PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 18290856-7 2008 RESULTS: Hyperglycaemia reduced LPS-induced mRNA expression of nuclear factor of kappa light polypeptide gene enhancer in B cells inhibitor alpha (NFKBIA), interleukin-1 alpha (IL1A) and chemokine (C-C motif) ligand 3 (CCL3), whereas during hyperinsulinaemia enhanced mRNA levels occurred in six out of eight measured inflammation-related genes, irrespective of plasma glucose levels. Glucose 369-376 interleukin 1 alpha Homo sapiens 177-181 15001844-5 2004 Neu5Ac-Gal-IL-1alpha exhibited reduction in activities in vivo, including induction of serum amyloid A and NOx, and down-regulation of serum glucose. Glucose 141-148 interleukin 1 alpha Homo sapiens 11-20 17189875-6 2007 Proinflammatory cytokines such as interleukin-1 and tumor necrosis factor-alpha (TNF-alpha) also stimulated NF-kappaB-dependent transcription and showed an additive effect with high glucose. Glucose 182-189 interleukin 1 alpha Homo sapiens 34-79 16249450-0 2005 Is there a role for locally produced interleukin-1 in the deleterious effects of high glucose or the type 2 diabetes milieu to human pancreatic islets? Glucose 86-93 interleukin 1 alpha Homo sapiens 37-50 15070811-9 2004 We conclude that IL-1 cytokines can regulate cellular Glc phosphorylating capacity via an IL-1 receptor-, Ras-, and classic MAPK pathway-mediated increase in HKII abundance. Glucose 54-57 interleukin 1 alpha Homo sapiens 17-21 15070811-9 2004 We conclude that IL-1 cytokines can regulate cellular Glc phosphorylating capacity via an IL-1 receptor-, Ras-, and classic MAPK pathway-mediated increase in HKII abundance. Glucose 54-57 interleukin 1 alpha Homo sapiens 90-94 10506586-9 1999 When cells were incubated in 25 mM glucose to mimic the diabetic state, IL-1beta induction was inhibited in all cases, but to a significantly lesser extent with the 14-repeat allele. Glucose 35-42 interleukin 1 alpha Homo sapiens 72-80 1665456-3 1991 In perifused islets, insulin secretion in response to IL-1 in the presence of 7 mM glucose averaged 313 +/- 43 pg/islet/min 35-40 min after the onset of stimulation. Glucose 83-90 interleukin 1 alpha Homo sapiens 54-58 9828188-4 1998 First, IL-1alpha was shown to increase the uptake of glucose substrate in a time- and dose-dependent manner. Glucose 53-60 interleukin 1 alpha Homo sapiens 7-16 7487926-6 1995 These results imply that the activation of distinct MAP kinase pathways is required for the stimulation of glucose transport by IL1/anisomycin and IGF1 in KB cells, and suggest that the combined use of SB 203580 and PD 98059 is a powerful new approach to explore the roles of different MAP kinase cascades in cell regulation. Glucose 107-114 interleukin 1 alpha Homo sapiens 128-131 1477295-0 1992 The effects of interleukin-1 on pancreatic beta cell function in vitro depend on the glucose concentration. Glucose 85-92 interleukin 1 alpha Homo sapiens 15-28 1511500-5 1992 Thus, the inflammatory cytokines IL-1 and TNF alpha reportedly detected in the circulation during severe sepsis may directly affect not only glucose uptake but also its subsequent metabolism within tissue fibroblasts. Glucose 141-148 interleukin 1 alpha Homo sapiens 33-37 9151802-6 1997 The ability of IL-1 to upregulate Glut1 and Glut3 transcripts proved time-, dose-, nitric oxide-, and protein biosynthesis-dependent but glucose independent. Glucose 137-144 interleukin 1 alpha Homo sapiens 15-19 1478189-2 1992 IL-1 significantly reduced serum insulin levels in ADX rats only, while it similarly decreased plasma glucose levels. Glucose 102-109 interleukin 1 alpha Homo sapiens 0-4 1665456-1 1991 The monokine interleukin-1 alpha (IL-1) induces a glucose-dependent increase in insulin secretion, an effect