PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 11961304-0 2002 Effects of high glucose on interleukin-6 production in human mesangial cells. Glucose 16-23 interleukin 6 Homo sapiens 27-40 11961304-7 2002 Incubation of mesangial cells with high glucose (450 mg/dL) reduced the ratio of PCR products for IL-6 to beta-actin on densitometric results, while AGII (10(-7)M) increased it. Glucose 40-47 interleukin 6 Homo sapiens 98-102 11961304-8 2002 The IL-6 secretion in the supernatant was also increased by AGII and decreased by high glucose. Glucose 87-94 interleukin 6 Homo sapiens 4-8 11961304-9 2002 The IL-6 mRNA expression and IL-6 secretion in combination of high glucose and AGII were higher than those in high glucose and similar with those in control media. Glucose 67-74 interleukin 6 Homo sapiens 4-8 11961304-9 2002 The IL-6 mRNA expression and IL-6 secretion in combination of high glucose and AGII were higher than those in high glucose and similar with those in control media. Glucose 67-74 interleukin 6 Homo sapiens 29-33 11961304-9 2002 The IL-6 mRNA expression and IL-6 secretion in combination of high glucose and AGII were higher than those in high glucose and similar with those in control media. Glucose 115-122 interleukin 6 Homo sapiens 4-8 11961304-12 2002 The IL-6 production of mesangial cells in diabetic milieu may be complicated and depend on the local effects of high glucose and/or AGII. Glucose 117-124 interleukin 6 Homo sapiens 4-8 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 interleukin 6 Homo sapiens 63-76 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 interleukin 6 Homo sapiens 47-51 11687509-8 2001 These findings also support the hypothesis that IL-6 may be produced by contracting myofibers when glycogen levels become critically low as a means of signaling the liver to increase glucose production. Glucose 183-190 interleukin 6 Homo sapiens 48-52 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 interleukin 6 Homo sapiens 78-82 10868978-3 2000 Subjects homozygous for the C allele at position -174 of the IL-6 gene (SfaNI genotype), associated to lower plasma IL-6 levels, showed significantly lower integrated area under the curve of serum glucose concentrations (AUCglucose) after an oral glucose tolerance test, lower blood glycosylated hemoglobin, lower fasting insulin levels, lower total and differential white blood cell count (a putative marker of peripheral IL-6 action), and an increased insulin sensitivity index than carriers of the G allele, despite similar age and body composition. Glucose 197-204 interleukin 6 Homo sapiens 61-65 11079743-9 2000 RESULTS: We show that cells grown in a medium with high glucose concentration underwent great ATP-mediated morphological changes, enhanced apoptosis, caspase 3 activation and interleukin-6 release. Glucose 56-63 interleukin 6 Homo sapiens 175-188 10868978-3 2000 Subjects homozygous for the C allele at position -174 of the IL-6 gene (SfaNI genotype), associated to lower plasma IL-6 levels, showed significantly lower integrated area under the curve of serum glucose concentrations (AUCglucose) after an oral glucose tolerance test, lower blood glycosylated hemoglobin, lower fasting insulin levels, lower total and differential white blood cell count (a putative marker of peripheral IL-6 action), and an increased insulin sensitivity index than carriers of the G allele, despite similar age and body composition. Glucose 224-231 interleukin 6 Homo sapiens 61-65 10868978-6 2000 In summary, a polymorphism of the IL-6 gene influences the relationship among insulin sensitivity, postload glucose levels, and peripheral white blood cell count. Glucose 108-115 interleukin 6 Homo sapiens 34-38 9853701-9 1998 Portal IL-6 levels were correlated with the corresponding fasting serum glucose values. Glucose 72-79 interleukin 6 Homo sapiens 7-11 8666148-0 1996 Glucose-dependent interleukin 6 and tumor necrosis factor production by human peripheral blood monocytes in vitro. Glucose 0-7 interleukin 6 Homo sapiens 18-31 9648083-9 1998 The concentration of IL-6 in the supernatant of stimulated monocytes was highest with Glu/Bic (1023 +/- 278 pg/ml) and Amino/Bic (776 +/- 296 pg/ml) an lowest with Glu/lac pH 5.5 (46 +/- 22 pg/ml) and Glu-poly/PBS (32 +/- 13 pg/ml). Glucose 86-89 interleukin 6 Homo sapiens 21-25 9648083-9 1998 The concentration of IL-6 in the supernatant of stimulated monocytes was highest with Glu/Bic (1023 +/- 278 pg/ml) and Amino/Bic (776 +/- 296 pg/ml) an lowest with Glu/lac pH 5.5 (46 +/- 22 pg/ml) and Glu-poly/PBS (32 +/- 13 pg/ml). Glucose 164-167 interleukin 6 Homo sapiens 21-25 9648083-9 1998 The concentration of IL-6 in the supernatant of stimulated monocytes was highest with Glu/Bic (1023 +/- 278 pg/ml) and Amino/Bic (776 +/- 296 pg/ml) an lowest with Glu/lac pH 5.5 (46 +/- 22 pg/ml) and Glu-poly/PBS (32 +/- 13 pg/ml). Glucose 164-167 interleukin 6 Homo sapiens 21-25 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 interleukin 6 Homo sapiens 76-80 9501294-12 1998 Both amniotic fluid NOx and IL-6 were also positively correlated with amniotic fluid leukocyte counts, leukocyte esterase activity and Gram stains, and negatively correlated with glucose levels. Glucose 179-186 interleukin 6 Homo sapiens 28-32 9398733-0 1997 Dose-dependent effects of recombinant human interleukin-6 on glucose regulation. Glucose 61-68 interleukin 6 Homo sapiens 44-57 9398733-2 1997 To examine the effects of interleukin 6 (IL-6), the main circulating cytokine, on glucose metabolism in man, we performed dose-response studies of recombinant human IL-6 in normal volunteers. Glucose 82-89 interleukin 6 Homo sapiens 41-45 9398733-8 1997 By 60 min after the 3 higher IL-6 doses, however, the decline in fasting blood glucose was arrested, and glucose levels increased in a dose-dependent fashion. Glucose 79-86 interleukin 6 Homo sapiens 29-33 9398733-8 1997 By 60 min after the 3 higher IL-6 doses, however, the decline in fasting blood glucose was arrested, and glucose levels increased in a dose-dependent fashion. Glucose 105-112 interleukin 6 Homo sapiens 29-33 9398733-11 1997 In conclusion, sc IL-6 administration induced dose-dependent increases in fasting blood glucose, probably by stimulating glucagon release and other counteregulatory hormones and/or by inducing peripheral resistance to insulin action. Glucose 88-95 interleukin 6 Homo sapiens 18-22 9134917-5 1997 The immediate postrun plasma glucose concentrations correlated negatively with those of plasma cortisol (r = -0.67, P < 0.001); postrun plasma cortisol (r = 0.70, P < 0.001) and IL-6 levels (r = 0.54, P = 0.003) correlated positively with levels of IL-1ra. Glucose 29-36 interleukin 6 Homo sapiens 184-188 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 interleukin 6 Homo sapiens 5-9 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 interleukin 6 Homo sapiens 5-9 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 interleukin 6 Homo sapiens 5-9 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 interleukin 6 Homo sapiens 138-142 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 interleukin 6 Homo sapiens 112-116 8811326-0 1996 Elevated glucose levels stimulate transforming growth factor-beta 1 (TGF-beta 1), suppress interleukin IL-2, IL-6 and IL-10 production and DNA synthesis in peripheral blood mononuclear cells. Glucose 9-16 interleukin 6 Homo sapiens 109-113 8811326-5 1996 Exposure to elevated glucose levels caused a significant and dose-dependent increase in the production of latent TGF-beta 1 by (PWM)-stimulated PBMC at 24 and 48 h. Production of the cytokines IL-2, IL-6 and IL-10 was suppressed by elevated glucose concentration dose- and time-dependently. Glucose 21-28 interleukin 6 Homo sapiens 199-203 8811326-6 1996 In contrast to the time-dependent decreased effect of glucose-induced TGF-beta 1 production the effects of elevated glucose levels on IL-2, IL-6 and IL-10 production increased with time indicating that TGF-beta 1 production is preceding the reduced IL production. Glucose 116-123 interleukin 6 Homo sapiens 140-144 8811326-8 1996 Our results indicate that high glucose-induced TGF-beta 1 production may suppress immune response by inhibiting the endogenous production of IL-2, IL-6 and IL-10. Glucose 31-38 interleukin 6 Homo sapiens 147-151 8769856-5 1996 These data indicate that modulation of astrocyte properties during oxygen deprivation results, in part, from intracellular glucose depletion and subsequent expression of GRP78, which sustains generation of neuroprotective IL-6 under the stress of H/R. Glucose 123-130 interleukin 6 Homo sapiens 222-226 7628063-4 1994 IL-6 produced a transient increase in plasma glucagon that was mirrored by elevated plasma glucose and a depletion of hepatic glycogen. Glucose 91-98 interleukin 6 Homo sapiens 0-4 7695204-1 1995 To clarify the mechanism that causes elevation of plasma fibrinogen levels in diabetes, we examined the effect of high concentration of glucose and/or advanced glycosylation end products (AGEs) on the production of interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha) by human monocytes. Glucose 136-143 interleukin 6 Homo sapiens 215-228 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 interleukin 6 Homo sapiens 0-4 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 interleukin 6 Homo sapiens 0-4 7695204-6 1995 Our serial observation with treatment for lowering glucose levels showed that the diabetics with decreasing plasma fibrinogen levels also showed decrease in plasma IL-6 levels. Glucose 51-58 interleukin 6 Homo sapiens 164-168 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 interleukin 6 Homo sapiens 79-83 2105658-0 1990 Interleukin 6 stimulates hepatic glucose release from prelabeled glycogen pools. Glucose 33-40 interleukin 6 Homo sapiens 0-13 2105658-4 1990 After the addition of a highly concentrated human monocyte-conditioned medium (MCM) or various cytokines to these prelabeled cells, [14C]glucose release was stimulated by MCM and recombinant human interleukin 6 (IL-6) but was not stimulated by other cytokines tested. Glucose 137-144 interleukin 6 Homo sapiens 197-210 2105658-4 1990 After the addition of a highly concentrated human monocyte-conditioned medium (MCM) or various cytokines to these prelabeled cells, [14C]glucose release was stimulated by MCM and recombinant human interleukin 6 (IL-6) but was not stimulated by other cytokines tested. Glucose 137-144 interleukin 6 Homo sapiens 212-216 33777140-5 2021 We found the following: (1) under the high-glucose condition, the HSF cell viability, the expression of TIMP-2 mRNA, and the collagen levels were reduced, while the apoptosis rate and the expression of MMP-2 mRNA increased (P < 0.05). Glucose 43-50 interleukin 6 Homo sapiens 66-69 33777140-6 2021 (2) In the high-glucose + PDC group, the PDC reversed the changes in the collagen level, viability, and apoptosis rate of the HSF cells caused by high glucose, with the expression of protein and TIMP-2 mRNA increased and the level of MMP-2 mRNA decreased (P < 0.05). Glucose 16-23 interleukin 6 Homo sapiens 126-129 33777140-6 2021 (2) In the high-glucose + PDC group, the PDC reversed the changes in the collagen level, viability, and apoptosis rate of the HSF cells caused by high glucose, with the expression of protein and TIMP-2 mRNA increased and the level of MMP-2 mRNA decreased (P < 0.05). Glucose 151-158 interleukin 6 Homo sapiens 126-129 33777140-7 2021 This is the first time attempting to reveal that PDC can exhibit protective effects on HSF under high-glucose conditions, which may be related to the upregulation of the TIMP-2 expression and inhibition of the MMP-2 expression. Glucose 102-109 interleukin 6 Homo sapiens 87-90 34917989-8 2022 Conclusions: Cardiovascular autonomic functioning and blood glucose control were significantly associated with stressor-evoked IL-6 responses when controlling for BMI and age. Glucose 60-67 interleukin 6 Homo sapiens 127-131 34319506-9 2021 However, as compared with baseline data, a reduction in weight, BMI, hipline, WHR, fasting glucose, homeostatic model assessment of insulin sensitivity, visfatin and HDL-C, and an increase in resistin and IL-6 were observed in the true acupuncture group (P<0.05). Glucose 91-98 interleukin 6 Homo sapiens 205-209 34402375-6 2021 Firstly, we found that Tamsulosin reduced high glucose-induced expressions of TNF-alpha, IL-6, and IL-8. Glucose 47-54 interleukin 6 Homo sapiens 89-93 34868528-12 2021 In the oxygen-glucose-deprived reoxygenation model group, SNHG15 expression increased, miR-141 expression decreased, SIRT1 expression increased, and the expressions of p65, TNF-alpha, ROS, iNOS, and IL-6 decreased. Glucose 14-21 interleukin 6 Homo sapiens 199-203 34946023-7 2021 Our results showed that insulin-mediated reduction of UPEC infection in a high-glucose environment was not only due to the downregulation of JAK1/2 and phosphorylated STAT-1/3, but also because of the decreased expression of TLR-4 proteins and pro-inflammatory IL-6. Glucose 79-86 interleukin 6 Homo sapiens 261-265 34402957-4 2021 Long-term exposure to high glucose significantly enhanced the increase in the production of pro-inflammatory cytokines, including tumor necrosis-alpha, interleukin (IL)-1beta, and IL-6, when macrophages were stimulated with LPS. Glucose 27-34 interleukin 6 Homo sapiens 180-184 34680892-1 2021 Interleukin 6 (IL-6) is a cytokine with both pro- and anti-inflammatory actions, but is also considered as a "metabolic hormone" involved in immune responses, affecting glucose, protein and lipid