunoassay [DIA]) from PMO isolated from the peritoneal cavities of patients exposed to conventional fluid (PD4 1.36% glucose) was lowest after 30 min of intraperitoneal dwell (3591+/-1200 versus 28,946+/-9359 for 240-min dwell [pg/ml], n=5, P < 0.05). Glucose 228-235 tumor necrosis factor Homo sapiens 38-65 9697673-2 1998 Initial experiments demonstrated that tumor necrosis factor-alpha (TNFalpha) release (assessed by TNF-direct immunoassay [DIA]) from PMO isolated from the peritoneal cavities of patients exposed to conventional fluid (PD4 1.36% glucose) was lowest after 30 min of intraperitoneal dwell (3591+/-1200 versus 28,946+/-9359 for 240-min dwell [pg/ml], n=5, P < 0.05). Glucose 228-235 tumor necrosis factor Homo sapiens 67-75 9697673-2 1998 Initial experiments demonstrated that tumor necrosis factor-alpha (TNFalpha) release (assessed by TNF-direct immunoassay [DIA]) from PMO isolated from the peritoneal cavities of patients exposed to conventional fluid (PD4 1.36% glucose) was lowest after 30 min of intraperitoneal dwell (3591+/-1200 versus 28,946+/-9359 for 240-min dwell [pg/ml], n=5, P < 0.05). Glucose 228-235 tumor necrosis factor Homo sapiens 67-70 9697673-5 1998 Exposure of PMO to TBL or TB (1.36% glucose) resulted in a significant increase in the generation of TNFalpha (pg/2 X 10(6) PMO) compared with PD4. Glucose 36-43 tumor necrosis factor Homo sapiens 101-109 9691088-3 1998 Treatment of human islets with a combination of tumor necrosis factor (TNF) + lipopolysaccharide (LPS) + interferon-gamma (IFN-gamma) stimulates inducible nitric oxide synthase (iNOS) expression, nitric oxide production, and inhibits glucose-stimulated insulin secretion. Glucose 234-241 tumor necrosis factor Homo sapiens 71-74 9709967-7 1998 The magnitude of weight loss and fall in TNFalpha were related to basal body weight (r = 0.57, P < 0.001) and basal TNFalpha (r = 0.55, P < 0.001) concentrations, respectively, but not to each other or to the glucose-induced insulin release (area under the curve). Glucose 215-222 tumor necrosis factor Homo sapiens 41-49 9492058-4 1998 Moreover, TNF-alpha caused an insulin resistance on the insulin-induced glucose uptake in brown adipocytes. Glucose 72-79 tumor necrosis factor Homo sapiens 10-19 11061332-0 1998 High glucose concentrations increase the tumor necrosis factor-alpha production capacity by human peripheral blood mononuclear cells. Glucose 5-12 tumor necrosis factor Homo sapiens 41-68 11061332-2 1998 It has been recently shown that glucose can induce the synthesis of TNF and IL-6 in human monocytes. Glucose 32-39 tumor necrosis factor Homo sapiens 68-71 11061332-3 1998 The aim of the present study was to investigate the effect of glucose on unstimulated and lipopolysaccharide (LPS)-induced TNF and IL-1 production by human peripheral blood mononuclear cells (PBMC). Glucose 62-69 tumor necrosis factor Homo sapiens 123-126 11061332-5 1998 The LPS-stimulated production of TNF was enhanced when cells were preincubated with increasing glucose concentrations. Glucose 95-102 tumor necrosis factor Homo sapiens 33-36 11061332-7 1998 In conclusion, high glucose concentrations can increase the stimulated TNF production capacity, with possible important consequences for patients with diabetes mellitus. Glucose 20-27 tumor necrosis factor Homo sapiens 71-74 9492058-9 1998 Our results indicate that TNF-alpha induced an IRS-2- but not IRS-1-mediated insulin resistance on glucose transport and lipid synthesis in fetal brown adipocytes. Glucose 99-106 tumor necrosis factor Homo sapiens 26-35 9469498-14 1998 High glucose concentration induced an increase in TNF-alpha production by unstimulated PBMCs, a decrease in TNF-alpha production by endotoxin-stimulated PBMCs, and an inhibition of PMN functions. Glucose 5-12 tumor necrosis factor Homo sapiens 50-59 9469498-14 1998 High glucose concentration induced an increase in TNF-alpha production by unstimulated PBMCs, a decrease in TNF-alpha production by endotoxin-stimulated PBMCs, and an inhibition of PMN functions. Glucose 5-12 tumor necrosis factor Homo sapiens 108-117 9595645-2 1998 We studied the influence of supernatants from stored whole blood and buffy-coat-depleted SAGM (saline, adenine, glucose and mannitol) blood in stimulating TNF-alpha and IL-2 release in an ex vivo assay. Glucose 112-119 tumor necrosis factor Homo sapiens 155-164 9482542-5 1998 The direct effects of interferon-alpha, interleukin-1beta, and tumor necrosis factor-alpha on glucose-sensitive neurons in two specific regions of the hypothalamus could cause profound changes in eating patterns in animals and humans. Glucose 