tentatively attributed to its ability to increase beta cell phosphoinositide (PI) hydrolysis. Glucose 50-57 interleukin 1 alpha Homo sapiens 13-32 1665456-1 1991 The monokine interleukin-1 alpha (IL-1) induces a glucose-dependent increase in insulin secretion, an effect tentatively attributed to its ability to increase beta cell phosphoinositide (PI) hydrolysis. Glucose 50-57 interleukin 1 alpha Homo sapiens 34-38 1665456-6 1991 This level of IL-1 caused significant increases in inositol phosphate accumulation in the presence of 7 mM glucose but not 2.75 mM glucose. Glucose 107-114 interleukin 1 alpha Homo sapiens 14-18 34139004-0 2021 Glucose regulates expression of pro-inflammatory genes IL-1beta and IL-12 through a mechanism involving hexosamine biosynthesis pathway dependent regulation of alphaEcatenin. Glucose 0-7 interleukin 1 alpha Homo sapiens 55-63 34651203-15 2022 HIF-1 activation increased IL-1beta and IL-8 in human uroepithelial cells treated with high glucose concentration. Glucose 92-99 interleukin 1 alpha Homo sapiens 27-35 34831052-3 2021 One of these mechanisms is related to NLRP3 activation, initiated by high levels of danger signals such as cholesterol, urate, and glucose, producing IL-1, IL-18, and cell death by pyroptosis. Glucose 131-138 interleukin 1 alpha Homo sapiens 150-154 34858390-4 2021 We now describe that the macrophage molecular clock, through Bmal1, regulates the uptake of glucose, its flux through glycolysis and the Krebs cycle, including the production of the metabolite succinate to drive Il-1beta production. Glucose 92-99 interleukin 1 alpha Homo sapiens 212-220 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 1 alpha Homo sapiens 152-174 34576117-1 2021 We aimed to investigate the effect of acute glucose shift on the activation of the NLRP3 inflammasome, IL-1beta secretion, and underlying signaling pathways in THP-1 cells. Glucose 44-51 interleukin 1 alpha Homo sapiens 103-111 34576117-6 2021 Further analysis using inhibitors of p38 MAPK, JNK, and NF-kappaB indicated that acute glucose shifts promoted IL-1beta secretion by activating the signaling pathway in a ROS-MAPK-NF-kappaB-NLRP3 inflammasome in THP-1 cells. Glucose 87-94 interleukin 1 alpha Homo sapiens 111-119 34139004-7 2021 We find that the reduction of alpha-E catenin level using siRNA attenuates the glucose induced changes of both IL-1beta and IL-12 mRNA levels under LPS stimulated condition but does not affect TNF-alpha expression. Glucose 79-86 interleukin 1 alpha Homo sapiens 111-119 34139004-8 2021 Together this indicates that alpha-E catenin can sense the changes in glucose levels in macrophages via hexosamine biosynthesis pathway and also can modulate the glucose induced gene expression of inflammatory markers such as IL-1beta and IL-12. Glucose 162-169 interleukin 1 alpha Homo sapiens 226-234 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 1 alpha Homo sapiens 22-30 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 1 alpha Homo sapiens 161-173 34198548-3 2021 Macrophage-specific deletion of Glucose Transporter 1 (GLUT1) significantly reduced tumor burden, which was accompanied by increased Natural Killer and CD8+ T cell activity and suppression of the NLRP3-IL1beta inflammasome axis. Glucose 32-39 interleukin 1 alpha Homo sapiens 202-209 35513427-4 2022 Stimulation of human mesangial cells with high glucose primed the inflammasome-driven interleukin 1 beta (IL-1beta) secretion, which in turn stimulated platelet-derived growth factor (PDGF-BB) release. Glucose 47-54 interleukin 1 alpha Homo sapiens 106-114 2689826-2 1989 Since an enhanced rate of whole-body glucose utilization is a consistent feature of the hypermetabolic phase of infection, the purpose of the present study was to