metabolism. Glucose 169-176 interleukin 6 Homo sapiens 0-13 34544857-4 2021 U-13C glucose tracing revealed that IL-6 knockout reduced 3-phosphoserine and serine production in TSC2-deficient cells, implicating IL-6 in de novo serine metabolism. Glucose 6-13 interleukin 6 Homo sapiens 36-40 34544857-4 2021 U-13C glucose tracing revealed that IL-6 knockout reduced 3-phosphoserine and serine production in TSC2-deficient cells, implicating IL-6 in de novo serine metabolism. Glucose 6-13 interleukin 6 Homo sapiens 133-137 34680892-1 2021 Interleukin 6 (IL-6) is a cytokine with both pro- and anti-inflammatory actions, but is also considered as a "metabolic hormone" involved in immune responses, affecting glucose, protein and lipid metabolism. Glucose 169-176 interleukin 6 Homo sapiens 15-19 34533012-7 2021 Interleukin 6 provides an energy substrate for contracting muscle fibers, fibroblast growth factor 21 activates the mechanisms of energy production during fasting and improves tissue sensitivity to insulin; irisin stimulates thermogenesis, glucose uptake by myocytes, and also contributes to an increase in bone mineral density. Glucose 240-247 interleukin 6 Homo sapiens 0-13 34288404-10 2021 Postprandial adiponectin was positively associated with malondialdehyde and inversely associated with interleukin-6 following DEX and also negatively associated with metabolic parameters after both test meals. Glucose 126-129 interleukin 6 Homo sapiens 102-115 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 interleukin 6 Homo sapiens 155-159 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 interleukin 6 Homo sapiens 117-121 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 interleukin 6 Homo sapiens 117-121 34247997-0 2021 Association of IL-6 & IL-1beta (pro-inflammatory cytokines) and related biochemical indexes in newly diagnosed diabetics subjected to glucose tolerance test. Glucose 134-141 interleukin 6 Homo sapiens 15-19 35264090-6 2022 IL-6 increases GLUT-4 vesicle mobilization to muscle cell periphery, increasing the glucose transport into the cell, and also glycogen synthesis. Glucose 84-91 interleukin 6 Homo sapiens 0-4 35457130-4 2022 As IL-6 and EGF signaling are growth and inflammatory-inducible responses, we examined if glucose challenge can increase STAT3 activation, promoting adaptive changes in XRCC1 expression in different cell types. Glucose 90-97 interleukin 6 Homo sapiens 3-7 35432729-5 2022 Furthermore, the oxygen-glucose deprivation/reoxygenation (OGD/R) model was used to validate the anti-inflammatory effects of the key ingredients by determining the levels of inflammatory cytokines, including interleukin (IL)-6, IL-1beta, and tumor necrosis factor (TNF)-alpha. Glucose 24-31 interleukin 6 Homo sapiens 209-227 35212163-3 2022 We initially found that the glycolytic inhibitor 2-deoxy-d-glucose (2-DG), a simple monosaccharide, attenuated cellular responses to IL-6 by inhibiting N-linked glycosylation of the IL-6 receptor gp130. Glucose 59-66 interleukin 6 Homo sapiens 182-186 35043090-7 2022 Although dipeptidyl peptidase-4 plays an important role in glucose homeostasis, additionally it also stimulates the production of proinflammatory cytokines such as IL-6 and TNF-alpha creating a cytokine storm. Glucose 59-66 interleukin 6 Homo sapiens 164-168 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 interleukin 6 Homo sapiens 176-180 2674559-4 1989 In contrast, low levels of IL-1 potentiate the secretion of insulin and thyroid hormones, and intermediate levels of IL-6 double glucose-induced insulin production by beta-cells. Glucose 129-136 interleukin 6 Homo sapiens 117-121 33615922-0 2021 MiR-29a Alleviates High Glucose-induced Inflammation and Mitochondrial Dysfunction via Modulation of IL-6/STAT3 in Diabetic Cataracts. Glucose 24-31 interleukin 6 Homo sapiens 101-105 33971617-13 2021 Plasma glucose was strongly correlated with hsCRP (p<0.001) and IL-6 (p<0.0001). Glucose 7-14 interleukin 6 Homo sapiens 64-68 33924229-6 2021 The analysis showed that IL-6 is significantly correlated with glucose (p = 0.001) and BMI value (p = 0.031). Glucose 63-70 interleukin 6 Homo sapiens 25-29 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 interleukin 6 Homo sapiens 73-77 33615922-1 2021 Background: This in vitro study was designed to reveal the role of miR-29a in high glucose-induced cellular injury through the modulation of IL-6/STAT3 in diabetic cataracts. Glucose 83-90 interleukin 6 Homo sapiens 141-145 33599871-6 2021 In subjects without diabetes (controls), we found an association between the G/C genotype of the -572 polymorphism and the G/C and C/C genotypes of the -597 polymorphism of IL-6 with the risk of glucose levels > 131 mg/dL. Glucose 195-202 interleukin 6 Homo sapiens 173-177 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 interleukin 6 Homo sapiens 126-130 33294275-0 2020 MOB1A regulates glucose deprivation-induced autophagy via IL6-STAT3 pathway in gallbladder carcinoma. Glucose 16-23 interleukin 6 Homo sapiens 58-61 33354576-0 2020 Tangeretin Inhibition of High-Glucose-Induced IL-1beta, IL-6, TGF-beta1, and VEGF Expression in Human RPE Cells. Glucose 30-37 interleukin 6 Homo sapiens 56-60 33328159-6 2020 The role of HRH4 in high glucose-induced regulation of VEGF, IL-6 and PEDF in ARPE-19 cells and the underlying regulatory mechanism were verified using an RNA interference-mediated knockdown study. Glucose 25-32 interleukin 6 Homo sapiens 61-65 33038372-5 2020 High glucose-induced NF-kappaB increased the migration and invasion of CCA cells and the expression of downstream NF-kappaB targeted genes associated with aggressiveness, including interleukin-6, a potent triggering signal of the signal transducer and activator of transcription 3 (STAT3) pathway. Glucose 5-12 interleukin 6 Homo sapiens 181-194 32907617-2 2020 Interleukin (IL)-6 is implicated in both the pathogenesis of RA and in glucose homeostasis; this post hoc analysis investigated the effects of IL-6 receptor vs. tumour necrosis factor inhibition on glycosylated haemoglobin (HbA1c) in patients with RA with or without diabetes. Glucose 71-78 interleukin 6 Homo sapiens 0-18 32946851-8 2020 Besides, patients with higher fasting plasma glucose (FPG) had higher IL-6, IL-8, CRP, and mortality. Glucose 45-52 interleukin 6 Homo sapiens 70-74 32833280-11 2020 Osteocytes secreted exosomes carrying miR-124-3p, Gal-3, and IL-6, which were influenced by high glucose. Glucose 97-104 interleukin 6 Homo sapiens 61-65 32863319-0 2020 Glucose transporter 4 mediates LPS-induced IL-6 production in osteoblasts under high glucose conditions. Glucose 0-7 interleukin 6 Homo sapiens 43-47 32863319-0 2020 Glucose transporter 4 mediates LPS-induced IL-6 production in osteoblasts under high glucose conditions. Glucose 85-92 interleukin 6 Homo sapiens 43-47 32863319-8 2020 RESULTS: LPS and glucose increased the mRNA expression of IL-6, coupled with a decrease in the mRNA expression of OCN, which is associated with IL-6 and glucose. Glucose 17-24 interleukin 6 Homo sapiens 58-62 32863319-8 2020 RESULTS: LPS and glucose increased the mRNA expression of IL-6, coupled with a decrease in the mRNA expression of OCN, which is associated with IL-6 and glucose. Glucose 17-24 interleukin 6 Homo sapiens 144-148 32863319-11 2020 Furthermore, GLUT4 inhibitor, WZB117, blocked the stimulatory effect of glucose on LPS-induced IL-6 mRNA expression. Glucose 72-79 interleukin 6 Homo sapiens 95-99 32863319-13 2020 CONCLUSION: These results suggest that high glucose levels increase LPS-induced IL-6 expression mediated by GLUT4. Glucose 44-51 interleukin 6 Homo sapiens 80-84 31792920-9 2020 High glucose increased the secretion of IL-6. Glucose 5-12 interleukin 6 Homo sapiens 40-44 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 interleukin 6 Homo sapiens 111-115 31787367-7 2020 Obesity and diet composition were both positively associated to pro-inflammatory biomarkers, CRP and IL1b; while diet composition shared with physical activity levels the correlation with IL6 (positive with energy, fat, carbohydrate and saturated fatty acid intake, and negative with cholesterol intake and average physical activity in boys), NGF and glucose (in both cases correlations were negative with diet composition and physical activity variables) (P < 0.05, in all cases). Glucose 351-358 interleukin 6 Homo sapiens 188-191 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 interleukin 6 Homo sapiens 94-98 32312819-4 2020 To explore this issue, we analyzed secretomes from glucose-deprived cells, which revealed up-regulation of multiple cytokines and chemokines, including IL-6 and IL-8, in response to starvation stress. Glucose 51-58 interleukin 6 Homo sapiens 152-156 30448438-11 2020 Furthermore, we observed negative correlations between CSF IL-6 levels and CSF glucose and CSF/blood glucose ratio in CNS infection. Glucose 79-86 interleukin 6 Homo sapiens 59-63 31960917-6 2020 Pre-treating ARPE-19 cells with quercetin clearly attenuated high glucose-induced viability loss, apoptosis, MCP-1 and IL-6 overproduction, and ROS generation. Glucose 66-73 interleukin 6 Homo sapiens 119-123 32365859-2 2020 In peripheral tissues, exercise induced IL-6 can result in GLUT4 translocation and increased glucose uptake through AMPK activation. Glucose 93-100 interleukin 6 Homo sapiens 40-44 32365859-4 2020 The aim of this study is to examine if IL-6 treatment: (1) results in AMPK activation in neuronal cells, (2) increases the activation of proteins involved in GLUT4 translocation, and (3) increases neuronal glucose uptake. Glucose 206-213 interleukin 6 Homo sapiens 39-43 32365859-10 2020 Importantly, IL-6 treatment increased glucose uptake. Glucose 38-45 interleukin 6 Homo sapiens 13-17 32365859-11 2020 Our findings demonstrate that IL-6 and insulin can phosphorylate AS160 via different signaling pathways (AMPK and PI3K/Akt, respectively) and promote GLUT4 translocation towards the neuronal plasma membrane, resulting in increased neuronal glucose uptake in SH-SY5Y cells. Glucose 240-247 interleukin 6 Homo sapiens 30-34 30448438-9 2020 Moreover, CSF IL-6 levels were strongly negatively correlated with CSF glucose and the CSF/blood glucose ratio (r = -0.4375, P = 0.0042; r = -0.4991, P = 0.0009). Glucose 71-78 interleukin 6 Homo sapiens 14-18 30448438-9 2020 Moreover, CSF IL-6 levels were strongly negatively correlated with CSF glucose and the CSF/blood glucose ratio (r = -0.4375, P = 0.0042; r = -0.4991, P = 0.0009). Glucose 97-104 interleukin 6 Homo sapiens 14-18 31764462-9 2020 Variations in the resting concentration of IL-6 were associated with lowered blood glucose, an increased perception of effort, and impaired exercise performance. Glucose 83-90 interleukin 6 Homo sapiens 43-47 30448438-11 2020 Furthermore, we observed negative correlations between CSF IL-6 levels and CSF glucose and CSF/blood glucose ratio in CNS infection. Glucose 101-108 interleukin 6 Homo sapiens 59-63 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 interleukin 6 Homo sapiens 147-151 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 interleukin 6 Homo sapiens 17-21 30975555-5 2020 RESULTS: Circulating IL-6 levels decreased after glucose and protein ingestion but slightly increased after oral lipid intake. Glucose 49-56 interleukin 6 Homo sapiens 21-25 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 interleukin 6 Homo sapiens 153-166 31944871-7 2020 Serum IL-6 exhibited significant inverse correlations with body mass index (r = -0.39/P < 0.0001), waist circumference (r = -0.42/P < 0.001), blood glucose (r = -0.40/P < 0.0001), triglycerides (r = -0.34/P < 0.0001), and TNF-alpha (r = -0.48/P < 0.0001), whereas a strongly positive correlation was found with IL-10 (r = 0.77/P < 0.0001). Glucose 154-161 interleukin 6 Homo sapiens 6-10 31823669-8 2020 IL-6 acts as an anti-inflammatory myokine by inhibiting TNF-alpha and improving glucose uptake through the stimulation of AMPK signaling. Glucose 80-87 interleukin 6 Homo sapiens 0-4 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 interleukin 6 Homo sapiens 389-393 30843768-5 2020 Treatment with alpha-tocopherol (10, 100, and 1,000 muM) and ascorbic acid (15, 150, and 1,500 muM) at the same time that the dextrose was added reduced IL-1beta, IL-6, and IL-8 levels in culture media from cells maintained at 5.5 mM dextrose but had no effect on IL-1beta, IL-6, and IL-8 levels in cells exposed to 27.5 mM dextrose. Glucose 126-134 interleukin 6 Homo sapiens 163-167 30843768-5 2020 Treatment with alpha-tocopherol (10, 100, and 1,000 muM) and ascorbic acid (15, 150, and 1,500 muM) at the same time that the dextrose was added reduced IL-1beta, IL-6, and IL-8 levels in culture media from cells maintained at 5.5 mM dextrose but had no effect on IL-1beta, IL-6, and IL-8 levels in cells exposed to 27.5 mM dextrose. Glucose 126-134 interleukin 6 Homo sapiens 274-278 31702814-11 2019 ELISA indicated that miR-217 inhibitor significantly reduced the expression of inflammatory factors, such as interleukin (IL)-1beta, tumor necrosis factor-alpha, and IL-6 in high glucose-treated ARPE-19 cells. Glucose 179-186 interleukin 6 Homo sapiens 166-170 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 interleukin 6 Homo sapiens 44-48 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 interleukin 6 Homo sapiens 51-55 31219767-9 2019 Our findings may have implications for the microvascular complications associated with T2DM.NEW & NOTEWORTHY Higher concentrations of serum factors, specifically Interleukin-6 and its soluble receptor found in individuals with