94-101 tumor necrosis factor Homo sapiens 63-90 9421370-10 1998 Our work provides further mechanisms for the effects of TNF-alpha and ceramides in increasing non-insulin-dependent glucose uptake and decreasing insulin-stimulated uptake in vivo. Glucose 116-123 tumor necrosis factor Homo sapiens 56-65 9440488-8 1998 The TNFalpha concentration also correlated significantly with fasting glucose and proinsulin concentrations, as well as glucose and proinsulin levels after glucose ingestion. Glucose 70-77 tumor necrosis factor Homo sapiens 4-12 9440488-10 1998 The present results provide clinical evidence for a basic role of TNFalpha in hypertriglyceridemia, glucose intolerance, and the etiology of premature CHD. Glucose 100-107 tumor necrosis factor Homo sapiens 66-74 9344602-0 1997 Influence of cycloheximide-mediated downregulation of glucose transport on TNF alpha-induced apoptosis. Glucose 54-61 tumor necrosis factor Homo sapiens 75-84 9655153-17 1997 When dextrose concentration in TB and TBL was increased from 1.5% to 4.25%, TNFalpha secretion by PMphi was not suppressed by more than 49%, even after 30 minutes incubation. Glucose 5-13 tumor necrosis factor Homo sapiens 76-84 9655153-18 1997 Moreover, suppression of TNFalpha mRNA levels could not be detected with TB or TBL even at high dextrose concentrations. Glucose 96-104 tumor necrosis factor Homo sapiens 25-33 9591299-8 1997 In acute phase of meningitis correlations between CSF concentration of TNF-alpha and IL-1 beta and other indexes of inflammation in CSF: pleocytosis, concentration of protein and glucose were found. Glucose 179-186 tumor necrosis factor Homo sapiens 71-80 9344602-10 1997 In conclusion, CX is proposed to contribute to TNF alpha-induced apoptosis predominantly by interference with glucose transport; the exact nature of this effect remains to be elucidated. Glucose 110-117 tumor necrosis factor Homo sapiens 47-56 9112394-4 1997 Firstly, TNF alpha was shown to increase the uptake of glucose substrate in a time- and dose-dependent manner. Glucose 55-62 tumor necrosis factor Homo sapiens 9-18 9287048-9 1997 The integrated area under the curve of serum insulin concentrations, measured in response to a 75-g oral glucose challenge, and the percent body fat, measured by bioelectric impedance, were significantly increased in TNF-2 subjects (226.8 +/- 33 vs. 139.4 +/- 17.8 mU/l, P = 0.032; 33.6 +/- 2.8 vs. 24.9 +/- 2%, P = 0.01). Glucose 105-112 tumor necrosis factor Homo sapiens 217-220 9287048-10 1997 TNF-2 subjects also showed a decreased insulin sensitivity index, as determined by the frequently sampled intravenous glucose tolerance test with minimal model analysis (1.9 +/- 0.4 vs. 3.05 +/- 0.3 min(-1) x mU(-1) x l(-1), P = 0.03). Glucose 118-125 tumor necrosis factor Homo sapiens 0-3 9411420-1 1997 In 27 patients with uncontrolled type 1 diabetes the changes of the endogenous TNF alpha serum concentration in correlation with blood glucose level were investigated. Glucose 135-142 tumor necrosis factor Homo sapiens 79-88 9160827-1 1997 Recombinant human tumor necrosis factor-alpha (TNF) injection in mice was associated with a reduced blood glucose level, already manifest 6 hours following cytokine administration. Glucose 106-113 tumor necrosis factor Homo sapiens 18-45 9160827-1 1997 Recombinant human tumor necrosis factor-alpha (TNF) injection in mice was associated with a reduced blood glucose level, already manifest 6 hours following cytokine administration. Glucose 106-113 tumor necrosis factor Homo sapiens 47-50 9411420-7 1997 The level of TNF alpha markedly decreases together with the decrease of blood glucose level in each patient. Glucose 78-85 tumor necrosis factor Homo sapiens 13-22 9411420-9 1997 The results presented above unequivocally show that there is a correlation between endogenous TNF alpha and glucose level in serum of the patients with type 1 diabetes (at the decompensation stage of the disease). Glucose 108-115 tumor necrosis factor Homo sapiens 94-103 9109412-2 1997 Tumor necrosis factor-alpha also markedly increased glucose consumption, and its cytotoxicity was modified by glucose concentrations in the growth medium; higher glucose levels were associated with increased cell survival. Glucose 52-59 tumor necrosis factor Homo sapiens 0-27 9139834-8 1997 After the isolated limb perfusion, TNF-alpha entered the systemic circulation and induced metabolic changes resulting in a doubling of arterial lactate concentrations, decreased arterial glucose concentrations and decreased arterial amino-acid concentrations. Glucose 187-194 tumor necrosis factor Homo sapiens 35-44 