determine whether IL-1 could increase glucose uptake and whether that increase was dependent on the concomitant elevation in plasma insulin. Glucose 201-208 interleukin 1 alpha Homo sapiens 181-185 2666106-15 1989 These combined observations suggest that exposure to IL-1 induces a preferential decrease in glucose-mediated insulin release and mitochondrial glucose metabolism. Glucose 93-100 interleukin 1 alpha Homo sapiens 53-57 2666106-17 1989 It is conceivable that the IL-1-induced suppression and shift in islet metabolism can be an explanation for the beta-cell insensitivity to glucose observed in the early phases of human and experimental insulin-dependent diabetes mellitus. Glucose 139-146 interleukin 1 alpha Homo sapiens 27-31 2539976-0 1989 Interleukin-1 alpha exerts glucose-dependent stimulatory and inhibitory effects on islet cell phosphoinositide hydrolysis and insulin secretion. Glucose 27-34 interleukin 1 alpha Homo sapiens 0-19 2539976-5 1989 1) In islets labeled for 2 h with [3H]inositol in the presence of 2.75 mM glucose, subsequent perifusion with 5.0 nM IL-1 increased insulin output, [3H]inositol efflux, and [3H]inositol phosphate accumulation in the simultaneous presence of 7 mM, but not 2.75 mM, glucose. Glucose 264-271 interleukin 1 alpha Homo sapiens 117-121 2539976-6 1989 2) Mannoheptulose, a competitive inhibitor of islet glucokinase, blocked the stimulatory effects of IL-1 noted in the presence of 7 mM glucose. Glucose 135-142 interleukin 1 alpha Homo sapiens 100-104 2539976-12 1989 6) These inhibitory effects of IL-1 were abolished if mannoheptulose was included during the 2-h incubation with 7 mM glucose plus 5.0 nM IL-1. Glucose 118-125 interleukin 1 alpha Homo sapiens 31-35 2539976-13 1989 7) The diacylglycerol kinase inhibitor 1-monooleoylglycerol (100 microM) significantly restored insulin output after IL-1 exposure (with 7 mM glucose). Glucose 155-162 interleukin 1 alpha Homo sapiens 130-134 2539976-14 1989 8) Similar to the results obtained with 7 mM glucose plus IL-1, incubation of islets with 8-10 mM glucose alone produced dose-dependent impairments of [3H]inositol efflux patterns and inositol phosphate accumulation. Glucose 98-105 interleukin 1 alpha Homo sapiens 58-62 2539976-16 1989 These results demonstrate that IL-1 has glucose-dependent stimulatory and inhibitory effects on beta-cell function. Glucose 40-47 interleukin 1 alpha Homo sapiens 31-35 2783675-0 1989 Modification of tissue-factor mRNA and protein response to thrombin and interleukin 1 by high glucose in cultured human endothelial cells. Glucose 94-101 interleukin 1 alpha Homo sapiens 72-85 2783675-6 1989 In contrast, the tissue-factor response to interleukin 1, a modulator of endothelial function in the context of host defense, was decreased in cells cultured in high glucose (P = .04). Glucose 166-173 interleukin 1 alpha Homo sapiens 43-56 2783675-8 1989 The reciprocal effects of high glucose on the tissue-factor response to thrombin and interleukin 1 points to different pathways of tissue-factor stimulation by the two agents and suggests functional consequences pertinent to the increased thrombin activity and compromised host-defense mechanisms observed in diabetes. Glucose 31-38 interleukin 1 alpha Homo sapiens 85-98 2507377-1 1989 Recombinant human interleukin 1 alpha (IL-1) has been found to induce prostaglandin E2 (PGE2) accumulation by isolated rat islets of Langerhans at concentrations similar to those at which the cytokine inhibits glucose-induced insulin secretion and islet glucose oxidation. Glucose 210-217 interleukin 1 alpha Homo sapiens 18-37 2507377-1 1989 Recombinant human interleukin 1 alpha (IL-1) has been found to induce prostaglandin E2 (PGE2) accumulation by isolated rat islets