type 2 diabetes (T2DM) appear to impair endothelial cell capillary-like network formation compared with those present in serum from individuals with impaired glucose tolerance and normal glucose tolerance. Glucose 389-396 interleukin 6 Homo sapiens 166-179 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 interleukin 6 Homo sapiens 132-136 30919933-7 2019 High levels of D-fructose compared to D-glucose led to activation of DCs in vitro by promoting interleukin (IL)-6 and IL-1beta production. Glucose 40-47 interleukin 6 Homo sapiens 95-113 31389609-10 2019 High glucose group had clearly increased the content of ROS (p<0.01), LDH (p<0.01), and interleukin-6 (IL-6) (p<0.01), but decreased the content of IL-10 (p<0.01). Glucose 5-12 interleukin 6 Homo sapiens 88-101 31389609-10 2019 High glucose group had clearly increased the content of ROS (p<0.01), LDH (p<0.01), and interleukin-6 (IL-6) (p<0.01), but decreased the content of IL-10 (p<0.01). Glucose 5-12 interleukin 6 Homo sapiens 103-107 31389609-12 2019 CONCLUSIONS: High glucose represses the activation of the Nrf2/anti-oxidation response element (ARE) signaling pathway in prostate cancer cells and increases the content of ROS, IL-6, and the expression of apoptotic proteins in the cells, thus promoting the apoptosis of prostate cancer cells. Glucose 18-25 interleukin 6 Homo sapiens 178-182 31934133-9 2019 High glucose significantly evoked MV generation, which contained increased protein level of IL-6, 8 and MCP-1. Glucose 5-12 interleukin 6 Homo sapiens 92-99 30365907-1 2019 Interleukin-6 (IL-6), IL-15, and heat shock protein 72 (Hsp72) are molecules that have significant metabolic effects on glucose and fat metabolism and a cell"s stress response. Glucose 120-127 interleukin 6 Homo sapiens 0-13 31212679-5 2019 The C. turczaninowii extract attenuated the increased mRNA expression of IL-6, TNF-alpha, and CHOP in hASMCs under high glucose conditions. Glucose 120-127 interleukin 6 Homo sapiens 73-77 30365907-1 2019 Interleukin-6 (IL-6), IL-15, and heat shock protein 72 (Hsp72) are molecules that have significant metabolic effects on glucose and fat metabolism and a cell"s stress response. Glucose 120-127 interleukin 6 Homo sapiens 15-19 30365907-9 2019 Since these molecules are involved in regulating glucose and fat metabolism, significant increases of IL-6, IL-15, and soluble Hsp72 may have health benefits that may be associated with long-distance trail runs, which are becoming more popular worldwide. Glucose 49-56 interleukin 6 Homo sapiens 102-106 30992036-5 2019 Interleukin-6 was also found to be a predictor of high cfDNA (>= 2.84 microg/mL, upper quartile) along with glucose. Glucose 111-118 interleukin 6 Homo sapiens 0-13 31223191-10 2019 Inflammatory cytokines, such as IL-6, and stress oxidative markers might play a role in underlying mechanisms modulating the glucose variability responses to exercise (clinicalTrials.gov NCT02262208). Glucose 125-132 interleukin 6 Homo sapiens 32-36 30741955-7 2019 Supporting this result, glucose metabolism-related enzyme IRS1 and interleukin-6 (IL-6) were abnormally expressed, and levels of lysophosphatidylcholine (LysoPC) and its related enzyme phospholipase A2 (PLA2) were significantly altered in allogeneic groups compared to those in autologous groups. Glucose 24-31 interleukin 6 Homo sapiens 82-86 30631154-3 2019 Mechanistically, high glucose, TGF-beta, CTGF, SHH, and IL-6 induce the expression of a long non-coding RNA, GAEA (Glucose Aroused for EMT Activation), which associates with an RNA-binding E3 ligase, MEX3C, and enhances its enzymatic activity, leading to the K27-linked polyubiquitination of PTEN. Glucose 115-122 interleukin 6 Homo sapiens 56-60 29932015-6 2019 Moreover, in vitro, we treated cells with IL-6 to simulate inflammatory microenvironment and found that glucose uptake, lactate production, and lactate dehydrogenase activity increased dramatically, mirroring what were observed in vivo. Glucose 104-111 interleukin 6 Homo sapiens 42-46 29932015-8 2019 With the inhibition of STAT3/c-Myc signaling, meanwhile, the upregulation of both cell glucose uptake and lactate production by IL-6 pretreatment was reduced simultaneously. Glucose 87-94 interleukin 6 Homo sapiens 128-132 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 interleukin 6 Homo sapiens 21-25 30390336-12 2018 IL-6 treatment induced the phosphorylation of Stat3 and Bmi-1 expression, increased cell viability, as well as elevated glucose consumption, lactate production, and HK2 expression; however, the effects of IL-6 were attenuated by icaritin or S3I-201 treatment. Glucose 120-127 interleukin 6 Homo sapiens 0-4 29199785-1 2019 BACKGROUND: Muscle-derived interleukin-6 (IL-6) not only enhances glucose and fat metabolism but also has an anti-inflammatory effect that can prevent the development of cardiovascular disease (CVD) and metabolic syndrome. Glucose 66-73 interleukin 6 Homo sapiens 27-40 29199785-1 2019 BACKGROUND: Muscle-derived interleukin-6 (IL-6) not only enhances glucose and fat metabolism but also has an anti-inflammatory effect that can prevent the development of cardiovascular disease (CVD) and metabolic syndrome. Glucose 66-73 interleukin 6 Homo sapiens 42-46 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 interleukin 6 Homo sapiens 135-139 29235373-8 2018 IL-6 was significantly associated with glycerol in all models (p < .05), with glycerol levels increasing by 106% in individuals with AGM after AP (p <.05) compared to a 30.3% increase in individuals with normal glucose metabolism (NGM) (p >.05). Glucose 217-224 interleukin 6 Homo sapiens 0-4 29851525-4 2018 RESULTS: In T2D patients with high blood glucose, IL-1beta expression showed a 2.69-fold increase (p = 0.0380), while IL-6 expression levels were 3.45 fold lower (p = 0.0045) versus control subjects. Glucose 41-48 interleukin 6 Homo sapiens 118-122 30383519-5 2018 High glucose (HG) significantly increased expression of IL-6, intercellular adhesion molecule (ICAM-1), matrix metalloproteinase-2 & 9, and migration of vascular smooth muscle cells. Glucose 5-12 interleukin 6 Homo sapiens 56-60 29851525-5 2018 Moreover, compared with control group the expression of IL1R1 and IL-6 genes both were downregulated in individuals with moderately high blood glucose levels by 2.38 (p = 0.0365) and 4.34 fold (p = 0.0027), respectively. Glucose 143-150 interleukin 6 Homo sapiens 66-70 29851525-6 2018 In addition, hemoglobin A1C (A1C) levels were positively correlated with IL-1beta expression and fasting plasma glucose (FPG) levels showed a positive correlation with IL-1beta and a negative correlation with IL-6 expression. Glucose 112-119 interleukin 6 Homo sapiens 209-213 30020457-8 2018 In youth with T1D, glucose rate of disappearance correlated with free fatty acid at the 80-mU/m2/min phase (P = 0.005), markers of inflammation (IL-6; P = 0.012), high-sensitivity C-reactive protein (P = 0.001), and leptin (P = 0.008)], but not hemoglobin A1c. Glucose 19-26 interleukin 6 Homo sapiens 145-149 29874560-1 2018 Actions of Interleukin-6 on Glucose Tolerance. Glucose 28-35 interleukin 6 Homo sapiens 11-24 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 interleukin 6 Homo sapiens 78-82 30128492-8 2018 Results: Expression levels of ANGPTL3, IL-1beta, IL-6, Bax, P53, VEGF, and integrin alphaVbeta3 were found to be upregulated after high-glucose stimulation or ANGPTL3 overexpression in HRMECs or diabetic retinal tissue. Glucose 136-143 interleukin 6 Homo sapiens 49-53 29874560-4 2018 (2018) demonstrate that IL-6 infusion has GLP-1-dependent and -independent actions with opposing effects on glucose tolerance, resulting in an overall improvement in healthy male volunteers but no improvement in male patients with diabetes. Glucose 108-115 interleukin 6 Homo sapiens 24-28 29508109-3 2018 On the other hand, an increasing number of evidence suggests that IL-6 has an anti-inflammatory role and improves glucose metabolism. Glucose 114-121 interleukin 6 Homo sapiens 66-70 28852907-7 2018 HK-2 cells with high glucose up-regulated IL-6 and MCP-1 in a dose- and time-dependent manner, and SUV39H1 expression was reduced with greater glucose and prolonged stimulation. Glucose 21-28 interleukin 6 Homo sapiens 42-46 29623201-8 2018 Immunoglobulin G, immunoglobulin A and interleukin 6 levels in the case cohort, respectively, associated weakly with fasting blood glucose (r = 0.252, p = 0.001; r = 0.170, p = 0.031; r = 0.296, p = 0.001). Glucose 131-138 interleukin 6 Homo sapiens 0-52 28881473-0 2018 The classic signalling and trans-signalling of interleukin-6 are both injurious in podocyte under high glucose exposure. Glucose 103-110 interleukin 6 Homo sapiens 47-60 29479468-5 2018 Conclusions: Findings in this study support the anti-inflammatory, anti-obesity and glucose homeostatic roles of IL6 in Mexican-American youth. Glucose 84-91 interleukin 6 Homo sapiens 113-116 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 interleukin 6 Homo sapiens 36-54 29142506-8 2017 Glycated hemoglobin levels measured after 6-month glucose-lowering treatment appeared to be inversely correlated with plasma anti-IL1alpha IgG (r=-0.477, df=17, p=0.039) and anti-IL6 IgG (r=-0.519, df=17, p=0.023) although such correlation failed to survive the Bonferroni correction. Glucose 50-57 interleukin 6 Homo sapiens 179-182 28852804-8 2017 RESULTS: Podocytes exposed to a diabetic environment (high glucose, high insulin and the proinflammatory cytokines TNF-alpha and IL-6) become insulin resistant with respect to glucose uptake and activation of phosphoinositide 3-kinase (PI3K) and mitogen-activated protein kinase (MAPK) signalling. Glucose 176-183 interleukin 6 Homo sapiens 129-133 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 interleukin 6 Homo sapiens 118-122 28722106-6 2017 Moreover, muscle-derived IL-6 appears to have direct anti-inflammatory effects and serves as a mechanism to improve glucose tolerance. Glucose 116-123 interleukin 6 Homo sapiens 25-29 28433754-10 2017 Overall, we report that miR-146a suppressed IL-6 signaling, leading to reduced levels of STAT3 and VEGF in REC in high glucose conditions, leading to decreased apoptosis. Glucose 119-126 interleukin 6 Homo sapiens 44-48 28507168-3 2017 Circulating IL-6 is thought to maintain energy status during exercise by acting as an energy sensor for contracting muscle and stimulating glucose production. Glucose 139-146 interleukin 6 Homo sapiens 12-16 28883755-3 2017 Here, we demonstrate that hypoxia, reactive oxygen species (ROS), and differential concentration of glucose influence the expression of cytokines and chemokines, such as IL-6, IL-8, and IP-10, in human glial cell lines. Glucose 100-107 interleukin 6 Homo sapiens 170-174 28503530-7 2017 When compared the changes between groups (postvalues minus prevalues), there was lower glucose in CAF group when compared to CHO group (CAF= 5.0+-10.4 vs. CHO=27.8+-20 vs. P=15.1+-14, P=0.031) and higher IL-6 levels (CAF=11.9+-9.2 vs. CHO=-2.4+-1.7 vs. P=4.3+- 11.7, P=0.017). Glucose 87-94 interleukin 6 Homo sapiens 204-208 28704555-1 2017 Interleukin-6 (IL-6) has been recently shown to play a central role in glucose homeostasis, since it stimulates the production and secretion of Glucagon-like Peptide-1 (GLP-1) from intestinal L-cells and pancreas, leading to an enhanced insulin response. Glucose 71-78 interleukin 6 Homo sapiens 0-13 28704555-1 2017 Interleukin-6 (IL-6) has been recently shown to play a central role in glucose homeostasis, since it stimulates the production and secretion of Glucagon-like Peptide-1 (GLP-1) from intestinal L-cells and pancreas, leading to an enhanced insulin response. Glucose 71-78 interleukin 6 Homo sapiens 15-19 27894955-6 2017 Among signaling pathways related to T-ICs, IL-6/STAT3 was identified to be responsible for the elevation of glucose uptake in liver T-ICs under glucose limitation. Glucose 108-115 interleukin 6 Homo sapiens 43-47 26874912-6 2017 RESULTS: Anti-inflammatory cytokines (interleukin-6 and interleukin-18) were increased in the fasting state and/or decreased in some women during the oral glucose tolerance test, as opposed to inflammatory mediators such as macrophage migration inhibitory factor and matrix metallopeptidase-9 that increased during the oral glucose tolerance test especially in subjects with weight excess. Glucose 155-162 interleukin 6 Homo sapiens 38-51 26874912-6 2017 RESULTS: Anti-inflammatory cytokines (interleukin-6 and interleukin-18) were increased in the fasting state and/or decreased in some women during the oral glucose tolerance test, as opposed to inflammatory mediators such as macrophage migration inhibitory factor and matrix metallopeptidase-9 that increased during the oral glucose tolerance test especially in subjects with weight excess. Glucose 324-331 interleukin 6 Homo sapiens 38-51 27397896-8 2017 RESULTS: High glucose stimulated a significant increase in the production of IL-6 and IL-8 by HGFs compared with normal glucose. Glucose 14-21 interleukin 6 Homo sapiens 77-81 27894955-6 2017 Among signaling pathways related to T-ICs, IL-6/STAT3 was identified to be responsible for the elevation of glucose uptake in liver T-ICs under glucose limitation. Glucose 144-151 interleukin 6 Homo sapiens 43-47 27894955-9 2017 Our findings suggest that blocking IL-6/STAT3-mediated preferential glucose uptake might be exploited for novel therapeutic targets during hepatocellular carcinoma (HCC) progression. Glucose 68-75 interleukin 6 Homo sapiens 35-39 28149010-0 2017 Association of Interleukin-6 and Myeloperoxidase with Insulin