9109412-2 1997 Tumor necrosis factor-alpha also markedly increased glucose consumption, and its cytotoxicity was modified by glucose concentrations in the growth medium; higher glucose levels were associated with increased cell survival. Glucose 110-117 tumor necrosis factor Homo sapiens 0-27 9110145-7 1997 High TNF production capacity was associated with faster fever clearance and parasite clearance and, in patients with severe malaria, with higher blood glucose levels. Glucose 151-158 tumor necrosis factor Homo sapiens 5-8 8988743-12 1997 Plasma concentrations of TNF-alpha might play a modulating role in the metabolic changes that occur after administration of a glucose load. Glucose 126-133 tumor necrosis factor Homo sapiens 25-34 8988743-13 1997 The role of TNF-alpha on glucose and lipid metabolism in cancer patients would be a worthy subject of future investigations. Glucose 25-32 tumor necrosis factor Homo sapiens 12-21 8666148-4 1996 Both IL-6 and TNF-alpha mRNA levels and immunoreactivity were significantly increased by treatment with 33 mmol/l glucose compared with treatment with 11 mmol/l glucose or 11 mmol/l glucose with 22 mmol/l mannitol. Glucose 114-121 tumor necrosis factor Homo sapiens 14-23 8914021-0 1996 Induction of TGF-beta 1 synthesis in D-glucose primed human proximal tubular cells by IL-1 beta and TNF alpha. Glucose 37-46 tumor necrosis factor Homo sapiens 100-109 8914021-1 1996 The aim of the present study was to examine whether the induction of TGF-beta 1 synthesis by the pro-inflammatory macrophage derived cytokines, IL-1 beta or TNF alpha, was modified by alterations in D-glucose concentrations. Glucose 199-208 tumor necrosis factor Homo sapiens 157-166 8940683-6 1996 Recent studies showed glucose uptake elevated in sepsis or TNF infusion. Glucose 22-29 tumor necrosis factor Homo sapiens 59-62 8894488-3 1996 Furthermore, TNF alpha expression and secretion are increased in adipose tissue from obese subjects and correlates with insulin resistance roughly measured as elevated fasting plasma insulin in spite of normal fasting blood glucose. Glucose 224-231 tumor necrosis factor Homo sapiens 13-22 8666148-0 1996 Glucose-dependent interleukin 6 and tumor necrosis factor production by human peripheral blood monocytes in vitro. Glucose 0-7 tumor necrosis factor Homo sapiens 36-57 8666148-4 1996 Both IL-6 and TNF-alpha mRNA levels and immunoreactivity were significantly increased by treatment with 33 mmol/l glucose compared with treatment with 11 mmol/l glucose or 11 mmol/l glucose with 22 mmol/l mannitol. Glucose 161-168 tumor necrosis factor Homo sapiens 14-23 8666148-4 1996 Both IL-6 and TNF-alpha mRNA levels and immunoreactivity were significantly increased by treatment with 33 mmol/l glucose compared with treatment with 11 mmol/l glucose or 11 mmol/l glucose with 22 mmol/l mannitol. Glucose 161-168 tumor necrosis factor Homo sapiens 14-23 8666148-5 1996 In addition, preincubation of the cells with an anti-TNF monoclonal antibody (mAb) blocked the stimulatory effect of 33 mmol/l glucose on IL-6 synthesis and secretion. Glucose 127-134 tumor necrosis factor Homo sapiens 53-56 8663078-0 1996 Glucose metabolism to glucosamine is necessary for glucose stimulation of transforming growth factor-alpha gene transcription. Glucose 51-58 tumor necrosis factor Homo sapiens 74-106 8783331-8 1996 Cryopreservation did not significantly modify the hormone response to glucose but it partially reversed the TNF alpha-induced inhibitory effect on insulin release in the presence of 20 mM glucose. Glucose 188-195 tumor necrosis factor Homo sapiens 108-117 8663078-1 1996 Transforming growth factor-alpha (TGFalpha) gene transcription can be increased when arterial smooth muscle cells are exposed to supraphysiological concentrations of glucose, and this effect of glucose can be mimicked by glucosamine. Glucose 166-173 tumor necrosis factor Homo sapiens 0-32 8663078-1 1996 Transforming growth factor-alpha (TGFalpha) gene transcription can be increased when arterial smooth muscle cells are exposed to supraphysiological concentrations of glucose, and this effect of glucose can be mimicked by glucosamine. Glucose 194-201 tumor necrosis factor Homo sapiens 0-32 8613535-3 1996 To more closely link TNF expression with whole body insulin action, we examined the expression of TNF by muscle, which is responsible for the majority of glucose uptake in vivo. Glucose 154-161 tumor necrosis factor Homo sapiens 98-101 8648229-4 1996 CSF glucose levels correlated highly with levels of IL-10, sTNFR-55, and sTNFR-75 and weakly with TNF-alpha and IL-6. Glucose 4-11 tumor necrosis