of Langerhans at concentrations similar to those at which the cytokine inhibits glucose-induced insulin secretion and islet glucose oxidation. Glucose 210-217 interleukin 1 alpha Homo sapiens 39-43 2507377-1 1989 Recombinant human interleukin 1 alpha (IL-1) has been found to induce prostaglandin E2 (PGE2) accumulation by isolated rat islets of Langerhans at concentrations similar to those at which the cytokine inhibits glucose-induced insulin secretion and islet glucose oxidation. Glucose 254-261 interleukin 1 alpha Homo sapiens 18-37 2507377-1 1989 Recombinant human interleukin 1 alpha (IL-1) has been found to induce prostaglandin E2 (PGE2) accumulation by isolated rat islets of Langerhans at concentrations similar to those at which the cytokine inhibits glucose-induced insulin secretion and islet glucose oxidation. Glucose 254-261 interleukin 1 alpha Homo sapiens 39-43 2507377-4 1989 Islets that had been pretreated with IL-1 for 18 h showed elevated rates of PGE2 production at basal (3-mM) and stimulatory (16.5-mM) glucose concentrations and converted exogenous arachidonic acid to PGE2 at twice the maximal rate of control islets. Glucose 134-141 interleukin 1 alpha Homo sapiens 37-41 2668949-3 1989 In these animal models, a single injection of a low dose of human recombinant IL-1 normalized glucose blood levels for several hours. Glucose 94-101 interleukin 1 alpha Homo sapiens 78-82 2689826-7 1989 SRIF prevented the IL-1 induced increase in insulin and tissue glucose utilization. Glucose 63-70 interleukin 1 alpha Homo sapiens 19-23 2689826-9 1989 These data suggest that the administration of IL-1 increases organ glucose utilization by insulin-dependent mechanisms. Glucose 67-74 interleukin 1 alpha Homo sapiens 46-50 3308437-5 1987 IL-1 was found to reduce insulin release in culture and totally inhibit glucose-stimulated insulin release in short-term incubations. Glucose 72-79 interleukin 1 alpha Homo sapiens 0-4 3046964-4 1988 Several studies have convincingly demonstrated that IL-1 is a potent modulator of beta-cell function and can potentiate or inhibit glucose-induced insulin secretion, depending on the concentration and length of exposure to IL-1. Glucose 131-138 interleukin 1 alpha Homo sapiens 52-56 3046964-4 1988 Several studies have convincingly demonstrated that IL-1 is a potent modulator of beta-cell function and can potentiate or inhibit glucose-induced insulin secretion, depending on the concentration and length of exposure to IL-1. Glucose 131-138 interleukin 1 alpha Homo sapiens 223-227 3259727-0 1988 Cachectin/TNF and IL-1 induced by glucose-modified proteins: role in normal tissue remodeling. Glucose 34-41 interleukin 1 alpha Homo sapiens 18-22 3128273-1 1988 Recombinant-derived human interleukin 1 (IL1) alpha and beta and interferon gamma (IFN-gamma) each produced similar increases in rheumatoid synovial cell (RSC) glycolysis, as judged by increased values for glucose uptake, lactate production and cellular fructose 2,6-bisphosphate [Fru(2,6)P2]. Glucose 206-213 interleukin 1 alpha Homo sapiens 26-51 2510238-5 1989 Glycolysis, estimated by glucose utilisation and measurements of the glycolytic regulatory metabolite fructose 2,6-bisphosphate was significantly stimulated by TGF beta, IL-1 alpha and IFN-gamma, but less so by TGF alpha. Glucose 25-32 interleukin 1 alpha Homo sapiens 170-180 3308437-6 1987 Islet (pro)insulin biosynthesis, glucose oxidation, and oxygen uptake at 16.7 mM glucose were partially inhibited by IL-1. Glucose 33-40 interleukin 1 alpha Homo sapiens 117-121 3093048-3 1986 In some cancer patients with weight loss there are many similarities to an interleukin-1 response including increases in resting energy expenditure, whole-body protein flux and synthesis and