Resistance in Impaired Fasting Glucose Subjects. Glucose 93-100 interleukin 6 Homo sapiens 15-28 28073126-5 2017 Results: Our results demonstrated that high levels of IL6 are associated with altered glucose levels in the WAT (p=0.01). Glucose 86-93 interleukin 6 Homo sapiens 54-57 27918955-12 2017 After proper glycemic control, release of IL-1beta was increased and of IL-6 decreased; cells of patients with improved glycemic control responded better to LPS stimulation under increased concentrations of glucose. Glucose 207-214 interleukin 6 Homo sapiens 72-76 26869278-3 2017 METHODS: Human mesothelial cells (Met-5A) were incubated with different concentrations of glucose and mannitol, and the effect of glucose and mannitol on the expression of IL-6 was determined. Glucose 130-137 interleukin 6 Homo sapiens 172-176 26869278-8 2017 High glucose and mannitol could upregulate IL-6 mRNA expression and IL-6 secretion in mesothelial cells significantly, and there was no difference of its effect between high glucose and mannitol. Glucose 5-12 interleukin 6 Homo sapiens 43-47 26869278-8 2017 High glucose and mannitol could upregulate IL-6 mRNA expression and IL-6 secretion in mesothelial cells significantly, and there was no difference of its effect between high glucose and mannitol. Glucose 5-12 interleukin 6 Homo sapiens 68-72 26869278-13 2017 CONCLUSION: The present study might provide evidence that high glucose upregulates IL-6 synthesis in Met-5A cells, to some extent, depending on its osmolality and that IL-6 trans-signalling could induce VEGF synthesis partly dependent on the JAK/STAT3 pathway. Glucose 63-70 interleukin 6 Homo sapiens 83-87 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 interleukin 6 Homo sapiens 170-174 28124586-8 2017 RESULTS: High glucose (30.5 mM) increased mRNA expression of interleukin (IL)-6 and secretion of both IL-6 and IL-8 by astrocytes. Glucose 14-21 interleukin 6 Homo sapiens 61-79 28124586-8 2017 RESULTS: High glucose (30.5 mM) increased mRNA expression of interleukin (IL)-6 and secretion of both IL-6 and IL-8 by astrocytes. Glucose 14-21 interleukin 6 Homo sapiens 102-106 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 interleukin 6 Homo sapiens 14-18 27652031-4 2016 Interleukin-6 (IL-6) released from the exercising muscles may be involved in and could therefore explain acute adaptations on glucose metabolism. Glucose 126-133 interleukin 6 Homo sapiens 0-13 27957415-0 2016 The role of local IL6/JAK2/STAT3 signaling in high glucose-induced podocyte hypertrophy. Glucose 51-58 interleukin 6 Homo sapiens 18-21 27957415-2 2016 We tested the hypothesis that IL6 and its downstream gp130/JAK2/STAT3 pathway participated in high glucose (HG)-induced podocyte hypertrophy. Glucose 99-106 interleukin 6 Homo sapiens 30-33 27652031-4 2016 Interleukin-6 (IL-6) released from the exercising muscles may be involved in and could therefore explain acute adaptations on glucose metabolism. Glucose 126-133 interleukin 6 Homo sapiens 15-19 27186361-6 2016 Exendin-4 and glucose-dependent insulinotropic polypepide elicited cyclic adenosine monophosphate generation, and suppressed the lipopolysaccharide-induced gene expression of inflammatory molecules, such as interleukin-1beta, interleukin-6 and tumor necrosis factor-alpha, in U937 human monocytes. Glucose 14-21 interleukin 6 Homo sapiens 226-271 27274108-4 2016 Interleukin-6 (IL-6) released from the exercising muscles may be involved in the acute adaptations of glucose metabolism after CE and non-muscle-damaging EE. Glucose 102-109 interleukin 6 Homo sapiens 0-13 27274108-4 2016 Interleukin-6 (IL-6) released from the exercising muscles may be involved in the acute adaptations of glucose metabolism after CE and non-muscle-damaging EE. Glucose 102-109 interleukin 6 Homo sapiens 15-19 26930265-10 2016 Secretion of sFlt-1, sEng, and IL-6 was increased while VEGF and PIGF were decreased in CTB-treated >=150 mg/dl of glucose (*p < 0.01 for each). Glucose 118-125 interleukin 6 Homo sapiens 31-35 26924495-9 2016 Glucose fluctuation also resulted in up-regulating gene expression of pro-inflammatory mediators, interleukin-6 and intercellular adhesion molecule-1. Glucose 0-7 interleukin 6 Homo sapiens 98-149 26537370-8 2016 RESULTS: High glucose levels inhibited PDLSC proliferation and differentiation into osteoblasts but induced NF-kappaB activation and subsequent interleukin (IL)-6 and IL-8 expression. Glucose 14-21 interleukin 6 Homo sapiens 144-162 26537370-9 2016 Treatment with an NF-kappaB inhibitor rescued the defects in cell proliferation and osteoblastic differentiation and inhibited the IL-6 expression caused by the high-glucose environment. Glucose 166-173 interleukin 6 Homo sapiens 131-135 26918832-6 2016 Frequencies of IL-6-producing T cells were correlated with glucose levels after glucose-tolerance tests (but not body mass index and waist circumference) and inversely correlated with HGK expression levels. Glucose 59-66 interleukin 6 Homo sapiens 15-19 26918832-6 2016 Frequencies of IL-6-producing T cells were correlated with glucose levels after glucose-tolerance tests (but not body mass index and waist circumference) and inversely correlated with HGK expression levels. Glucose 80-87 interleukin 6 Homo sapiens 15-19 26926996-2 2016 Here, we report that in monocytes and macrophages of patients with atherosclerotic coronary artery disease (CAD), overutilization of glucose promotes excessive and prolonged production of the cytokines IL-6 and IL-1beta, driving systemic and tissue inflammation. Glucose 133-140 interleukin 6 Homo sapiens 202-206 26911440-2 2016 The cytokine interleukin-6 may impact on glucose homeostasis. Glucose 41-48 interleukin 6 Homo sapiens 13-26 26924930-4 2016 In present study, agmatine attenuated the cell death and the expression of pro-inflammatory cytokines such as IL-6, TNF-alpha and CCL2 in high glucose in vitro conditions. Glucose 143-150 interleukin 6 Homo sapiens 110-114 25565094-7 2016 IL-6 was inversely related to birth weight adjusted for gestational age at delivery (r=-0.3382, p<0.001) and glucose levels at oral glucose test. Glucose 112-119 interleukin 6 Homo sapiens 0-4 26568029-7 2016 In addition, IL-6 has direct impact on glucose and lipid metabolism. Glucose 39-46 interleukin 6 Homo sapiens 13-17 27042306-4 2016 Additional in vitro studies of human peripheral blood mononuclear cells (PBMCs) exposed to high glucose confirmed decreased IL-6 expression, most prominently in CD14(+)CD16(+) intermediate monocytes. Glucose 96-103 interleukin 6 Homo sapiens 124-128 27003399-4 2016 Similarly, adiponectin, leptin and IL-6 enhance glucose uptake and increase fatty acid oxidation in skeletal muscle. Glucose 48-55 interleukin 6 Homo sapiens 35-39 26839875-5 2016 Fasting glucose positively correlated with hs-CRP, interleukin-6, tumor necrosis factor-alpha, oxidized low density lipoprotein (LDL) and malondialdehyde. Glucose 8-15 interleukin 6 Homo sapiens 51-93 26141422-7 2015 The GG genotype of the -179C/G polymorphism (IL6) was associated with higher glucose levels, while the GA and AA genotypes of the -1082A/G polymorphism (IL10), CT and TT genotypes of the -819A/T polymorphism (IL10), CA and AA genotypes of the -522A/G (IL10) polymorphism, and TA genotype of the +874T/A polymorphism (IFN-gamma) were associated with lower total cholesterol and triglycerides levels. Glucose 77-84 interleukin 6 Homo sapiens 45-48 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 interleukin 6 Homo sapiens 27-31 26854669-6 2016 Covariance analysis confirmed that differences in IL-1beta and IL-6 levels were determined by pharmacotherapy and fasting plasma glucose, whereas in IL-10 levels by the therapy only. Glucose 129-136 interleukin 6 Homo sapiens 63-67 26190660-11 2015 Increased interleukin (IL)-6 concentrations were associated with increased glucose (estimate [EST]: 0.55 (+-0.13) mmol/L; P < .001) and insulin (EST: 1.14 (+-0.12) mumol/L; P < .001) in linear regression adjusted for repeated measures. Glucose 75-82 interleukin 6 Homo sapiens 10-28 26885173-9 2015 RESULTS: Compared with those in normal glucose condition, IL-6 and IL-8 expression were increased in high glucose condition. Glucose 39-46 interleukin 6 Homo sapiens 58-62 26885173-9 2015 RESULTS: Compared with those in normal glucose condition, IL-6 and IL-8 expression were increased in high glucose condition. Glucose 106-113 interleukin 6 Homo sapiens 58-62 25410618-7 2015 Our data showed that high glucose induced the protein expressions of cyclooxygenase-2 (COX-2) and production of prostaglandin-E2 (PGE2 ), interleukin-6 (IL-6), and metalloproteinase-13 (MMP-13), but decreased the protein expression of collagen II and PPARgamma in human chondrocytes. Glucose 26-33 interleukin 6 Homo sapiens 138-151 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 interleukin 6 Homo sapiens 90-94 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 interleukin 6 Homo sapiens 112-116 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 interleukin 6 Homo sapiens 116-120 26040375-9 2015 Interleukin-6 correlated positively with levels of C-reactive protein and negatively with blood glucose. Glucose 96-103 interleukin 6 Homo sapiens 0-13 25394884-5 2015 RESULTS: Increasing concentrations of glucose significantly increased trophoblast secretion of the inflammatory cytokines/chemokines: IL-1beta, IL-6, IL-8, GRO-alpha, RANTES, and G-CSF; significantly increased trophoblast secretion of the anti-angiogenic factors sFlt-1 and sEndoglin; and significantly decreased trophoblast migration. Glucose 38-45 interleukin 6 Homo sapiens 144-148 25681539-5 2015 The endothelial production of high-glucose-induced interleukin (IL)-4, IL-6, IL-13 and signal transducer and activator of transcription-3 (STAT-3) phosphorylation were significantly inhibited by the pretreatment with GA at concentrations of 10, 15 and 20muM based on enzyme-linked immunosorbent assay (ELISA), western blot or/and RT-PCR experiments. Glucose 35-42 interleukin 6 Homo sapiens 71-75 25410618-7 2015 Our data showed that high glucose induced the protein expressions of cyclooxygenase-2 (COX-2) and production of prostaglandin-E2 (PGE2 ), interleukin-6 (IL-6), and metalloproteinase-13 (MMP-13), but decreased the protein expression of collagen II and PPARgamma in human chondrocytes. Glucose 26-33 interleukin 6 Homo sapiens 153-157 27167911-10 2015 Both glucose and nLDL increased IL-6 levels in a dose-dependent manner at 6 and 24 h. In conclusion, glucose treatment on HMEC-1 cells exerted a mild stimulus on NO and IL-6 production. Glucose 5-12 interleukin 6 Homo sapiens 32-36 25790769-6 2015 RESULTS: Neither high glucose nor low LPS (<=5 ng/ml) alone had an effect on TNF-a and IL-6 levels, but the combination of low LPS and high glucose stimulated the inflammatory response. Glucose 143-150 interleukin 6 Homo sapiens 90-94 25213007-2 2015 This increase in IL-6 is reported to have pleiotropic effects including increased glucose uptake, increased fat oxidation, and anti-inflammatory actions. Glucose 82-89 interleukin 6 Homo sapiens 17-21 27167911-10 2015 Both glucose and nLDL increased IL-6 levels in a dose-dependent manner at 6 and 24 h. In conclusion, glucose treatment on HMEC-1 cells exerted a mild stimulus on NO and IL-6 production. Glucose 5-12 interleukin 6 Homo sapiens 169-173 27167911-10 2015 Both glucose and nLDL increased IL-6 levels in a dose-dependent manner at 6 and 24 h. In conclusion, glucose treatment on HMEC-1 cells exerted a mild stimulus on NO and IL-6 production. Glucose 101-108 interleukin 6 Homo sapiens 32-36 27167911-10 2015 Both glucose and nLDL increased IL-6 levels in a dose-dependent manner at 6 and 24 h. In conclusion, glucose treatment on HMEC-1 cells exerted a mild stimulus on NO and IL-6 production. Glucose 101-108 interleukin 6 Homo sapiens 169-173 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 interleukin 6 Homo sapiens 168-181 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 interleukin 6 Homo sapiens 183-187 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 interleukin 6 Homo sapiens 56-60 24947356-0 2014 GLP-1 secretion is increased by inflammatory stimuli in an IL-6-dependent manner, leading to hyperinsulinemia and blood glucose lowering. Glucose 120-127 interleukin 6 Homo sapiens 59-63 24878329-9 2014 The expression of interleukin (IL)-6, IL-8, and monocyte chemoattractant protein-1 were significantly increased in HGECs while challenged with LPS in the context of high glucose; however, the expression inflammatory cytokines were decreased significantly, whereas TLR4 was blocked by TAK-242. Glucose 170-177 interleukin 6 Homo sapiens 18-36 24673855-8 2014 Our data indicate that high concentrations of IL-6 during the glucose clamp may be limited to the atypical subgroup of patients with MDD. Glucose 62-69 interleukin 6 Homo sapiens 46-50 24702712-0 2014 Interleukin-6 in combination with the interleukin-6 receptor stimulates glucose uptake in resting human skeletal muscle independently of insulin action. Glucose 72-79 interleukin 6 Homo sapiens 0-13 24702712-1 2014 AIM: To examine if the physiological concentrations of both interleukin-6 (IL-6), in combination with IL-6 receptor (IL-6R), are able to stimulate glucose uptake in human skeletal muscle and to identify the associated signalling pathways. Glucose 147-154 interleukin 6 Homo sapiens 60-73 24702712-1 2014 AIM: To examine if the physiological concentrations of both interleukin-6 (IL-6), in combination with IL-6 receptor (IL-6R), are able to stimulate glucose uptake in human skeletal muscle and to identify the