factor Homo sapiens 98-107 8617880-10 1996 In summary, the data suggest that TNF-alpha and high glucose modulate insulin receptor-signaling through different mechanisms: (a) TNF-alpha modulates insulin receptor signals by PTPase activation, whereas glucose acts through activation of PKC. Glucose 53-60 tumor necrosis factor Homo sapiens 131-140 8617880-10 1996 In summary, the data suggest that TNF-alpha and high glucose modulate insulin receptor-signaling through different mechanisms: (a) TNF-alpha modulates insulin receptor signals by PTPase activation, whereas glucose acts through activation of PKC. Glucose 206-213 tumor necrosis factor Homo sapiens 34-43 8613535-7 1996 TNF expression in the insulin resistant subjects and the diabetic patients was fourfold higher than in the insulin sensitive subjects, and there was a significant inverse linear relationship between maximal glucose disposal rate and muscle TNF (r = -0.60, P < 0.02). Glucose 207-214 tumor necrosis factor Homo sapiens 0-3 8543058-0 1995 TNF-alpha inhibits glucose-induced insulin secretion in a pancreatic beta-cell line (INS-1). Glucose 19-26 tumor necrosis factor Homo sapiens 0-9 8543058-3 1995 The possibility that TNF-alpha might directly reduce glucose-stimulated insulin secretion in pancreatic beta-cells was examined by using an established pancreatic beta-cell line (INS-1). Glucose 53-60 tumor necrosis factor Homo sapiens 21-30 8543058-5 1995 However, over a longer time period (24 h), TNF-alpha decreased glucose-induced insulin secretion without affecting the total amount of insulin in the cell. Glucose 63-70 tumor necrosis factor Homo sapiens 43-52 8543058-6 1995 In the presence of TNF-alpha levels of 0, 10, 100 and 1000 U/ml, the respective 20 mM glucose-induced insulin secretion was 1.736 +/- 0.166, 1.750 +/- 0.302, 1.550 +/- 0.200, and 1.400 +/- 0.112 mU/ml per 3 x 10(5) cells in 24 h. Glucose 86-93 tumor necrosis factor Homo sapiens 19-28 7556976-0 1995 Effects of tumour necrosis factor alpha (TNF alpha) on glucose transport and lipid metabolism of newly-differentiated human fat cells in cell culture. Glucose 55-62 tumor necrosis factor Homo sapiens 41-50 7492275-7 1995 RESULTS: The incorporation of 14C-labeled glucose (D-[U-14C]glucose) into phosphatidylcholine and phosphatidylglycerol was selectively inhibited either by 8-Br-cGMP or in the presence of TNF-alpha, PGE2, or nitroprusside, all of which caused an increase in the intracellular levels of cGMP. Glucose 42-49 tumor necrosis factor Homo sapiens 187-196 7695204-4 1995 IL-6 and TNF-alpha levels of culture supernatants incubated with 22 mM or 33 mM glucose showed considerable increase over basal levels incubated with 11 mM glucose, whereas those levels incubated with high concentration of mannitol showed no increase. Glucose 80-87 tumor necrosis factor Homo sapiens 9-18 7695204-4 1995 IL-6 and TNF-alpha levels of culture supernatants incubated with 22 mM or 33 mM glucose showed considerable increase over basal levels incubated with 11 mM glucose, whereas those levels incubated with high concentration of mannitol showed no increase. Glucose 156-163 tumor necrosis factor Homo sapiens 9-18 7695204-7 1995 In this study, we revealed the effect of glucose and AGEs on the production of IL-6 or TNF-alpha by human monocytes. Glucose 41-48 tumor necrosis factor Homo sapiens 87-96 8197147-4 1994 Chronic exposure of adipocytes to low concentrations of TNF-alpha strongly inhibits insulin-stimulated glucose uptake. Glucose 103-110 tumor necrosis factor Homo sapiens 56-65 7812976-1 1995 It has been reported that the cytotoxic effect of tumor necrosis factor (TNF) on cells of several tumor cell lines was potentiated in culture media lacking glucose. Glucose 156-163 tumor necrosis factor Homo sapiens 50-71 7812976-1 1995 It has been reported that the cytotoxic effect of tumor necrosis factor (TNF) on cells of several tumor cell lines was potentiated in culture media lacking glucose. Glucose 156-163 tumor necrosis factor Homo sapiens 73-76 7812976-3 1995 The present study was aimed to reveal whether (a) the administration of the glucose antimetabolite 2-deoxy-D-glucose (2DG) has an effect similar to that of reduction of the extracellular glucose concentration; (b) the combined treatment with TNF and 2DG, similar to TNF alone, leads to apoptosis; and (c) there is a preference of cells in a particular phase of the cell cycle to undergo apoptosis in the presence of these agents. Glucose 76-83 tumor necrosis factor Homo sapiens 242-245 7812976-3 1995 The present study was aimed to reveal whether (a) the administration of the glucose antimetabolite 