glucose flux and recycling, hypoalbuminemia and increased albumin catabolic rates, and an adaptive low T3 state that suggest a similar injury/infection response. Glucose 191-198 interleukin 1 alpha Homo sapiens 75-88 3297891-1 1987 The effects of interleukin 1 (IL-1) on glucose-induced insulin secretion from isolated rat islets of Langerhans have been examined. Glucose 39-46 interleukin 1 alpha Homo sapiens 30-34 3297891-9 1987 In addition to the inhibitory effects of IL-1 on glucose-induced insulin secretion, purified IL-1 and human rIL-1 had stimulatory effects on glucose-induced insulin secretion under the following conditions: a 90-min incubation with purified IL-1 (10% vol/vol) or in the presence of human rIL-1 (1400 pM) or a 15-h incubation with relatively low concentrations of human rIL-1 (0.5 or 5 pM). Glucose 141-148 interleukin 1 alpha Homo sapiens 93-97 3297891-9 1987 In addition to the inhibitory effects of IL-1 on glucose-induced insulin secretion, purified IL-1 and human rIL-1 had stimulatory effects on glucose-induced insulin secretion under the following conditions: a 90-min incubation with purified IL-1 (10% vol/vol) or in the presence of human rIL-1 (1400 pM) or a 15-h incubation with relatively low concentrations of human rIL-1 (0.5 or 5 pM). Glucose 141-148 interleukin 1 alpha Homo sapiens 93-97 32968210-9 2021 Cultured human and mouse podocytes were treated with high glucose (30 mM), which significantly increased the expression levels of caspase-11 or caspase-4 (the homolog of caspase-11 in human), GSDMD-N, NF-kappaB, IL-1beta, and IL-18, and decreased the expression of nephrin and podocin. Glucose 58-65 interleukin 1 alpha Homo sapiens 212-220 3514344-1 1986 Addition of highly purified human Interleukin-1 to the culture medium of isolated rat islets of Langerhans for 6 days led to 88% inhibition of glucose-induced insulin-release, reduction of islet contents of insulin and glucagon to 31% and 8% respectively, and disintegration of the islets. Glucose 143-150 interleukin 1 alpha Homo sapiens 34-47 33989405-7 2021 TNFalpha measurably increased secretion of IL-8 and IL-1beta, which was enhanced at 60 mM glucose. Glucose 90-97 interleukin 1 alpha Homo sapiens 52-60 33979025-7 2021 Together, this suggests that the IL-1beta-stimulated energy shift is driven by shunting of glucose-derived pyruvate into mitochondria to maintain elevated oxygen consumption in HUVECs. Glucose 91-98 interleukin 1 alpha Homo sapiens 33-41 33729569-10 2021 RESULTS: High glucose could induce IL-1beta-driven inflammatory responses in HGFs via the activation of NLRP3 inflammasome regulated by TLR2/TLR4 coupled ROS in NF-kappaB-dependent manner. Glucose 14-21 interleukin 1 alpha Homo sapiens 35-43 33739224-8 2022 Logistic regression analysis identified the CC+CT genotype as an independent risk factor for the development of diabetes in patients with normal glucose metabolism (OR = 2.457, 95% CI: 1.238-4.877).Conclusions: The IL-1beta gene rs16944 C/T polymorphism may cause genetic susceptibility to T2DM in the Luzhou population. Glucose 145-152 interleukin 1 alpha Homo sapiens 215-223 33729569-12 2021 CONCLUSION: Taiwanese green propolis could elicit protective effects against IL-1beta-driven inflammation in high glucose-exposed HGFs through TLR2/TLR4 combined ROS/NF-kappaB/NLRP3 inflammasome pathway. Glucose 114-121 interleukin 1 alpha Homo sapiens 77-85 33629290-8 2021 RESULTS: HIF-1alpha and Runx2 were increased, and glucose uptake and ATP generation were decreased in the degenerative CHs from both OA and IL-1beta conditions. Glucose 50-57 interleukin 1 alpha Homo sapiens 140-148 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 1 alpha Homo sapiens 59-67 33038372-4 2020 KEY FINDINGS: Data indicated that