PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 24357461-9 2014 In cultured macrophages, combinatorial treatment with high glucose and palmitate amplifies MRP8 expression in a Tlr4-dependent manner, and recombinant MRP8 protein markedly increases gene expression of the inflammatory cytokines interleukin-1beta and tumor necrosis factor alpha. Glucose 59-66 interleukin 1 beta Mus musculus 229-278 24013028-6 2013 To address this hypothesis, we examined the effect of glucose on IL-1alpha and IL-1beta mRNA expression in the hypothalamus. Glucose 54-61 interleukin 1 beta Mus musculus 79-87 25077824-17 2014 Either high glucose or LPS increased the levels of IL-1beta and TNF-alpha in the conditional medium of peritoneal macrophages. Glucose 12-19 interleukin 1 beta Mus musculus 51-59 25077824-18 2014 Glibenclamide treatment suppressed the increase of IL-1beta level induced by high glucose and LPS. Glucose 82-89 interleukin 1 beta Mus musculus 51-59 24013028-8 2013 Levels of IL-1alpha and IL-1beta mRNA in the hypothalamus were increased in response to feeding and intraperitoneal injection of glucose, and were positively correlated with blood glucose levels in mice. Glucose 129-136 interleukin 1 beta Mus musculus 24-32 24013028-8 2013 Levels of IL-1alpha and IL-1beta mRNA in the hypothalamus were increased in response to feeding and intraperitoneal injection of glucose, and were positively correlated with blood glucose levels in mice. Glucose 180-187 interleukin 1 beta Mus musculus 24-32 24013028-9 2013 Exposure of hypothalamic explants to high glucose (10 mM) media increased IL-1alpha and IL-1beta mRNA levels compared to low glucose (1 mM) media. Glucose 42-49 interleukin 1 beta Mus musculus 88-96 22595195-4 2012 Our results showed that spinasterol-Glc inhibited the production of NO and proinflammatory cytokines such as TNF-alpha, IL-6 and IL-1beta in dose-dependent manners in LPS-treated RAW264.7 cells. Glucose 36-39 interleukin 1 beta Mus musculus 129-137 23766264-7 2013 In vitro, the inhibitors of PKCbeta and extracellular signal-regulated kinase 1/2, as well as small interfering RNA to Egr-1, significantly decreased high-glucose-induced expression of CD11c (integrin, alpha X 9 complement component 3 receptor 4 subunit]), chemokine (C-C motif) ligand 2, and interleukin-1beta in U937 macrophages. Glucose 155-162 interleukin 1 beta Mus musculus 293-310 24000330-7 2013 The expression of IL-6 and IL-1beta was significantly increased under 10 mM glucose in the presence of NT, while IL-1beta and IL-12 expression significantly decreased under inflammatory and hyperglycemic conditions. Glucose 76-83 interleukin 1 beta Mus musculus 27-35 22595195-8 2012 Administration of the spinasterol-Glc significantly decreased the plasma levels of these inflammatory mediators including TNF-alpha, IL-6 and IL-1beta in LPS-injected mice and improved survival of septic mice with lethal endotoxemia. Glucose 34-37 interleukin 1 beta Mus musculus 142-150 23773309-0 2013 Interleukin-1beta (IL-1beta) increases pain behavior and the blood glucose level: possible involvement of glucocorticoid system. Glucose 67-74 interleukin 1 beta Mus musculus 0-17 23773309-0 2013 Interleukin-1beta (IL-1beta) increases pain behavior and the blood glucose level: possible involvement of glucocorticoid system. Glucose 67-74 interleukin 1 beta Mus musculus 19-27 23773309-11 2013 In addition, the adrenalectomy caused the reductions of the blood glucose level and pain behavior induced by IL-1beta injected i.t. Glucose 66-73 interleukin 1 beta Mus musculus 109-117 23773309-14 2013 pretreatment with RU486 (100mg/kg) attenuated the blood glucose level and pain behavior induced by IL-1beta administered i.t. Glucose 56-63 interleukin 1 beta Mus musculus 99-107 23836031-3 