associated signalling pathways. Glucose 147-154 interleukin 6 Homo sapiens 75-79 24702712-6 2014 IL-6 did not stimulate glucose uptake but combined with IL-6R, induced 1.5-fold increase in glucose uptake (p < 0.05) and phosphorylation of AMPK (0.95 +- 0.19; phosphorylated: total, p < 0.05). Glucose 92-99 interleukin 6 Homo sapiens 0-4 24702712-7 2014 CONCLUSIONS: IL-6 in combination with IL-6R and not IL-6 alone increased glucose uptake in human skeletal muscle. Glucose 73-80 interleukin 6 Homo sapiens 13-17 24702712-7 2014 CONCLUSIONS: IL-6 in combination with IL-6R and not IL-6 alone increased glucose uptake in human skeletal muscle. Glucose 73-80 interleukin 6 Homo sapiens 38-42 24702712-8 2014 IL-6/IL-6R-mediated glucose uptake occurred independently of PKB/Akt phosphorylation, showing that IL-6/IL-6R-induced glucose uptake is dependent on a divergent pathway. Glucose 20-27 interleukin 6 Homo sapiens 0-4 24702712-8 2014 IL-6/IL-6R-mediated glucose uptake occurred independently of PKB/Akt phosphorylation, showing that IL-6/IL-6R-induced glucose uptake is dependent on a divergent pathway. Glucose 20-27 interleukin 6 Homo sapiens 5-9 24702712-8 2014 IL-6/IL-6R-mediated glucose uptake occurred independently of PKB/Akt phosphorylation, showing that IL-6/IL-6R-induced glucose uptake is dependent on a divergent pathway. Glucose 118-125 interleukin 6 Homo sapiens 0-4 24702712-8 2014 IL-6/IL-6R-mediated glucose uptake occurred independently of PKB/Akt phosphorylation, showing that IL-6/IL-6R-induced glucose uptake is dependent on a divergent pathway. Glucose 118-125 interleukin 6 Homo sapiens 5-9 24702172-8 2014 The rise in IL-6 from baseline to peak concentration significantly correlated inversely with blood glucose area under the curve (r=-0.65, P=0.041). Glucose 99-106 interleukin 6 Homo sapiens 12-16 25002027-3 2014 The mechanism involves the regulation of cellular redox through an mTORC1/c-Myc pathway of stromal glucose and amino acid metabolism, resulting in increased stromal IL-6 production, which is required for tumor promotion in the epithelial compartment. Glucose 99-106 interleukin 6 Homo sapiens 165-169 24896536-2 2014 A new study shows that modulation of macrophage activation by IL-6 maintains glucose homeostasis in diet-induced obesity while limiting inflammation in endotoxemia (Mauer et al., 2014). Glucose 77-84 interleukin 6 Homo sapiens 62-66 24714919-6 2014 RESULTS: There was a significant inverse correlation between IL-6 levels and FMD (-0.042; p=0.02) after adjustment for age, gender, race/ethnicity, education, income, low-density lipoprotein, diabetes, glucose, hypertension status and treatment, waist circumference, triglycerides, baseline brachial diameter, recent infection and use of medications that may alter inflammation. Glucose 202-209 interleukin 6 Homo sapiens 61-65 24308966-6 2014 High glucose induced gene profiling in Jurkat T-lymphocytes showed significantly increased expression of 64 proinflammatory genes including IL-6 and IL-17A and most of these genes were Nuclear Factor (NF)-kappaB and AP-1 regulated. Glucose 5-12 interleukin 6 Homo sapiens 140-144 24576416-8 2014 In response to glucose ingestion, plasma IL-6 and sVCAM-1 increased and CRP suppression was attenuated in both PCOS groups and obese controls compared with lean controls. Glucose 15-22 interleukin 6 Homo sapiens 41-45 24473436-2 2014 We investigated the effect of IL-6 on insulin-stimulated glucose metabolism in type 2 diabetes patients and hypothesized that an acute, moderate IL-6 elevation would increase the insulin-mediated glucose uptake. Glucose 57-64 interleukin 6 Homo sapiens 30-34 24473436-2 2014 We investigated the effect of IL-6 on insulin-stimulated glucose metabolism in type 2 diabetes patients and hypothesized that an acute, moderate IL-6 elevation would increase the insulin-mediated glucose uptake. Glucose 57-64 interleukin 6 Homo sapiens 145-149 24473436-2 2014 We investigated the effect of IL-6 on insulin-stimulated glucose metabolism in type 2 diabetes patients and hypothesized that an acute, moderate IL-6 elevation would increase the insulin-mediated glucose uptake. Glucose 196-203 interleukin 6 Homo sapiens 30-34 24473436-2 2014 We investigated the effect of IL-6 on insulin-stimulated glucose metabolism in type 2 diabetes patients and hypothesized that an acute, moderate IL-6 elevation would increase the insulin-mediated glucose uptake. Glucose 196-203 interleukin 6 Homo sapiens 145-149 24575367-1 2014 Aim The objective of the study was to identify the association if any, of inflammatory markers (adiponectin and IL-6) with fasting glucose in normoglycemic (healthy), prediabetic (impaired fasting glucose), and hyperglycemic (diabetic) people in Indian population. Glucose 131-138 interleukin 6 Homo sapiens 112-116 24397394-1 2014 OBJECTIVE: The aim of this study is to compare galanin and IL-6 levels in pregnant women with gestational diabetes mellitus (GDM) and normal glucose tolerance (NGT). Glucose 141-148 interleukin 6 Homo sapiens 59-63 24586431-8 2014 Activation of PAR-4 by a selective agonist was found to elicit the pro-inflammatory and pro-fibrotic phenotypes in PTEC while blockade of the receptor by specific antagonist attenuated high glucose-induced IL-6, CCL-2, CTGF and collagen IV expression. Glucose 190-197 interleukin 6 Homo sapiens 206-210 24575367-6 2014 Similarly significant increase was also observed in IL-6 level in hyperglycemic and impaired fasting glucose groups compared with normoglycemic group. Glucose 101-108 interleukin 6 Homo sapiens 52-56 24575367-7 2014 Conclusions From our data it can be summarized that there is a significant change in both adiponectin (reduction) and IL-6 (increase) levels in normoglycemic (healthy), prediabetic (impaired fasting glucose), and hyperglycemic (diabetic) population in Indian population. Glucose 199-206 interleukin 6 Homo sapiens 118-122 24200052-6 2014 Interaction between PPARgamma Pro12Ala and IL6 -174G>C improved prediction of high fasting blood glucose (chi(2)=13.99; df=1; p<0.001). Glucose 100-107 interleukin 6 Homo sapiens 43-46 24200052-7 2014 PPARgamma Ala12 variant was found protective in patients with IL6 -174GG genotype (OR=0.10; 95% CI: 0.02-0.57, p=0.01), while in the case of IL6 -174C allele carriers, for PPARgamma Ala12 carriers, larger odds for high glucose levels compared with Pro12 variant were observed (OR=2.39; 95% CI: 1.11-5.17, p=0.026). Glucose 219-226 interleukin 6 Homo sapiens 141-144 24177007-5 2013 These dual effects would be mediated through endoplasmic reticulum (ER) stress, because we observed (1) up-regulation of GRP78 and CHOP under glucose-deprived condition, which was inhibited by chemical chaperon TMAO, and (2) treatment with TMAO inhibited IL-6 production under glucose-deprived condition. Glucose 142-149 interleukin 6 Homo sapiens 255-259 23656570-5 2013 RESULTS: Statistical analysis showed three doses of 0.5 (p = 0.049), 1 (p = 0.027), and 2 J/cm(2) (p = 0.004) stimulated the release of IL-6 in HSFs cultured in high glucose concentration medium compared with that of non-irradiated HSFs that were cultured in the same medium. Glucose 166-173 interleukin 6 Homo sapiens 136-140 23656570-7 2013 CONCLUSION: Our study showed that LLLT stimulated the release of IL-6 and bFGF from HSFs cultured in high glucose concentration medium. Glucose 106-113 interleukin 6 Homo sapiens 65-69 24063815-2 2013 Interleukin-6 (IL-6), a multifunctional cytokine, could influence conditions of altered glucose metabolism such as insulin resistance in diabetic patients. Glucose 88-95 interleukin 6 Homo sapiens 0-13 24063815-2 2013 Interleukin-6 (IL-6), a multifunctional cytokine, could influence conditions of altered glucose metabolism such as insulin resistance in diabetic patients. Glucose 88-95 interleukin 6 Homo sapiens 15-19 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 interleukin 6 Homo sapiens 96-109 23135962-5 2013 In AMI group, individuals carrying IL6 -174CC genotype had higher serum triglycerides, VLDL cholesterol and glucose compared to the IL6 -174GG/GC genotype carriers (p < 0.05). Glucose 108-115 interleukin 6 Homo sapiens 35-38 23767858-7 2013 In multiple regression analysis, postload glucose concentration was independently associated with circulating hsCRP and IL-6 concentrations when the data was controlled for age, gender, BMI and lipid concentrations (p < 0.05 for hsCRP, and IL-6). Glucose 42-49 interleukin 6 Homo sapiens 120-124 21997325-9 2013 "In vitro" results demonstrate that glucose directly and significantly induced MCP-1 and IL6 and reduced TLR2 mRNA expression. Glucose 36-43 interleukin 6 Homo sapiens 89-92 21997325-10 2013 Insulin at high dose (100 IU/ml) dramatically enhanced the upregulatory effects of glucose on MCP-1 and IL-6 and reduced per se TLR2 mRNA expression. Glucose 83-90 interleukin 6 Homo sapiens 104-108 23767858-7 2013 In multiple regression analysis, postload glucose concentration was independently associated with circulating hsCRP and IL-6 concentrations when the data was controlled for age, gender, BMI and lipid concentrations (p < 0.05 for hsCRP, and IL-6). Glucose 42-49 interleukin 6 Homo sapiens 243-247 23735697-0 2013 High glucose modulates IL-6 mediated immune homeostasis through impeding neutrophil extracellular trap formation. Glucose 5-12 interleukin 6 Homo sapiens 23-27 23693076-11 2013 Furthermore, high glucose increased the secretion of IL-6 and ICAM, as well as decreased phospho-eNOS protein expression and NOS activity. Glucose 18-25 interleukin 6 Homo sapiens 53-57 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 interleukin 6 Homo sapiens 158-162 23776669-1 2013 BACKGROUND: Plasma interleukin-6 (IL-6) concentrations decrease acutely 1 h after ingestion of a glucose load or mixed meals and this may be mediated by an anti-inflammatory effect of insulin. Glucose 97-104 interleukin 6 Homo sapiens 19-32 23776669-1 2013 BACKGROUND: Plasma interleukin-6 (IL-6) concentrations decrease acutely 1 h after ingestion of a glucose load or mixed meals and this may be mediated by an anti-inflammatory effect of insulin. Glucose 97-104 interleukin 6 Homo sapiens 34-38 23776669-6 2013 Plasma IL-6 decreased (13-20%) significantly (P = 0.009) at 30 min to 90 min following the oral glucose load and did not change significantly following the other two interventions. Glucose 96-103 interleukin 6 Homo sapiens 7-11 23776669-7 2013 The incremental area under the curve for plasma IL-6 concentrations following oral intake of glucose was significantly lower compared with concentrations following intravenous glucose (P = 0.005) and water control (P = 0.02). Glucose 93-100 interleukin 6 Homo sapiens 48-52 23780308-4 2013 EGCG inhibited high glucose(HG)-induced TNF-alpha and IL-6 production in human embryonic kidney (HEK) cells. Glucose 20-27 interleukin 6 Homo sapiens 54-58 23371411-2 2013 Therefore, this study was aimed to investigate the association between concentration of IL-6 in relation to glucose control, lipid profile, and body mass index (BMI) in 69 DM1 patients subdivided according to the absence or presence of microvascular complications. Glucose 108-115 interleukin 6 Homo sapiens 88-92 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 interleukin 6 Homo sapiens 9-13 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 interleukin 6 Homo sapiens 178-182 23529237-6 2013 High glucose promoted NF-kappaB nuclear translocation and significantly enhanced the expression and secretion of both MCP-1 and IL-6 (P<0.01). Glucose 5-12 interleukin 6 Homo sapiens 128-132 23529237-7 2013 Pretreatment with high glucose significantly promoted LPS-induced NF-kappaB nuclear translocation (P<0.01) and the mRNA expression and secretion of MCP-1 and IL-6. Glucose 23-30 interleukin 6 Homo sapiens 161-165 23086036-2 2013 We determined the effect of IL-6 exposure on glucose and lipid metabolism in cultured myotubes established from people with normal glucose tolerance or type 2 diabetes. Glucose 45-52 interleukin 6 Homo sapiens 28-32 23086036-3 2013 Acute IL-6 exposure increased glycogen synthesis, glucose uptake, and signal transducer and activator of transcription 3 (STAT3) phosphorylation in cultured myotubes from normal glucose tolerant subjects. Glucose 50-57 interleukin 6 Homo sapiens 6-10 23086036-3 2013 Acute IL-6 exposure increased glycogen synthesis, glucose uptake, and signal transducer and activator of transcription 3 (STAT3) phosphorylation in cultured myotubes from normal glucose tolerant subjects. Glucose 178-185 interleukin 6 Homo sapiens 6-10 23086036-5 2013 IL-6 increased fatty acid oxidation in myotubes from type 2 diabetic and normal glucose tolerant subjects. Glucose 80-87 interleukin 6 Homo sapiens 0-4 23086036-8 2013 In summary, skeletal muscle cells from type 2 diabetic patients display selective IL-6 resistance for glucose rather than lipid metabolism. Glucose 102-109 interleukin 6 Homo sapiens 82-86 23086036-9 2013 In conclusion, IL-6 appears to play a differential role in regulating metabolism in type 2 diabetic patients compared with normal glucose tolerant subjects. Glucose 130-137 interleukin 6 Homo sapiens 15-19 22494810-0 2012 Correlation between high blood IL-6 level, hyperglycemia, and glucose control in septic patients. Glucose 62-69 interleukin 6 Homo sapiens 31-35 23420163-10 2013 CONCLUSION: The multiple regression model demonstrated that in addition to age and glycemia (two well-known factors that are directly involved in glucose metabolism), adrenomedullin and IL-6 levels were independent factors associated with lower insulin concentrations. Glucose 