high glucose increased the expression of interleukin-1beta (IL-1beta), an upstream regulator of nuclear factor-kappaB (NF-kappaB) pathway, through the nuclear localization of NF-kappaB. Glucose 39-46 interleukin 1 alpha Homo sapiens 94-102 32455427-4 2021 Specifically, we provide evidence that the key diabetogenic cytokine IL-1beta disrupts functionality of the beta cell circadian clock and impairs circadian regulation of glucose-stimulated insulin secretion. Glucose 170-177 interleukin 1 alpha Homo sapiens 69-77 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 1 alpha Homo sapiens 46-54 32699039-8 2020 CONCLUSION: In conclusion, we demonstrated that GLUT1-mediated glucose uptake is instrumental during the inflammatory IL-1beta response induced by MSU and CPP crystals. Glucose 63-70 interleukin 1 alpha Homo sapiens 118-126 33136275-7 2022 HBMVECs were injured by exposure to glucose and/or hypoxia, as assessed by release of LDH, interleukin (IL)-1beta, and reactive oxygen species (ROS). Glucose 36-43 interleukin 1 alpha Homo sapiens 91-113 32908567-11 2020 There were medium-to-strong correlation between CML with SOD (r = 0.58, p < 0.05) and IL-1alpha with SOD (r = 0.70, p < 0.05) in well-controlled blood glucose. Glucose 151-158 interleukin 1 alpha Homo sapiens 86-95 32733443-0 2020 Glucose Induces IL-1alpha-Dependent Inflammation and Extracellular Matrix Proteins Expression and Deposition in Renal Tubular Epithelial Cells in Diabetic Kidney Disease. Glucose 0-7 interleukin 1 alpha Homo sapiens 16-25 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 1 alpha Homo sapiens 90-98 32650532-4 2020 Although the mechanism is very complex and needs further explanation, it appears that high levels of cholesterol, urate, and glucose activates NLRP3 inflammasome, which produces IL-1beta, IL-18, and gasdermin D. Glucose 125-132 interleukin 1 alpha Homo sapiens 178-186 32733443-4 2020 Human proximal tubular kidney HK-2 cells exposed to high glucose (HG) gradually increase the expression of IL-1alpha but not IL-1beta and induce the expression and deposition of extracellular matrix (ECM) proteins. Glucose 57-64 interleukin 1 alpha Homo sapiens 107-116 32733443-5 2020 We further demonstrate that in vitro ectopic addition of recombinant IL-1alpha in low glucose concentration leads to a similar effect as in HG, while supplementing excess amounts of IL-1Ra in HG significantly attenuates the ECM protein overexpression and deposition. Glucose 86-93 interleukin 1 alpha Homo sapiens 69-78 32587797-11 2020 Moreover, the highest ROS and the lowest insulin secretion were found in FAC combined with IL-1beta and TNF-alpha in the high-glucose condition of human pancreatic beta cell, which could be involved in the mechanism of DM development in beta-thalassemia patients. Glucose 126-133 interleukin 1 alpha Homo sapiens 91-99 32561825-2 2020 At basal time, the T polymorphic allele of the rs16944 was associated with lower IL-1beta mRNA expression (p = 0.006); and higher glucose level was positive correlated to IL-1beta protein levels (p = 0.015). Glucose 130-137 interleukin 1 alpha Homo sapiens 171-179 32350565-11 2020 GPR44 inhibition antagonised the reduction in glucose-stimulated insulin secretion induced by HG and IL-1beta in human islets. Glucose 46-53 interleukin 1 alpha Homo sapiens 101-109 32561825-4 2020 Surprisingly, we observed that the greater decreases in glucose level were associated to increased IL-1beta serum levels (p = 0.040). Glucose 56-63 interleukin 1 alpha Homo sapiens 99-107 32439949-5 2020 An in vitro study indicated that high glucose increased IL-1beta and IL-18 expression and activated the NLRP3 inflammasome via upregulation of MARK4 in human umbilical vein endothelial cells (HUVECs). Glucose 