2013 Overnight exposure to IL-1B+IL-6 in islets isolated from normal mice and humans disrupted glucose-stimulated intracellular calcium responses; cytokine-induced effects were more severe among islets from prediabetic db/db mice that otherwise showed no signs of dysfunction. Glucose 90-97 interleukin 1 beta Mus musculus 22-27 23836031-4 2013 IL-1B+IL-6 exposure reduced endoplasmic reticulum (ER) calcium storage, activated ER stress responses (Nos2, Bip, Atf4, and Ddit3 [CHOP]), impaired glucose-stimulated insulin secretion, and increased cell death only in islets from prediabetic db/db mice. Glucose 148-155 interleukin 1 beta Mus musculus 0-5 20332197-0 2010 XOMA 052, an anti-IL-1{beta} monoclonal antibody, improves glucose control and {beta}-cell function in the diet-induced obesity mouse model. Glucose 59-66 interleukin 1 beta Mus musculus 18-27 20920427-3 2010 For the present studies, we utilized these transgenic mice to determine the role of IL-1B in glucose sensor function in vivo. Glucose 93-100 interleukin 1 beta Mus musculus 84-89 22548833-0 2012 Interleukin-1beta (IL-1beta) increases pain behavior and the blood glucose level: possible involvement of sympathetic nervous system. Glucose 67-74 interleukin 1 beta Mus musculus 0-17 22548833-0 2012 Interleukin-1beta (IL-1beta) increases pain behavior and the blood glucose level: possible involvement of sympathetic nervous system. Glucose 67-74 interleukin 1 beta Mus musculus 19-27 22548833-5 2012 IL-1beta injection caused an elevation of the blood glucose level. Glucose 52-59 interleukin 1 beta Mus musculus 0-8 22548833-9 2012 injection of IL-1beta enhanced the blood glucose level when mice were orally fed with d-glucose. Glucose 41-48 interleukin 1 beta Mus musculus 13-21 22548833-9 2012 injection of IL-1beta enhanced the blood glucose level when mice were orally fed with d-glucose. Glucose 86-95 interleukin 1 beta Mus musculus 13-21 22548833-15 2012 pretreatment with phentolamine (an alpha(1)-adrenergic blocker) or yohimbine (an alpha(2)-adrenergic blocker) significantly attenuated the blood glucose level and pain behavior induced by IL-1beta administered i.t. Glucose 145-152 interleukin 1 beta Mus musculus 188-196 22548833-16 2012 However, the blood glucose level and pain behavior were not affected by butoxamine (a beta(2)-adrenergic blocker), whereas metoprolol (a beta(2)-adrenergic blocker) enhanced IL-1beta-induced blood glucose level and pain behavior in mice fed with d-glucose. Glucose 197-204 interleukin 1 beta Mus musculus 174-182 22548833-16 2012 However, the blood glucose level and pain behavior were not affected by butoxamine (a beta(2)-adrenergic blocker), whereas metoprolol (a beta(2)-adrenergic blocker) enhanced IL-1beta-induced blood glucose level and pain behavior in mice fed with d-glucose. Glucose 246-255 interleukin 1 beta Mus musculus 174-182 20332197-2 2010 Although previous work has shown that inhibiting IL-1beta can lead to improvements in glucose control and beta-cell function, we hypothesized that more efficient targeting of IL-1beta with a novel monoclonal antibody, XOMA 052, would reveal an effect on additional parameters affecting metabolic disease. Glucose 86-93 interleukin 1 beta Mus musculus 49-57 20067833-7 2010 Glucose-induced attenuation of IRS-2/Akt-mediated signalling was associated with increased IL-1beta expression. Glucose 0-7 interleukin 1 beta Mus musculus 91-99 20067833-0 2010 High glucose induces suppression of insulin signalling and apoptosis via upregulation of endogenous IL-1beta and suppressor of cytokine signalling-1 in mouse pancreatic beta cells. Glucose 5-12 interleukin 1 beta Mus musculus 100-108 20067833-4 2010 The aim of this study was to investigate whether high glucose can influence endogenous interleukin-1beta (IL-1beta) and SOCS expression thus affecting insulin signalling and survival in insulin-producing mouse pancreatic beta cells (betaTC-6). Glucose 54-61 interleukin 1 beta Mus musculus 87-104 20067833-4 2010 The aim of this study was to investigate whether high glucose can influence endogenous interleukin-1beta (IL-1beta) and SOCS expression thus affecting insulin signalling and survival in insulin-producing mouse pancreatic beta cells (betaTC-6). Glucose 54-61 interleukin 1 beta Mus musculus 106-114 20067833-11 2010 These results indicated that glucose-induced endogenous IL-1beta expression increased betaTC-6 cells apoptosis by inhibiting, at least in part, IRS-2/Akt-mediated signalling through SOCS-1 upregulation. Glucose 29-36 interleukin 1 beta Mus musculus 56-64 17003335-11 2006 Consistent with our in vitro results, IL-1beta knockout mice displayed glucose intolerance along with a decrease in islet Fas, FLIP, Pax4, and PDX-1 transcripts. Glucose 71-78 interleukin 1 beta Mus musculus 38-46 19777841-12 2009 CONCLUSION: Gastrodine can inhibit the expression of IL-1 beta, IL-6 in cultured BV-2 cells induced by high concentration of glucose. Glucose 125-132 interleukin 1 beta Mus musculus 53-62 17035503-7 2006 These findings, together with the present demonstration that this effect is integrated in the brain and is paralleled by IL-1beta expression in the hypothalamus, indicate that this cytokine can reset glucose homeostasis at central levels. Glucose 200-207 interleukin 1 beta Mus musculus 121-129 19666548-7 2009 Islets from mice deficient in IL-1beta or MyD88 challenged with glucose and palmitate in vitro also produced significantly less IL-6 and chemokines. Glucose 64-71 interleukin 1 beta Mus musculus 30-38 18723371-2 2008 In this study we describe the therapeutic effects by an IL-1beta antibody to improve glucose control in hyperglycemic mice with diet-induced obesity. Glucose 85-92 interleukin 1 beta Mus musculus 56-64 18383346-4 2008 In our study, we report that a combination of IL-1beta and TNFalpha exerts a synergistic effect on glucose utilization and markedly modifies the metabolic phenotype of astrocytes. Glucose 99-106 interleukin 1 beta Mus musculus 46-54 18383346-6 2008 Glutamate-stimulated glucose utilization and lactate release, a typical feature of astrocyte energy metabolism, are altered after pretreatment with IL-1beta+TNFalpha. Glucose 21-28 interleukin 1 beta Mus musculus 148-156 18383346-8 2008 Interestingly, stimulation of glucose utilization by IL-1beta+TNFalpha is not affected by the antioxidant N-acetyl-L-cysteine, suggesting that cellular stress does not account for this effect. Glucose 30-37 interleukin 1 beta Mus musculus 53-61 17583797-6 2007 Also, in primary islets of reporter gene mice, IL-1beta reduced glucose-stimulated INS transcription. Glucose 64-71 interleukin 1 beta Mus musculus 47-55 16023781-4 2005 Islets from iNOS-/- and wt mice exposed to IL-1beta or (IL-1beta + IFN-gamma) for 2-20 h showed different kinetics of glucose-stimulated insulin secretion. Glucose 118-125 interleukin 1 beta Mus musculus 43-51 16023781-4 2005 Islets from iNOS-/- and wt mice exposed to IL-1beta or (IL-1beta + IFN-gamma) for 2-20 h showed different kinetics of glucose-stimulated insulin secretion. Glucose 118-125 interleukin 1 beta Mus musculus 56-64 16023781-5 2005 In iNOS-/- islets, IL-1beta at high glucose induced a delayed and prolonged stimulation of insulin secretion, and this was followed by an increase in phospholipase D mRNA expression. Glucose 36-43 interleukin 1 beta Mus musculus 19-27 15194409-5 2004 Following a 21-hour incubation with IL-1 beta, CoPP islets secreted significantly more insulin upon glucose stimulation and preserved significantly more IC than control islets. Glucose 