146-153 interleukin 6 Homo sapiens 186-190 23037942-7 2013 Importantly, contraction-dependent IL-6 up-regulation was markedly suppressed in the presence of high levels of glucose along with increased glycogen accumulations. Glucose 112-119 interleukin 6 Homo sapiens 35-39 23037942-8 2013 Experimental manipulation of intracellular glycogen contents by modulating available glucose or pyruvate during a certain EPS period further established the suppressive effect of glycogen accumulations on contraction-induced IL-6 up-regulation, which appeared to be independent of calcineurin activity. Glucose 85-92 interleukin 6 Homo sapiens 225-229 23095208-10 2013 In logistic regression analysis, IL-6, neopterin and Lp-PLA2 levels were detected to be related to high blood glucose levels at 30 min (OR 1.11, p=0.01; OR 9.03, p=0.013; OR 1.01, p=0.004 respectively). Glucose 110-117 interleukin 6 Homo sapiens 33-37 22494810-1 2012 INTRODUCTION: The aim of the present study was to investigate the relationship between the blood IL-6 level, the blood glucose level, and glucose control in septic patients. Glucose 138-145 interleukin 6 Homo sapiens 97-101 22494810-4 2012 RESULTS: A significant positive correlation between blood IL-6 level and blood glucose level on ICU admission was observed in the overall study population (n = 153; r = 0.24, P = 0.01), and was stronger in the nondiabetic subgroup (n = 112; r = 0.42, P < 0.01). Glucose 79-86 interleukin 6 Homo sapiens 58-62 22494810-5 2012 The rate of successful glucose control (blood glucose level < 150 mg/dl maintained for 6 days or longer) decreased with increase in blood IL-6 level on ICU admission (P < 0.01). Glucose 23-30 interleukin 6 Homo sapiens 141-145 22494810-7 2012 CONCLUSIONS: High blood IL-6 level was correlated with hyperglycemia and with difficulties in glucose control in septic patients. Glucose 94-101 interleukin 6 Homo sapiens 24-28 22391518-10 2012 A positive correlation was found between IL-6 and glucose or triglyceride concentrations, while the correlation with HDL cholesterol was negative. Glucose 50-57 interleukin 6 Homo sapiens 41-45 22426798-7 2012 mRNA relative abundance of nuclear factor kappa-light-chain-enhancer of activated B cells was elevated in OBDM with anemia, and mRNA expression of interleukin-6 and toll-like receptor (TLR) 2 was increased in OBDM group in basal high Fe and high glucose concentrations. Glucose 246-253 interleukin 6 Homo sapiens 147-160 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 interleukin 6 Homo sapiens 14-18 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 interleukin 6 Homo sapiens 77-81 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 interleukin 6 Homo sapiens 114-118 22318941-10 2012 CONCLUSION: Based on these data, we conclude that gluconeogenesis is severely compromised in HCC by IL6-Stat3-mediated activation of miR-23a, which directly targets PGC-1alpha and G6PC, leading to decreased glucose production. Glucose 207-214 interleukin 6 Homo sapiens 100-103 22086137-9 2012 Our results show that high glucose concentrations (12 mM and particularly 24 mM) alter the biomineralization process in osteoblastic cells and provoke the following: i) a rise in mineralization, ii) an increase in the mRNA expression of RANKL and a decrease of OPG, iii) an increase in the mRNA expression of osteocalcin, bone sialoprotein and the transcription factor Runx2, iv) a diminished quality of the mineral, and v) an increase in the expression of IL1beta, IL6, IL8, MCP-1 and IL10 mRNAs. Glucose 27-34 interleukin 6 Homo sapiens 466-469 21633399-8 2012 The oral glucose challenge was associated with a significant increase in the expression of inflammatory cytokines, including interleukin (IL)-1alpha/beta, IL-6, and IL-8, that may result from ER stress. Glucose 9-16 interleukin 6 Homo sapiens 155-159 22428468-10 2012 Fasting plasma glucose (FPG) level and HbA1c showed a significant positive correlation (p < 0.001) with Hs-CRP (r = 0.531) (r = 0.750), and IL-6 (r = 0. Glucose 15-22 interleukin 6 Homo sapiens 143-147 22035595-5 2012 Our data indicated that diabetes as whole was strongly associated with elevated levels of IL-6, leptin, CRP and TNF-alpha, whereas worsening of glucose control was positively and linearly associated with high levels of IL-6, and leptin. Glucose 144-151 interleukin 6 Homo sapiens 219-223 22021706-6 2012 In vitro, high glucose induced TLR4 expression via protein kinase C activation in a time- and dose-dependent manner, resulting in upregulation of IL-6 and chemokine (C-C motif) ligand 2 (CCL-2) expression via IkappaB/NF-kappaB activation in human proximal tubular epithelial cells. Glucose 15-22 interleukin 6 Homo sapiens 146-185 22347395-7 2012 MSD, R&D, and ULX, but not LX, detected increases in IL-6 in response to glucose. Glucose 77-84 interleukin 6 Homo sapiens 57-61 22474579-7 2012 We speculate that the observed increases in postprandial IL6, without increases in any other markers of inflammation, may indicate a normal IL6 response to enhance glucose uptake, similar to its role postexercise. Glucose 164-171 interleukin 6 Homo sapiens 57-60 22474579-7 2012 We speculate that the observed increases in postprandial IL6, without increases in any other markers of inflammation, may indicate a normal IL6 response to enhance glucose uptake, similar to its role postexercise. Glucose 164-171 interleukin 6 Homo sapiens 140-143 22962620-0 2012 In vivo screening for secreted proteins that modulate glucose handling identifies interleukin-6 family members as potent hypoglycemic agents. Glucose 54-61 interleukin 6 Homo sapiens 82-95 22347395-11 2012 Plasma IL-6 concentrations increase in response to glucose and insulin, consistent with both an early glucose-dependent response (detectable at 1-2 hours) and a late insulin-dependent response (detectable after 2 hours). Glucose 51-58 interleukin 6 Homo sapiens 7-11 22347395-11 2012 Plasma IL-6 concentrations increase in response to glucose and insulin, consistent with both an early glucose-dependent response (detectable at 1-2 hours) and a late insulin-dependent response (detectable after 2 hours). Glucose 102-109 interleukin 6 Homo sapiens 7-11 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 interleukin 6 Homo sapiens 82-86 22086794-4 2011 RESULTS: In the analysis with leptin as a dependent variable, the IL-6 and glucose levels remained in the model (F = 6.2; P<0.05), with an increase of 5.8 (CI 95%:2.7-7.6) ng/ml with each 1 pg/ml of IL-6 and of 5.2 (CI95%:2.5-5.8) ng/ml with each 1 mg/dl of glucose. Glucose 75-82 interleukin 6 Homo sapiens 202-206 22086794-4 2011 RESULTS: In the analysis with leptin as a dependent variable, the IL-6 and glucose levels remained in the model (F = 6.2; P<0.05), with an increase of 5.8 (CI 95%:2.7-7.6) ng/ml with each 1 pg/ml of IL-6 and of 5.2 (CI95%:2.5-5.8) ng/ml with each 1 mg/dl of glucose. Glucose 261-268 interleukin 6 Homo sapiens 66-70 22086794-6 2011 In the third multivariate analysis with IL-6 as a dependent variable, the glucose level remained in the model (F = 10.1; P<0.01), with an increase of 0.09 (CI95%:0.06-0.12) pg/ml with each 1 mg/dl of glucose. Glucose 74-81 interleukin 6 Homo sapiens 40-44 21811961-8 2011 (2) Arterial interleukin-6 (p=0.002) and subcutaneous venous interleukin-6 (p=0.014) were negatively associated with forearm glucose uptake in obese. Glucose 125-132 interleukin 6 Homo sapiens 13-26 21811961-8 2011 (2) Arterial interleukin-6 (p=0.002) and subcutaneous venous interleukin-6 (p=0.014) were negatively associated with forearm glucose uptake in obese. Glucose 125-132 interleukin 6 Homo sapiens 61-74 21487312-0 2011 Resistance and aerobic exercise: the influence of mode on the relationship between IL-6 and glucose tolerance in young men who are obese. Glucose 92-99 interleukin 6 Homo sapiens 83-87 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 interleukin 6 Homo sapiens 147-160 21458563-6 2011 The high glucose incubation increased NF-kappaB, RAGE and IL-6 expressions in HEK293 cells. Glucose 9-16 interleukin 6 Homo sapiens 58-62 22219634-9 2011 The result of ELISA also showed that the release of IL-6 and IL-8 can be inhibited by high glucose, but these inhibitions were partly counteracted after pretreatment with anti-TLR2 and/or anti-TLR4 monoclonal antibody. Glucose 91-98 interleukin 6 Homo sapiens 52-56 21609290-11 2011 Furthermore, there was a significant correlation between changes in serum IL-6 levels and changes in fasting blood glucose levels (rho = 0.883; p = 0.0306). Glucose 115-122 interleukin 6 Homo sapiens 74-78 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 interleukin 6 Homo sapiens 87-91 24331010-5 2011 IL-6 at a concentration comparable to that in CM from visceral fat reduced insulin-stimulated glucose uptake by 53% (P < 0.05), an effect abolished by inhibiting NFkappaB or mTORC1. Glucose 94-101 interleukin 6 Homo sapiens 0-4 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 interleukin 6 Homo sapiens 142-155 20887798-4 2010 Microarray analysis revealed that myostatin upregulates several genes involved in regulating glucose metabolism such as Glut1, Glut4, Hk2, and IL-6. Glucose 93-100 interleukin 6 Homo sapiens 143-147 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 interleukin 6 Homo sapiens 157-161 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 interleukin 6 Homo sapiens 98-102 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 interleukin 6 Homo sapiens 98-102 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 interleukin 6 Homo sapiens 76-80 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 interleukin 6 Homo sapiens 76-80 21831781-7 2010 In addition, in human nutritional experiments we observed that whole grain products could counteract a glucose-induced tumour necrosis factor alpha and interleukin-6 increase which was associated with increased plasma butyrate concentrations. Glucose 103-110 interleukin 6 Homo sapiens 152-165 20225236-5 2010 We found that IL-6 is a powerful stimulator for MMP-1 expression and high glucose further augmented IL-6-stimulated MMP-1 expression. Glucose 74-81 interleukin 6 Homo sapiens 100-104 20950383-7 2010 Change in interleukin-6 was also significantly correlated with change in 2 h glucose after adjustment for the same variables (r = 0.26, P = 0.03). Glucose 77-84 interleukin 6 Homo sapiens 10-23 20170929-6 2010 Plasma IL-1beta and IL-6 levels in nonoverweight subjects were positively and strongly associated with fasting blood glucose and hemoglobin A(1c); in contrast, these cytokines were strongly associated with homeostasis model assessment of insulin resistance and fasting glucose in overweight subjects. Glucose 117-124 interleukin 6 Homo sapiens 20-24 20170929-6 2010 Plasma IL-1beta and IL-6 levels in nonoverweight subjects were positively and strongly associated with fasting blood glucose and hemoglobin A(1c); in contrast, these cytokines were strongly associated with homeostasis model assessment of insulin resistance and fasting glucose in overweight subjects. Glucose 269-276 interleukin 6 Homo sapiens 20-24 20578705-8 2010 Incubation of ARPE-19 cells with 33 mM glucose for 9 days significantly induced the accumulation of VEGF, IL-6, IL-8, TGF-beta, and COX-2, activation of PKCbeta, and reduction of Cx43 and GJIC. Glucose 39-46 interleukin 6 Homo sapiens 106-110 20578705-9 2010 Incubation of ARPE-19 cells with 33 mM glucose in the presence of 0-10 microM trans-resveratrol dose-dependently inhibited VEGF, TGF-beta1, COX-2, IL-6, and IL-8 accumulation, PKCbeta activation, and Cx43 degradation and enhanced GJIC. Glucose 39-46 interleukin 6 Homo sapiens 147-151 20189706-7 2010 While TNFalpha (-308) and IL-10 (-1082) genotypes did not influence clinical/laboratory parameters in PCOS, IL-6 (-174) CC or pooled CG+CC genotypes have lower glucose, insulin, HOMA, cholesterol, triglyceride, and LDL-C, and higher GIR and HDL-C values than GG genotypes. Glucose 160-167 interleukin 6 Homo sapiens 108-112 20358354-8 2009 The association between body fat mass and plasma glucose was influenced by the -174G/C polymorphism of the IL6 gene. Glucose 49-56 interleukin 6 Homo sapiens 107-110 20168253-12 2010 No relationship was observed between PO IL-6 and IGR, but PR IL-6 was negatively related to both PR (r = -0.043, p < 0.05) and 60 minutes (r = -0.59, p < 0.01) glucose (n = 14). Glucose 166-173 interleukin 6 Homo sapiens 61-65 20016056-7 2010 Mice with very high plasma levels of aAb-IL6 developed elevated fasting plasma glucose (mM, 4.8+/-0.4 vs 3.3+/-0.1, P<0.001) and impaired glucose tolerance (AUC glucose, 1340+/-38 vs 916+/-25, P<0.001) as compared with sham-control mice on normal chow. Glucose 79-86 interleukin 6 Homo sapiens 41-44 20016056-7 2010 Mice with very high plasma levels of aAb-IL6 developed elevated fasting plasma glucose (mM, 4.8+/-0.4 vs 3.3+/-0.1, P<0.001) and impaired glucose tolerance (AUC glucose, 1340+/-38 vs 916+/-25, P<0.001) as compared with sham-control mice on normal chow. Glucose 141-148 interleukin 6 Homo sapiens 41-44 19923143-2 2010 METHODS AND RESULTS: High-glucose (HG) super-induced interleukin (IL)-6, CCL-2, transforming growth factor (TGF)-beta, vascular endothelial growth factor (VEGF) and B(2)K receptor (B(2)KR) mRNA in cultured proximal tubular epithelial cells (PTEC), whereas bradykinin (BK) upregulated IL-6, CCL-2 and TGF-beta mRNA. Glucose 26-33 interleukin 6 Homo sapiens 284-288 20007708-0 2010 Adipocyte-mononuclear cell interaction, Toll-like receptor 4 activation, and high glucose synergistically up-regulate osteopontin expression via an interleukin 