2-deoxy-D-glucose (2DG) has an effect similar to that of reduction of the extracellular glucose concentration; (b) the combined treatment with TNF and 2DG, similar to TNF alone, leads to apoptosis; and (c) there is a preference of cells in a particular phase of the cell cycle to undergo apoptosis in the presence of these agents. Glucose 76-83 tumor necrosis factor Homo sapiens 266-269 7812976-3 1995 The present study was aimed to reveal whether (a) the administration of the glucose antimetabolite 2-deoxy-D-glucose (2DG) has an effect similar to that of reduction of the extracellular glucose concentration; (b) the combined treatment with TNF and 2DG, similar to TNF alone, leads to apoptosis; and (c) there is a preference of cells in a particular phase of the cell cycle to undergo apoptosis in the presence of these agents. Glucose 109-116 tumor necrosis factor Homo sapiens 242-245 7812976-3 1995 The present study was aimed to reveal whether (a) the administration of the glucose antimetabolite 2-deoxy-D-glucose (2DG) has an effect similar to that of reduction of the extracellular glucose concentration; (b) the combined treatment with TNF and 2DG, similar to TNF alone, leads to apoptosis; and (c) there is a preference of cells in a particular phase of the cell cycle to undergo apoptosis in the presence of these agents. Glucose 109-116 tumor necrosis factor Homo sapiens 266-269 7598438-4 1995 The CSFs with detectable TNF alpha or IL1 beta had higher levels of IL6 (p < 0.02), protein (NS) and lower glucose levels (p < 0.02), compared with those in which TNF alpha and IL1 beta were absent. Glucose 110-117 tumor necrosis factor Homo sapiens 25-34 8314347-1 1994 The reduction of glucose supply induced the killing of tumor cells by tumor necrosis factor (TNF) in vivo and in vitro. Glucose 17-24 tumor necrosis factor Homo sapiens 70-91 7514190-6 1994 Combinations of cytokines, notably IL-1 beta plus IFN-gamma plus TNF-alpha, induced increased expression of inducible NO synthase mRNA after 6 h and resulted in a fivefold increase in medium nitrite accumulation after 48 h. These cytokines did not impair glucose metabolism or insulin release in response to 16.7 mM glucose, but there was an 80% decrease in islet insulin content. Glucose 255-262 tumor necrosis factor Homo sapiens 65-74 8314347-1 1994 The reduction of glucose supply induced the killing of tumor cells by tumor necrosis factor (TNF) in vivo and in vitro. Glucose 17-24 tumor necrosis factor Homo sapiens 93-96 8314347-4 1994 Therefore, the killing mechanism of TNF under conditions of reduced glucose supply was investigated. Glucose 68-75 tumor necrosis factor Homo sapiens 36-39 8314347-9 1994 We conclude that, under conditions of low glucose supply, TNF can assume the role of a growth factor in transformed cells. Glucose 42-49 tumor necrosis factor Homo sapiens 58-61 8142598-1 1993 The cytokine cachectin/TNF induces a rapid increase in lactate production and in glucose metabolism in L6 myocytes in culture; glucose uptake was maximal after 17 h, while elevated glucose utilization and lactate production persisted for up to 32 h. These increases are suggestive of increased glycolytic activity, and were associated with a 10% decrease in cellular oxygen consumption and a comparable decrease in the production of 14C-labelled CO2 from 14C-labelled glucose. Glucose 81-88 tumor necrosis factor Homo sapiens 13-22 8286511-6 1993 RESULTS: All three cytokines, particularly TNF-alpha, inhibited the incorporation of D-glucose uniformly labelled with 14C (D-(U-14C) glucose) into phosphatidylcholine. Glucose 85-94 tumor necrosis factor Homo sapiens 43-52 8286512-5 1993 MAIN OUTCOME MEASURES: Effect of TNF-alpha on the incorporation of D-glucose and palmitate, both of which had been uniformly labelled with 14C (D-(U-14C) glucose and (U-14C) palmitate), into various phospholipid fractions by pneumocytes isolated from both healthy lungs and those from patients with lung cancer. Glucose 67-76 tumor necrosis factor Homo sapiens 33-42 8142598-1 1993 The cytokine cachectin/TNF induces a rapid increase in lactate production and in glucose metabolism in L6 myocytes in culture; glucose uptake was maximal after 17 h, while elevated glucose utilization and lactate production persisted for up to 32 h. These increases are suggestive of increased glycolytic activity, and were associated with a 10% decrease in cellular oxygen consumption and a comparable decrease in the production of 14C-labelled CO2 from 14C-labelled glucose. Glucose 127-134 tumor necrosis factor Homo sapiens 13-22 8142598-1 1993 The cytokine cachectin/TNF induces a rapid