38-45 interleukin 1 alpha Homo sapiens 56-64 32028854-2 2020 Biological function experiments showed that miR-218 and inflammatory factors TNF-alpha and IL-1beta were highly expressed in renal proximal tubule under high-glucose conditions. Glucose 158-165 interleukin 1 alpha Homo sapiens 91-99 32018221-3 2020 Notably, we found that high-glucose (50 mM) increased the expression levels of Caspase-1, Gasdermin D, NLRP3, IL-1beta and IL-18 in ARPE-19 cells, which indicated that high-glucose triggered pyroptotic cell death. Glucose 173-180 interleukin 1 alpha Homo sapiens 110-118 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 1 alpha Homo sapiens 70-92 32197070-0 2020 Postprandial Hypoglycemia in Patients after Gastric Bypass Surgery Is Mediated by Glucose-Induced IL-1beta. Glucose 82-89 interleukin 1 alpha Homo sapiens 98-106 32550560-2 2020 In this study, we investigated whether high glucose and/or tumor necrosis factor (TNF) would enhance pro-inflammatory cytokine expression of tumor necrosis factor (TNF) and interleukin (IL)-1beta (IL1B) by altering histone modifications in U937, a juvenile macrophage cell line. Glucose 44-51 interleukin 1 alpha Homo sapiens 173-195 32197070-7 2020 Our study proposes a role for glucose-induced IL-1beta in postprandial hypoglycemia after gastric bypass surgery and suggests that SGLT2-inhibitors and IL-1 antagonism may improve this condition. Glucose 30-37 interleukin 1 alpha Homo sapiens 46-54 32018221-3 2020 Notably, we found that high-glucose (50 mM) increased the expression levels of Caspase-1, Gasdermin D, NLRP3, IL-1beta and IL-18 in ARPE-19 cells, which indicated that high-glucose triggered pyroptotic cell death. Glucose 28-35 interleukin 1 alpha Homo sapiens 110-118 32420343-6 2020 Our data showed that high glucose induced NLRP3-caspase-1-GSDMD activation and pore formation in a dose- and time-dependent manner (p < 0.05) and resulted in the inflammatory cytokines IL-1beta and IL-18 and lactate dehydrogenase (LDH) release from HRPs (p < 0.05), which are all signs of HRP pyroptosis. Glucose 26-33 interleukin 1 alpha Homo sapiens 185-193 32197070-3 2020 Here, we hypothesized that glucose-induced IL-1beta leads to an exaggerated insulin response in this condition. Glucose 27-34 interleukin 1 alpha Homo sapiens 43-51 32062019-7 2020 Our findings suggest that high glucose and PA could induce excessive ER stress and apoptosis via promoting the overexpression of GLUT3 and FATP1, and ER stress could suppress BDNF and SYN expression through negatively regulating p38/ERK-CREB pathway and positively regulating NLRP3-IL-1beta pathway, which could be reversed by activated Nrf2-HO-1 pathway. Glucose 31-38 interleukin 1 alpha Homo sapiens 282-290 32209983-8 2020 IL-1beta secretion did not differ between conditions but was lower 60 min post-glucose ingestion compared to the fasting baseline (main effect of time, p = 0.014). Glucose 79-86 interleukin 1 alpha Homo sapiens 0-8 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 1 alpha Homo sapiens 379-387 31705795-0 2020 Allopurinol inhibits excess glucose-induced trophoblast IL-1beta and ROS production. Glucose 28-35 interleukin 1 alpha Homo sapiens 56-64 31705795-2 2020 Using an in vitro model, we previously reported that hyperglycemic levels of glucose induced a pro-inflammatory (IL-1beta, IL-8, RANTES, GRO-alpha), anti-angiogenic (sFlt-1) and anti-migratory profile in a human trophoblast cell line. Glucose 77-84 interleukin 1 alpha Homo sapiens 113-121 31705795-3 2020 The IL-1beta response to excess glucose was mediated by uric acid-induced activation of the NLRP3 inflammasome. Glucose 32-39 interleukin 1 alpha Homo sapiens 4-12 31705795-5 2020 Thus, we sought to test the effects of allopurinol on the IL-1beta and