6-mediated mechanism. Glucose 82-89 interleukin 6 Homo sapiens 148-161 20164544-2 2010 Interleukin-6 (IL-6) is a cytokine involved in inflammatory process, as well as in glucose and lipid metabolism. Glucose 83-90 interleukin 6 Homo sapiens 0-13 20164544-2 2010 Interleukin-6 (IL-6) is a cytokine involved in inflammatory process, as well as in glucose and lipid metabolism. Glucose 83-90 interleukin 6 Homo sapiens 15-19 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 interleukin 6 Homo sapiens 42-46 19592412-1 2009 Glucose ingestion during exercise attenuates the release of the myokine interleukin-6 (IL-6) from working skeletal muscle, which results in a diminished increase in plasma IL-6. Glucose 0-7 interleukin 6 Homo sapiens 72-85 19592412-1 2009 Glucose ingestion during exercise attenuates the release of the myokine interleukin-6 (IL-6) from working skeletal muscle, which results in a diminished increase in plasma IL-6. Glucose 0-7 interleukin 6 Homo sapiens 87-91 19592412-1 2009 Glucose ingestion during exercise attenuates the release of the myokine interleukin-6 (IL-6) from working skeletal muscle, which results in a diminished increase in plasma IL-6. Glucose 0-7 interleukin 6 Homo sapiens 172-176 19592412-7 2009 The IL-6Ralpha density increased to a lesser extent in the Glc-leg, suggesting that glucose ingestion attenuates the effect of training on IL-6Ralpha by blunting the IL-6 response. Glucose 84-91 interleukin 6 Homo sapiens 4-8 18842114-10 2009 Log interleukin-6 was found to be significantly correlated with periodontal diagnosis, leukocyte count and level of fasting blood glucose after adjusting for the confounders (p = 0.000, p = 0.009 and p = 0.013, respectively). Glucose 130-137 interleukin 6 Homo sapiens 4-17 19604525-9 2009 We also found that postprandial plasma concentrations of IL-6 were lower in subjects with a normal glucose tolerance (n = 69) compared with individuals with an impaired glucose tolerance (n = 11). Glucose 99-106 interleukin 6 Homo sapiens 57-61 19882048-9 2009 Thus, by increasing direct absorption of blood glucose by skeletal muscle, IL-6 can have a beneficial role in continuing the activities of diabetic patients. Glucose 47-54 interleukin 6 Homo sapiens 75-79 19375766-10 2009 Insulin-induced rise in IL-6 correlated negatively to BMI (P = .001), waist to hip ratio (P = .05), and baseline (fasting) insulin (P = .03) and IL-6 (P = .02) levels and positively to insulin-stimulated glucose uptake in isolated adipocytes (P = .07). Glucose 204-211 interleukin 6 Homo sapiens 24-28 19399017-6 2009 The action of IL-6 on glucose homeostasis is also complex and integrates central and peripheral mechanisms. Glucose 22-29 interleukin 6 Homo sapiens 14-18 19307187-0 2009 Interleukin-6 released from fibroblasts is essential for up-regulation of matrix metalloproteinase-1 expression by U937 macrophages in coculture: cross-talking between fibroblasts and U937 macrophages exposed to high glucose. Glucose 217-224 interleukin 6 Homo sapiens 0-13 19307187-10 2009 In conclusion, this study demonstrates that IL-6 derived from fibroblasts is essential for MMP-1 up-regulation by cross-talking between fibroblasts and U937 macrophages exposed to high glucose, revealing an IL-6-dependent mechanism in MMP-1 up-regulation. Glucose 185-192 interleukin 6 Homo sapiens 44-48 19307187-10 2009 In conclusion, this study demonstrates that IL-6 derived from fibroblasts is essential for MMP-1 up-regulation by cross-talking between fibroblasts and U937 macrophages exposed to high glucose, revealing an IL-6-dependent mechanism in MMP-1 up-regulation. Glucose 185-192 interleukin 6 Homo sapiens 207-211 19188427-2 2009 We hypothesized that IL-6 promotes endothelial cell signaling and capillary recruitment in vivo, contributing to increased glucose uptake. Glucose 123-130 interleukin 6 Homo sapiens 21-25 19188427-6 2009 In contrast, IL-6 increased Akt phosphorylation (Ser473) in hindlimb skeletal muscle and enhanced whole-body glucose disappearance and glucose uptake during the clamp. Glucose 109-116 interleukin 6 Homo sapiens 13-17 19188427-6 2009 In contrast, IL-6 increased Akt phosphorylation (Ser473) in hindlimb skeletal muscle and enhanced whole-body glucose disappearance and glucose uptake during the clamp. Glucose 135-142 interleukin 6 Homo sapiens 13-17 18752089-2 2009 AIMS: This joint analysis aimed to clarify whether IL6 -174G>C was associated with glucose and circulating interleukin-6 concentrations as well as body mass index (BMI). Glucose 86-93 interleukin 6 Homo sapiens 51-54 19092166-9 2009 Elevated fasting glucose (>6.2 mmol/l) markedly increased the predictive power of inflammatory markers (IL-18: 5.5 [1.4-21.1], IL-6: 3.5 [1.0-11.8], and CRP: 3.5 [1.0-11.9]). Glucose 17-24 interleukin 6 Homo sapiens 130-134 19218094-8 2009 Cells cultured in a medium with glucose 30 mmol/L generated more free radicals (+20%, P < 0.05) and released more MCP-1 (+113%, P < 0.001) and IL-6 (+26%, P < 0.05). Glucose 32-39 interleukin 6 Homo sapiens 149-153 18752089-6 2009 IL6 -174 C-allele carriers had significantly lower fasting glucose (-0.091 mmol/L, P=0.014). Glucose 59-66 interleukin 6 Homo sapiens 0-3 18752089-8 2009 CONCLUSIONS: Our data suggest that C-allele carriers of the IL6 -174G>C polymorphism have lower fasting glucose levels on average, which substantiates previous findings of decreased T2DM risk of these subjects. Glucose 107-114 interleukin 6 Homo sapiens 60-63 19156623-5 2009 In glucose-intolerant subjects, sCD36 was negatively associated with insulin sensitivity and positively with interleukin-6 (IL-6), fasting glucose, fasting triglycerides, fat-free mass and platelet count. Glucose 3-10 interleukin 6 Homo sapiens 109-122 18818415-2 2008 METHODS AND RESULTS: Monocyte and lymphocyte cytokine gene and protein expression of interleukin (IL)-6 were first shown to be greater in subjects with impaired glucose tolerance (IGT) than in subjects with normal glucose tolerance. Glucose 161-168 interleukin 6 Homo sapiens 85-103 19251052-5 2009 In contrast to its role in liver, IL-6 is believed to be beneficial for insulin-regulated glucose metabolism in muscle. Glucose 90-97 interleukin 6 Homo sapiens 34-38 18319319-5 2008 Finally, when subjects were stratified on the basis of their respective concentrations of IL-6 and TNF-alpha (using the 50th percentile of their overall distribution), an ANOVA revealed an independent contribution of IL-6 to the variation of fasting insulin (P < 0.01) and each of these two cytokines to the variation of insulin levels measured after a 75-g oral glucose challenge (P <0.01 for IL-6 and P < 0.05 for TNF-alpha). Glucose 366-373 interleukin 6 Homo sapiens 217-221 18803936-6 2008 The 30-minute decrease in plasma IL-6 was correlated significantly and inversely with the concomitant increase in plasma insulin (r = -0.410, P = .02) and with the ratio of insulin to glucose at 30 minutes during the OGTT (r = -0.366, P = .04). Glucose 184-191 interleukin 6 Homo sapiens 33-37 18803936-7 2008 These data suggest that plasma concentrations of IL-6 are acutely decreased possibly because of the predominance of the anti-inflammatory effect of hyperinsulinemia over the proinflammatory effect of hyperglycemia after ingestion of a large quantity of glucose in obese individuals. Glucose 253-260 interleukin 6 Homo sapiens 49-53 18481110-5 2008 Acute exposure of HPMC to conventional low-glucose-based PD solution resulted in a time-dependent increase in heat-shock protein (HSP-72) expression, impaired viability, and reduced ability to release IL-6 in response to stimulation. Glucose 43-50 interleukin 6 Homo sapiens 201-205 18446686-4 2008 The subjects with abnormal glucose challenge test results had higher IL-6 levels (0.9 [0.7-1.3] pg/ml, p=0.005) and similar levels of other cytokines as compared with the women with normal glucose tolerance. Glucose 27-34 interleukin 6 Homo sapiens 69-73 18319319-5 2008 Finally, when subjects were stratified on the basis of their respective concentrations of IL-6 and TNF-alpha (using the 50th percentile of their overall distribution), an ANOVA revealed an independent contribution of IL-6 to the variation of fasting insulin (P < 0.01) and each of these two cytokines to the variation of insulin levels measured after a 75-g oral glucose challenge (P <0.01 for IL-6 and P < 0.05 for TNF-alpha). Glucose 366-373 interleukin 6 Homo sapiens 217-221 17956334-6 2007 In more recent experiments, it has been shown that IL-6 infusion increases glucose disposal during a hyperinsulinaemic euglycaemic clamp in healthy humans. Glucose 75-82 interleukin 6 Homo sapiens 51-55 18171428-0 2008 Role of interleukin-6 signalling in glucose and lipid metabolism. Glucose 36-43 interleukin 6 Homo sapiens 8-21 18171428-7 2008 This review aims at summarizing the current data on mechanisms by which IL-6 may impact on glucose and lipid metabolism. Glucose 91-98 interleukin 6 Homo sapiens 72-76 17956545-5 2008 On the other hand, IL-6 produced in the working muscle during physical activity could act as an energy sensor by activating AMP-activated kinase and enhancing glucose disposal, lipolysis and fat oxidation. Glucose 159-166 interleukin 6 Homo sapiens 19-23 17956334-7 2007 IL-6 treatment of myotubes increases fatty acid oxidation, basal and insulin-stimulated glucose uptake and translocation of GLUT4 to the plasma membrane. Glucose 88-95 interleukin 6 Homo sapiens 0-4 18059606-3 2007 IL-6 increases insulin-stimulated glucose disposal and fatty acid oxidation in humans in vivo. Glucose 34-41 interleukin 6 Homo sapiens 0-4 17363741-10 2007 IL-6 also increased skeletal muscle glucose incorporation into glycogen, as well as glucose oxidation (1.5- and 1.3-fold, respectively; P < 0.05). Glucose 36-43 interleukin 6 Homo sapiens 0-4 17615159-2 2007 This IL-6 production is discussed as one possible mediator of the beneficial effects of physical activity on glucose and fatty acid metabolism. Glucose 109-116 interleukin 6 Homo sapiens 5-9 17416792-0 2007 Interleukin-6 in obese children and adolescents with and without glucose intolerance. Glucose 65-72 interleukin 6 Homo sapiens 0-13 17363741-0 2007 Interleukin-6 directly increases glucose metabolism in resting human skeletal muscle. Glucose 33-40 interleukin 6 Homo sapiens 0-13 17363741-4 2007 Thus, IL-6 has also been suggested to promote insulin-mediated glucose utilization. Glucose 63-70 interleukin 6 Homo sapiens 6-10 17363741-5 2007 In this study, we determined the direct effects of IL-6 on glucose transport and signal transduction in human skeletal muscle. Glucose 59-66 interleukin 6 Homo sapiens 51-55 17363741-8 2007 We found that IL-6 increased glucose transport in human skeletal muscle 1.3-fold (P < 0.05). Glucose 29-36 interleukin 6 Homo sapiens 14-18 17414493-4 2007 Acute interleukin-6 administration to humans increases lipolysis, fat oxidation and insulin-mediated glucose disposal. Glucose 101-108 interleukin 6 Homo sapiens 6-19 17363741-13 2007 In conclusion, acute IL-6 exposure increases glucose metabolism in resting human skeletal muscle. Glucose 45-52 interleukin 6 Homo sapiens 21-25 17185492-8 2007 IL-6 is a cytokine that may have beneficial systemic effects by mobilizing glucose from the liver and free fatty acids from the adipose tissue and providing them to the strenuously working respiratory muscles. Glucose 75-82 interleukin 6 Homo sapiens 0-4 16945991-0 2006 Signaling specificity of interleukin-6 action on glucose and lipid metabolism in skeletal muscle. Glucose 49-56 interleukin 6 Homo sapiens 25-38 16952201-2 2007 METHODS: To this end, we examined the relationship between plasma IL-6 concentration and different degrees of glucose homeostasis in a cohort of 470 Italian Caucasian subjects comprising 236 normal glucose tolerant (NGT), 49 IFG, 51 IGT, and 134 type 2 diabetic subjects. Glucose 110-117 interleukin 6 Homo sapiens 66-70 16952201-4 2007 Univariate correlations between IL-6 concentrations and metabolic variables in the whole cohort showed that IL-6 levels were positively correlated with age, BMI, waist, systolic and diastolic blood pressure, fasting plasma glucose, triglycerides, CRP, fibrinogen, and negatively correlated with insulin sensitivity, IGF-I and HDL. Glucose 223-230 interleukin 6 Homo sapiens 108-112 16952201-5 2007 In a subgroup analysis including NGT, IFG and IGT (n = 336), IL-6 levels were positively correlated with age, BMI, waist, systolic and diastolic blood pressure, triglycerides, CRP, fibrinogen, fasting insulin, 2 h post-load glucose, and negatively correlated with insulin sensitivity, IGF-I and HDL. Glucose 224-231 interleukin 6 Homo sapiens 61-65 16945991-4 2006 IL-6 increased glucose incorporation into glycogen, glucose uptake, lactate production, and fatty acid uptake and oxidation, concomitant with increased phosphorylation of AMP-activated protein kinase (AMPK), signal transducer and activator of transcription 3, and ERK1/2. Glucose 15-22 interleukin 6 Homo sapiens 0-4 16945991-4 2006 IL-6 increased glucose incorporation into glycogen, glucose uptake, lactate production, and fatty acid uptake and oxidation, concomitant with increased phosphorylation of AMP-activated protein kinase (AMPK), signal transducer and activator of transcription 3, and ERK1/2. Glucose 52-59 interleukin 6 Homo sapiens 0-4 16945991-6 2006 IL-6-mediated glucose metabolism was suppressed, but lipid metabolism was unaltered, by inhibition of PI3-kinase with LY294002. Glucose 14-21 interleukin 6 Homo sapiens 0-4 16896935-11 2006 CONCLUSIONS/INTERPRETATION: Homocysteine upregulates the MMP-TIMP pathway and IL6 