increase in lactate production and in glucose metabolism in L6 myocytes in culture; glucose uptake was maximal after 17 h, while elevated glucose utilization and lactate production persisted for up to 32 h. These increases are suggestive of increased glycolytic activity, and were associated with a 10% decrease in cellular oxygen consumption and a comparable decrease in the production of 14C-labelled CO2 from 14C-labelled glucose. Glucose 127-134 tumor necrosis factor Homo sapiens 23-26 8142598-3 1993 Furthermore, maximal stimulation of pyruvate dehydrogenase (PDH) by dichloroacetate (DCA) treatment in conjunction with cachectin/TNF abolished lactate production, but increased glucose uptake persisted. Glucose 178-185 tumor necrosis factor Homo sapiens 130-133 8142598-1 1993 The cytokine cachectin/TNF induces a rapid increase in lactate production and in glucose metabolism in L6 myocytes in culture; glucose uptake was maximal after 17 h, while elevated glucose utilization and lactate production persisted for up to 32 h. These increases are suggestive of increased glycolytic activity, and were associated with a 10% decrease in cellular oxygen consumption and a comparable decrease in the production of 14C-labelled CO2 from 14C-labelled glucose. Glucose 81-88 tumor necrosis factor Homo sapiens 23-26 8142598-1 1993 The cytokine cachectin/TNF induces a rapid increase in lactate production and in glucose metabolism in L6 myocytes in culture; glucose uptake was maximal after 17 h, while elevated glucose utilization and lactate production persisted for up to 32 h. These increases are suggestive of increased glycolytic activity, and were associated with a 10% decrease in cellular oxygen consumption and a comparable decrease in the production of 14C-labelled CO2 from 14C-labelled glucose. Glucose 127-134 tumor necrosis factor Homo sapiens 13-22 8142598-1 1993 The cytokine cachectin/TNF induces a rapid increase in lactate production and in glucose metabolism in L6 myocytes in culture; glucose uptake was maximal after 17 h, while elevated glucose utilization and lactate production persisted for up to 32 h. These increases are suggestive of increased glycolytic activity, and were associated with a 10% decrease in cellular oxygen consumption and a comparable decrease in the production of 14C-labelled CO2 from 14C-labelled glucose. Glucose 127-134 tumor necrosis factor Homo sapiens 23-26 1727716-12 1992 These results suggest that sustained elevations of TNF during chronic therapy and prolonged production of TNF by patients and experimental animals with malignancies or infectious diseases may be an important mechanism for the enhanced glucose flux as well as the insulin resistance seen in these conditions. Glucose 235-242 tumor necrosis factor Homo sapiens 51-54 1511500-5 1992 Thus, the inflammatory cytokines IL-1 and TNF alpha reportedly detected in the circulation during severe sepsis may directly affect not only glucose uptake but also its subsequent metabolism within tissue fibroblasts. Glucose 141-148 tumor necrosis factor Homo sapiens 42-51 1314824-2 1992 Tumor necrosis factor alpha (TNF alpha), 12-O-tetradecanoylphorbol-13-acetate and cAMP stimulate hexose transport in quiescent 3T3-L1 preadipocytes by stabilizing the relatively labile mRNA coding for the basal glucose transporter, GLUT-1. Glucose 211-218 tumor necrosis factor Homo sapiens 0-27 1314824-2 1992 Tumor necrosis factor alpha (TNF alpha), 12-O-tetradecanoylphorbol-13-acetate and cAMP stimulate hexose transport in quiescent 3T3-L1 preadipocytes by stabilizing the relatively labile mRNA coding for the basal glucose transporter, GLUT-1. Glucose 211-218 tumor necrosis factor Homo sapiens 29-38 1727716-12 1992 These results suggest that sustained elevations of TNF during chronic therapy and prolonged production of TNF by patients and experimental animals with malignancies or infectious diseases may be an important mechanism for the enhanced glucose flux as well as the insulin resistance seen in these conditions. Glucose 235-242 tumor necrosis factor Homo sapiens 106-109 2141005-4 1990 The activity of rh TNF was enhanced by the absence of glucose, while it was reduced by addition of extraneous ATP. Glucose 54-61 tumor necrosis factor Homo sapiens 19-22 1928337-2 1991 TNF induced a transient stress hormone response, associated with an early and sustained rise in plasma glucose concentrations (percentage increase at 2 h 23 +/- 7; P less than 0.05). Glucose 103-110 tumor necrosis factor Homo sapiens 0-3 1997633-0 1991 Tumor necrosis factor increases in vivo glucose uptake in hepatic nonparenchymal cells. Glucose 