other inflammatory, angiogenic and migratory responses that are triggered in the trophoblast by excess glucose. Glucose 174-181 interleukin 1 alpha Homo sapiens 58-66 31705795-10 2020 Together, our findings indicate that the xanthine oxidase inhibitor allopurinol inhibited excess glucose-induced trophoblast IL-1beta secretion. Glucose 97-104 interleukin 1 alpha Homo sapiens 125-133 31473434-7 2019 We found high glucose could increase Propidium Iodide (PI) positive cells and elevate release of lactate dehydrogenase (LDH), Interleukin 1 beta (IL-1beta) and Interleukin 18 (IL-18); protein levels of GSDMD, GSDMD N-terminal domain (GSDMD-N) and cleaved-caspase-1 were also elevated. Glucose 14-21 interleukin 1 alpha Homo sapiens 146-154 31850631-4 2020 High levels of glucose, reactive oxygen species, and advanced glycation end-products are found in the periodontium of diabetic individuals and lead to increased activation of nuclear factor-kappa B and expression of inflammatory cytokines such as tumor necrosis factor and interleukin-1. Glucose 15-22 interleukin 1 alpha Homo sapiens 273-286 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 1 alpha Homo sapiens 118-126 31302140-7 2019 Notably, dulaglutide treatment suppressed high glucose- induced maturation of IL-1beta and IL-18. Glucose 47-54 interleukin 1 alpha Homo sapiens 78-86 31485193-7 2019 In addition, levels of ROS, caspase1, and IL-1beta increased in a time- and dose-dependent manner in the high glucose group, even with an increased expression of LC3 (p < 0.01). Glucose 110-117 interleukin 1 alpha Homo sapiens 42-50 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 1 alpha Homo sapiens 130-138 24588826-3 2014 These aspects are complementary because stimulatory actions of IL-1 may be due to its capacity to increase glucose uptake by immune cells in the periphery and to affect the control of glucose homeostasis at brain levels, so as to deviate this main fuel to immune cells during inflammatory and infectious diseases. Glucose 107-114 interleukin 1 alpha Homo sapiens 63-67 21233852-4 2011 Preliminary results from clinical trials with salicylates and interleukin-1 antagonists support this notion and have opened the door for immunomodulatory strategies for the treatment of T2D that simultaneously lower blood glucose levels and potentially reduce the severity and prevalence of the associated complications of this disease. Glucose 222-229 interleukin 1 alpha Homo sapiens 62-75 20019678-7 2010 Fasting glucose related to VAT expression of TNFalpha, MIP, serum amyloid A (SAA), IL-1alpha, IL-1beta, IL-8, and IL-8 receptor. Glucose 8-15 interleukin 1 alpha Homo sapiens 83-92 31178664-5 2019 The results demonstrate that compared with the low-glucose culture, high glucose triggered higher cell death and increased IL-18 and IL-1beta mRNA expression and protein production. Glucose 73-80 interleukin 1 alpha Homo sapiens 133-141 31178664-7 2019 Notably, NAC, a ROS scavenger, could attenuate high glucose-induced ROS formation and IL-18 and IL-1beta mRNA and protein expression and block inflammasome activation. Glucose 52-59 interleukin 1 alpha Homo sapiens 96-104 31178664-9 2019 Intrudingly, H2S could ameliorate high glucose-induced ROS formation, IL-18 and IL-1beta expression, and inflammasome activation. Glucose 39-46 interleukin 1 alpha Homo sapiens 80-88 28553653-6 2017 Our study revealed several unexpected correlations which are indicative of a much more complex relationship between glucose and lipid factors (namely, glycosylated haemoglobin Hb1Ac, the presence of one but not multiple chronic diabetic complications, and atherogenic indexes) and proinflammatory cytokines (IL-1alpha and TNF-alpha). Glucose 116-123 interleukin 1 alpha Homo sapiens 308-317