release, the effect being stronger in the presence of high glucose. Glucose 141-148 interleukin 6 Homo sapiens 78-81 17003332-2 2006 Here, we show that IL-6 infusion increases glucose disposal without affecting the complete suppression of endogenous glucose production during a hyperinsulinemic-euglycemic clamp in healthy humans. Glucose 43-50 interleukin 6 Homo sapiens 19-23 17003332-0 2006 Interleukin-6 increases insulin-stimulated glucose disposal in humans and glucose uptake and fatty acid oxidation in vitro via AMP-activated protein kinase. Glucose 43-50 interleukin 6 Homo sapiens 0-13 17375405-3 2006 Glucose, glucose metabolites and AGEs alter endothelial cell functions, induce adhesion molecule overexpression (ICAM-1, VCAM), cytokine release (IL-6, MCP-1) and tissue factor production. Glucose 0-7 interleukin 6 Homo sapiens 146-150 16919544-10 2006 In conclusion, this study shows that in Asian Indians, inflammatory markers (CRP, IL-6, and VCAM-1) increase with increasing degrees of glucose intolerance. Glucose 136-143 interleukin 6 Homo sapiens 82-86 17003332-4 2006 IL-6 treatment increased fatty acid oxidation, basal and insulin-stimulated glucose uptake, and translocation of GLUT4 to the plasma membrane. Glucose 76-83 interleukin 6 Homo sapiens 0-4 17003332-8 2006 Our results demonstrate that acute IL-6 treatment enhances insulin-stimulated glucose disposal in humans in vivo, while the effects of IL-6 on glucose and fatty acid metabolism in vitro appear to be mediated by AMPK. Glucose 78-85 interleukin 6 Homo sapiens 35-39 17003332-8 2006 Our results demonstrate that acute IL-6 treatment enhances insulin-stimulated glucose disposal in humans in vivo, while the effects of IL-6 on glucose and fatty acid metabolism in vitro appear to be mediated by AMPK. Glucose 143-150 interleukin 6 Homo sapiens 135-139 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 interleukin 6 Homo sapiens 99-117 16477538-5 2006 Serum IL-6 and TNFalpha concentrations were elevated during glucose loading (for each comparison, p < 0.01). Glucose 60-67 interleukin 6 Homo sapiens 6-10 16804071-3 2006 Fasting plasma IL-6 concentration was negatively correlated with the rate of insulin-stimulated glucose disposal (M) (P = 0.001). Glucose 96-103 interleukin 6 Homo sapiens 15-19 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 interleukin 6 Homo sapiens 335-339 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 interleukin 6 Homo sapiens 341-354 16118251-5 2006 Suppression of basal glucose R(a) correlated with plasma adiponectin (r=0.44, P=0.02) and inversely with plasma IL-6 (r=-0.49, P<0.001). Glucose 21-28 interleukin 6 Homo sapiens 112-116 16118251-6 2006 Stimulation of glucose R(d) correlated directly with adiponectin (r=0.48, P<0.01) and inversely with IL-6 (r=-0.49, P=0.02). Glucose 15-22 interleukin 6 Homo sapiens 104-108 17167225-0 2006 Increased glucose uptake and metabolism in mesangial cells overexpressing glucose transporter 1 increases interleukin-6 and vascular endothelial growth factor production: role of AP-1 and HIF-1alpha. Glucose 10-17 interleukin 6 Homo sapiens 106-119 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 interleukin 6 Homo sapiens 6-10 16235156-7 2005 In addition, fasting plasma glucose was a significant determinant of adiponectin, CRP, and IL-6 plasma concentrations, whereas body fat content was only a significant predictor of CRP plasma concentration. Glucose 28-35 interleukin 6 Homo sapiens 91-95 15899942-8 2005 Taken together, our study suggests that IL-6 might influence glucose tolerance in part by regulation of the novel insulin-mimetic adipocytokine visfatin. Glucose 61-68 interleukin 6 Homo sapiens 40-44 15965659-2 2005 METHODS: We tested for associations between the -174 IL-6 G/C promoter polymorphism and fasting plasma glucose (FPG) and type 2 diabetes in a sample of 1,428 individuals from the largest 182 families in the National Heart, Lung and Blood Institute"s Framingham Heart Study population. Glucose 103-110 interleukin 6 Homo sapiens 53-57 15867169-8 2005 High-fat load and glucose alone produced a decrease in endothelial function and increases in nitrotyrosine, C-reactive protein, intercellular adhesion molecule-1, and interleukin-6. Glucose 18-25 interleukin 6 Homo sapiens 167-180 16200844-13 2005 Furthermore, IGFBP-1 and IL-6 increase steeply, presumably aimed at diminishing insulin-like activity of IGF-I, thereby reducing peripheral glucose utilization. Glucose 140-147 interleukin 6 Homo sapiens 25-29 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 interleukin 6 Homo sapiens 146-150 15616014-9 2005 Pan-protein kinase C (PKC) inhibitors significantly decreased high-glucose-induced IL-6 release. Glucose 67-74 interleukin 6 Homo sapiens 83-87 15616014-11 2005 Furthermore, the PKC-alpha/beta2 inhibitor decreased p38MAPK and the resulting high-glucose-induced IL-6 release. Glucose 84-91 interleukin 6 Homo sapiens 100-104 15616014-12 2005 Both antisense oligos to PKC-beta and -alpha as well as small interfering RNA (siRNA) to PKC-alpha and -beta resulted in significantly decreased high-glucose-induced IL-6 release. Glucose 150-157 interleukin 6 Homo sapiens 166-170 15528032-2 2004 We examined the hypothesis that 17beta-estradiol and trivalent chromium inhibit secretion of the pro-inflammatory cytokine interleukin (IL)-6 and oxidative stress in monocytes exposed to high glucose (HG). Glucose 192-199 interleukin 6 Homo sapiens 123-141 15569129-14 2004 Furthermore, the increase in myocardial glucose uptake correlated inversely with interleukin-6 (IL-6) concentrations (r = -0.58, P = 0.03). Glucose 40-47 interleukin 6 Homo sapiens 81-94 15569129-14 2004 Furthermore, the increase in myocardial glucose uptake correlated inversely with interleukin-6 (IL-6) concentrations (r = -0.58, P = 0.03). Glucose 40-47 interleukin 6 Homo sapiens 96-100 15180970-0 2004 Influence of the interleukin-6 -174 G/C gene polymorphism on exercise training-induced changes in glucose tolerance indexes. Glucose 98-105 interleukin 6 Homo sapiens 17-30 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 interleukin 6 Homo sapiens 31-44 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 interleukin 6 Homo sapiens 46-50 15180970-9 2004 In conclusion, fasting glucose and the extent to which glucose tolerance changes with exercise training may be influenced by the IL-6 -174 gene polymorphism. Glucose 23-30 interleukin 6 Homo sapiens 129-133 15180970-9 2004 In conclusion, fasting glucose and the extent to which glucose tolerance changes with exercise training may be influenced by the IL-6 -174 gene polymorphism. Glucose 55-62 interleukin 6 Homo sapiens 129-133 15180970-6 2004 The training-induced change in glucose area under the curve during the oral glucose tolerance test varied between the IL-6 -174 genotype groups (P = 0.05, covariates age, gender, ethnicity, baseline glucose area under the curve, and percent body fat change) with a significant decrease occurring only in the GG genotype group. Glucose 31-38 interleukin 6 Homo sapiens 118-122 15304054-0 2004 Intermittent high glucose enhances ICAM-1, VCAM-1, E-selectin and interleukin-6 expression in human umbilical endothelial cells in culture: the role of poly(ADP-ribose) polymerase. Glucose 18-25 interleukin 6 Homo sapiens 66-79 15304054-6 2004 We found that oscillating glucose was more effective in triggering the generation of nitrotyrosine and inducing the expression of adhesion molecules and IL-6 than stable high glucose. Glucose 26-33 interleukin 6 Homo sapiens 153-157 14676217-0 2004 High glucose enhances interleukin-6-induced vascular endothelial growth factor 165 expression via activation of gp130-mediated p44/42 MAPK-CCAAT/enhancer binding protein signaling in gingival fibroblasts. Glucose 5-12 interleukin 6 Homo sapiens 22-35 15001458-5 2004 Inhibition of IL-6 using a neutralizing antibody significantly reduced glucose-mediated monocyte adhesion by 50%, and addition of IL-6 directly to human EC stimulated monocyte adhesion. Glucose 71-78 interleukin 6 Homo sapiens 14-18 14676217-2 2004 Our purpose was to determine the effect of a high glucose (HG) condition on the interleukin-6/soluble interleukin-6 receptor (IL-6/sIL-6R)-induced activation of signaling and vascular endothelial growth factor (VEGF) expression in human gingival fibroblasts (HGFs). Glucose 50-57 interleukin 6 Homo sapiens 80-93 14676217-2 2004 Our purpose was to determine the effect of a high glucose (HG) condition on the interleukin-6/soluble interleukin-6 receptor (IL-6/sIL-6R)-induced activation of signaling and vascular endothelial growth factor (VEGF) expression in human gingival fibroblasts (HGFs). Glucose 50-57 interleukin 6 Homo sapiens 126-130 12952969-7 2003 Consistent with the reduced GLUT-4 mRNA, insulin-stimulated glucose transport was also significantly reduced by IL-6. Glucose 60-67 interleukin 6 Homo sapiens 112-116 14605496-9 2003 Mesothelial cells chronically exposed to glucose became activated after subsequent exposure to the dialysis fluid, as reflected by the increased release of interleukin (IL)-6, in contrast to control mesothelial cells, in which IL-6 synthesis was suppressed. Glucose 41-48 interleukin 6 Homo sapiens 156-174 14605496-9 2003 Mesothelial cells chronically exposed to glucose became activated after subsequent exposure to the dialysis fluid, as reflected by the increased release of interleukin (IL)-6, in contrast to control mesothelial cells, in which IL-6 synthesis was suppressed. Glucose 41-48 interleukin 6 Homo sapiens 227-231 14686093-6 2003 IL-6 can enhance lipolysis in humans and might play a role in glucose metabolism. Glucose 62-69 interleukin 6 Homo sapiens 0-4 14519071-1 2003 Interleukin (IL)-6 is a multifunctional immune-modulating cytokine that has been suggested to have important functions in glucose and lipid metabolism. Glucose 122-129 interleukin 6 Homo sapiens 0-18 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 interleukin 6 Homo sapiens 104-108 12702735-0 2003 Glucose ingestion attenuates interleukin-6 release from contracting skeletal muscle in humans. Glucose 0-7 interleukin 6 Homo sapiens 29-42 12702735-1 2003 To examine whether glucose ingestion during exercise affects the release of interleukin-6 (IL-6) from the contracting limb, seven men performed 120 min of semi-recumbent cycling on two occasions while ingesting either 250 ml of a 6.4 % carbohydrate (GLU trial) or sweet placebo (CON trial) beverage at the onset of, and at 15 min intervals throughout, exercise. Glucose 19-26 interleukin 6 Homo sapiens 91-95 12702735-8 2003 These results demonstrate that glucose ingestion during exercise attenuates leg IL-6 release but does not decrease intramuscular expression of IL-6 mRNA. Glucose 31-38 interleukin 6 Homo sapiens 80-84 12540635-7 2003 The rates of both oxidative (P = 0.013) and nonoxidative (P = 0.016) glucose disposal were significantly affected by the IL-6 promoter polymorphism. Glucose 69-76 interleukin 6 Homo sapiens 121-125 12509497-1 2003 In this study, the hypothesis that the release of interleukin (IL)-6 from human muscle is linked to exercise intensity and muscle glucose uptake was investigated. Glucose 130-137 interleukin 6 Homo sapiens 50-68 12509497-5 2003 Also, thigh IL-6 release (0.4 +/- 0.1, 1.3 +/- 0.5, 1.5 +/- 0.6 and 2.5 +/- 0.7 ng min(-1) thigh(-1) at rest and 25 %, 65 % and 85 % W(max), respectively) and thigh glucose uptake (0.05 +/- 0.01, 0.3 +/- 0.05, 0.75 +/- 0.16, 1.07 +/- 0.15 mmol min(-1) thigh(-1) at rest and 25 %, 65 % and 85 % W(max), respectively) increased with increasing exercise intensity (P < 0.05). Glucose 165-172 interleukin 6 Homo sapiens 12-16 12509497-7 2003 During exercise, thigh IL-6 release was positively related to both thigh glucose uptake (P < 0.001) and thigh glucose delivery (P < 0.005), but not to thigh glucose extraction. Glucose 73-80 interleukin 6 Homo sapiens 23-27 12509497-7 2003 During exercise, thigh IL-6 release was positively related to both thigh glucose uptake (P < 0.001) and thigh glucose delivery (P < 0.005), but not to thigh glucose extraction. Glucose 113-120 interleukin 6 Homo sapiens 23-27 12509497-7 2003 During exercise, thigh IL-6 release was positively related to both thigh glucose uptake (P < 0.001) and thigh glucose delivery (P < 0.005), but not to thigh glucose extraction. Glucose 113-120 interleukin 6 Homo sapiens 23-27 12509497-10 2003 In conclusion, the study indicates that IL-6 release from human muscle is positively related to exercise intensity, arterial adrenaline concentration and muscle glucose uptake. Glucose 161-168 interleukin 6 Homo sapiens 40-44 12379575-2 2002 We assessed the role of glucose in the regulation of circulating levels of IL-6, TNF-alpha, and interleukin-18 (IL-18) in subjects with normal or impaired glucose tolerance (IGT), as well as the effect of the antioxidant glutathione. Glucose 24-31 interleukin 6 Homo sapiens 75-79 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 interleukin 6 Homo sapiens 54-58 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 interleukin 6 Homo sapiens 100-113 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 interleukin 6 Homo sapiens 115-119 11994345-0 2002 Adipose tissue IL-6 content correlates with resistance to insulin activation of glucose uptake both in vivo and in vitro. Glucose 80-87 interleukin 6 Homo sapiens 15-19 12107724-0 2002 Impaired glucose tolerance is associated with increased serum concentrations of interleukin 6 and co-regulated acute-phase proteins but not TNF-alpha or its receptors. Glucose 9-16 interleukin 6 Homo sapiens 80-93