40-47 tumor necrosis factor Homo sapiens 0-21 1997633-3 1991 Following TNF administration glucose uptake was increased in the liver, lung, spleen, and skin while it was not changed in muscle and testis. Glucose 29-36 tumor necrosis factor Homo sapiens 10-13 1997633-7 1991 In vivo glucose uptake in response to TNF was doubled in the Kupffer cells and increased by 56% in hepatic endothelial cells. Glucose 8-15 tumor necrosis factor Homo sapiens 38-41 1997633-9 1991 The prompt increase of glucose uptake in the reticuloendothelial cells of the liver, primarily in the Kupffer cells, following TNF administration suggests that a similar metabolic response of these cells to sepsis may be mediated at least in part by TNF. Glucose 23-30 tumor necrosis factor Homo sapiens 127-130 1997633-9 1991 The prompt increase of glucose uptake in the reticuloendothelial cells of the liver, primarily in the Kupffer cells, following TNF administration suggests that a similar metabolic response of these cells to sepsis may be mediated at least in part by TNF. Glucose 23-30 tumor necrosis factor Homo sapiens 250-253 1997633-10 1991 It is suggested that the increased glucose uptake by the hepatic nonparenchymal cells is a reflection of the immunomodulatory effect of TNF. Glucose 35-42 tumor necrosis factor Homo sapiens 136-139 2195296-1 1990 We studied the effect of recombinant human interleukin-1 beta (IL-1) and recombinant human tumor necrosis factor alpha/cachectin (TNF) on glucose kinetics in healthy rats by means of a primed constant infusion of D-(6-3H)glucose and D-[U-14C]glucose. Glucose 138-145 tumor necrosis factor Homo sapiens 91-118 2195296-1 1990 We studied the effect of recombinant human interleukin-1 beta (IL-1) and recombinant human tumor necrosis factor alpha/cachectin (TNF) on glucose kinetics in healthy rats by means of a primed constant infusion of D-(6-3H)glucose and D-[U-14C]glucose. Glucose 138-145 tumor necrosis factor Homo sapiens 130-133 34922513-10 2021 According to the genetic results, glucose activated TNF family to initiate apoptosis. Glucose 34-41 tumor necrosis factor Homo sapiens 52-55 34673277-8 2022 In addition, TMAO significantly increased TNF-alpha-induced P-selectin production in mesothelial cells, as well as high glucose-induced TNF-alpha and CCL2 expression in endothelial cells. Glucose 120-127 tumor necrosis factor Homo sapiens 136-145 34185112-6 2021 RESULTS: Compared with the high glucose group, the proliferation rate, migration rate, and the expression of alpha-SMA, bcl-2, TLR4, NF-kappaB, TNF-alpha, IL-6, IL- and IL-1 were significantly decreased in the high glucose + MSC-Exo-miR-26a mimics group, while the apoptosis rate and the expression of miR-26a, cleaved-caspase 3, cleaved-caspase 9 and Bax were significantly increased. Glucose 215-222 tumor necrosis factor Homo sapiens 144-153 34909822-8 2021 Moreover, multiple correlations revealed that in active women both IL-10 and TNF-alpha serum levels positively correlate with fasting glucose levels, and were negatively associated with HDL levels. Glucose 134-141 tumor necrosis factor Homo sapiens 77-86 34562655-0 2021 WJCPR11 reverses the TNF-alpha-induced inhibition of adipocyte differentiation and glucose uptake. Glucose 83-90 tumor necrosis factor Homo sapiens 21-30 34562655-6 2021 Furthermore, the tumor necrosis factor-alpha (TNF-alpha)-induced inhibition of adipocyte differentiation and downregulation of glucose uptake were markedly reversed by WJCPR11 treatment. Glucose 127-134 tumor necrosis factor Homo sapiens 17-44 34562655-6 2021 Furthermore, the tumor necrosis factor-alpha (TNF-alpha)-induced inhibition of adipocyte differentiation and downregulation of glucose uptake were markedly reversed by WJCPR11 treatment. Glucose 127-134 tumor necrosis factor Homo sapiens 46-55 34265211-8 2021 Changes in fasting glucose and AUC of OGTT (0-120 min) were positively correlated with changes in MCP-1 and TNF-alpha (p < 0.05). Glucose 19-26 tumor necrosis factor Homo sapiens 108-117 34439425-1 2021 In diabetic patients, high glucose and high oxidative states activate gene expression of transforming growth factor beta (TGF-beta) and further translocate Smad proteins into the nucleus of renal cells. Glucose 27-34 tumor necrosis factor Homo sapiens 89-120 34402375-6 2021 Firstly, we found that Tamsulosin reduced high glucose-induced expressions of TNF-alpha, IL-6, and IL-8. Glucose 47-54 tumor necrosis factor Homo sapiens 78-87 34469050-6 2021 Luminex assay of EAT-secretome identified increased release of various proinflammatory cytokines, including tumor necrosis factor-alpha (TNF-alpha), interferon-alpha 2 (IFNA2), interleukin 1 beta (IL1B), interleukin 5 (IL5), interleukin 13 (IL13), and CCL5, among others, in response to high glucose, high palmitate, and lipopolysaccharide. Glucose 292-299 tumor necrosis factor Homo sapiens 108-135 34469050-6 2021 Luminex assay of EAT-secretome identified increased release of various proinflammatory cytokines, including tumor necrosis factor-alpha (TNF-alpha), interferon-alpha 2 (IFNA2), interleukin 1 beta (IL1B), interleukin 5 (IL5), interleukin 13 (IL13), and CCL5, among others, in response to high glucose, high palmitate, and lipopolysaccharide. Glucose 292-299 tumor necrosis factor Homo sapiens 137-146 34210601-3 2021 METHODS: We characterized 265 T2D and non-diabetic Latin American subjects and assessed the relationship between the TNF system and fasting plasma glucose (FPG), hemoglobin-A1C (A1C), insulin (FPI), C-peptide and HOMA-Beta. Glucose 147-154 tumor necrosis factor Homo sapiens 117-120 34253808-8 2021 Finally, we found that inhibition of the two GTPases by TNFalpha abrogated the ability of MOTS-c to prompt GLUT4 translocation and glucose uptake. Glucose 131-138 tumor necrosis factor Homo sapiens 56-64 34371884-7 2021 Tumor necrosis factor-alpha (TNFalpha) correlated positively with change in fasting plasma glucose (r = 0.70, p < 0.001) and negatively with change in insulin sensitivity (r = -0.68, p < 0.01). Glucose 91-98 tumor necrosis factor Homo sapiens 0-27 34371884-7 2021 Tumor necrosis factor-alpha (TNFalpha) correlated positively with change in fasting plasma glucose (r = 0.70, p < 0.001) and negatively with change in insulin sensitivity (r = -0.68, p < 0.01). Glucose 91-98 tumor necrosis factor Homo sapiens 29-37 35506311-0 2022 circFTO upregulates transforming growth factor-alpha through sponging miR-148a-3p to regulate high glucose-induced ARPE-19 cells injury. Glucose 99-106 tumor necrosis factor Homo sapiens 20-52 35285061-7 2022 In the cell model, activated HDFs exposed to high-glucose medium enhanced the expression of Sec31a and collagen I through the activation of transforming growth factor beta, a profibrotic molecule. Glucose 50-57 tumor necrosis factor Homo sapiens 140-171 34100500-8 2021 Furthermore, DHA-PL and EPA-PL improved glucose uptake and glucose transporter type 4 translocation to the plasma membrane in TNF-alpha-treated adipocytes. Glucose 40-47 tumor necrosis factor Homo sapiens 126-135 34100500-8 2021 Furthermore, DHA-PL and EPA-PL improved glucose uptake and glucose transporter type 4 translocation to the plasma membrane in TNF-alpha-treated adipocytes. Glucose 59-66 tumor necrosis factor Homo sapiens 126-135 34064969-6 2021 Exposure to macrophages and elevated glucose levels (25 mM glucose) impacted gene expression of EMT inducers such as IL-6 and TNF-alpha as well as EMT transcription factors in benign (H6c7-pBp) and premalignant (H6c7-kras) PDEC. Glucose 37-44 tumor necrosis factor Homo sapiens 126-135 34064969-6 2021 Exposure to macrophages and elevated glucose levels (25 mM glucose) impacted gene expression of EMT inducers such as IL-6 and TNF-alpha as well as EMT transcription factors in benign (H6c7-pBp) and premalignant (H6c7-kras) PDEC. Glucose 59-66 tumor necrosis factor Homo sapiens 126-135 35610661-8 2022 At 5 and 20 ng/ml hTNF-alpha, lactate production diminished on day 3 up to day 5, while glucose uptake increased on day 5. Glucose 88-95 tumor necrosis factor Homo sapiens 18-28 35315086-8 2022 Moreover, ROSE-70 potently suppressed high glucose- and H2 O2 -induced accumulation of tumor necrosis factor-alpha (TNF-alpha) and nuclear factor-kappa B (NF-kappaB) were investigated in human umbilical vein endothelial cells (HUVECs). Glucose 43-50 tumor necrosis factor Homo sapiens 87-114 35321702-6 2022 RESULTS: AE reduced the lipid peroxidation (17%), nitric oxide (NO) (47-50%), tumor necrosis factor-alpha (TNF-alpha) (32%) and free radicals (50%) induced by glucose on macrophages. Glucose 159-166 tumor necrosis factor Homo sapiens 78-105 35315086-8 2022 Moreover, ROSE-70 potently suppressed high glucose- and H2 O2 -induced accumulation of tumor necrosis factor-alpha (TNF-alpha) and nuclear factor-kappa B (NF-kappaB) were investigated in human umbilical vein endothelial cells (HUVECs). Glucose 43-50 tumor necrosis factor Homo sapiens 116-125 35282448-4 2022 Subsequently, MSCs were stimulated with insulin and glucose thrice daily, resembling food uptake and both glucose uptake/GLUT-4 translocation and the expression of LIPE, ATGL, IL-6 and TNF-alpha genes were analyzed at predefined timepoints over three days. Glucose 52-59 tumor necrosis factor Homo sapiens 185-194