100-107 interleukin 1 beta Mus musculus 36-45 15803864-0 2005 Effects of antioxidants coenzyme Q10 and lipoic acid on interleukin-1 beta-mediated inhibition of glucose-stimulated insulin release from cultured mouse pancreatic islets. Glucose 98-105 interleukin 1 beta Mus musculus 56-74 15803864-5 2005 In this study, the antioxidants coenzyme Q10 and lipoic acid were able to block IL-1beta-mediated inhibition of glucose-stimulated insulin secretion from islet cells at 10(-12) M and 10(-9) M, respectively. Glucose 112-119 interleukin 1 beta Mus musculus 80-88 15297440-0 2004 Inhibition of hepatic gluconeogenesis and enhanced glucose uptake contribute to the development of hypoglycemia in mice bearing interleukin-1beta- secreting tumor. Glucose 51-58 interleukin 1 beta Mus musculus 128-145 15297440-1 2004 Mice bearing IL-1beta-secreting tumor were used to study the chronic effect of IL-1beta on glucose metabolism. Glucose 91-98 interleukin 1 beta Mus musculus 79-87 15297440-11 2004 We concluded that both decreased glucose production by the liver and enhanced glucose disposal lead to the development of hypoglycemia in mice bearing IL-1beta-secreting tumor. Glucose 33-40 interleukin 1 beta Mus musculus 151-159 15297440-11 2004 We concluded that both decreased glucose production by the liver and enhanced glucose disposal lead to the development of hypoglycemia in mice bearing IL-1beta-secreting tumor. Glucose 78-85 interleukin 1 beta Mus musculus 151-159 15194409-6 2004 After 65-hour incubation with IL-1 beta, CoPP islets secreted significantly less insulin upon glucose stimulation than control islets and preserved significantly less IC compared to islets incubated without IL-1 beta. Glucose 94-101 interleukin 1 beta Mus musculus 30-39 9989930-2 1999 IL-1beta and TNF-alpha inhibited insulin release and glucose utilization and oxidation. Glucose 53-60 interleukin 1 beta Mus musculus 0-8 10967106-6 2000 The decrease in glucose-stimulated insulin secretion induced by IL-1beta and IFN-gamma was however not prevented. Glucose 16-23 interleukin 1 beta Mus musculus 64-72 12947309-1 2003 BACKGROUND: Interferon (IFN)-gamma acts synergistically with interleukin (IL)-1beta and tumor necrosis factor (TNF)-alpha to activate isoform of nitric oxide synthetase (iNOS) gene expression, induce apoptosis, and impair glucose-stimulated insulin release (GSIR) in pancreatic islets. Glucose 222-229 interleukin 1 beta Mus musculus 61-83 11181061-5 2001 Both IL-1 beta and (IL-1 beta + IFN-gamma) impaired glucose-stimulated insulin release and reduced the insulin content of wt islets, while (IL-1 beta + IFN-gamma) reduced glucose oxidation rates and cell viability. Glucose 52-59 interleukin 1 beta Mus musculus 5-14 11181061-5 2001 Both IL-1 beta and (IL-1 beta + IFN-gamma) impaired glucose-stimulated insulin release and reduced the insulin content of wt islets, while (IL-1 beta + IFN-gamma) reduced glucose oxidation rates and cell viability. Glucose 52-59 interleukin 1 beta Mus musculus 20-29 11181061-5 2001 Both IL-1 beta and (IL-1 beta + IFN-gamma) impaired glucose-stimulated insulin release and reduced the insulin content of wt islets, while (IL-1 beta + IFN-gamma) reduced glucose oxidation rates and cell viability. Glucose 52-59 interleukin 1 beta Mus musculus 20-29 11181061-6 2001 IL-1 beta exposure to iNOS -/- islets impaired glucose-stimulated insulin release, increased insulin accumulation and reduced the insulin content, without any increase in cell death. Glucose 47-54 interleukin 1 beta Mus musculus 0-9 11181061-8 2001 Our data suggest that IL-1 beta may inhibit glucose-stimulated insulin release by pathways that are not NO-dependent and not related to glucose metabolism or cell death. Glucose 44-51 interleukin 1 beta Mus musculus 22-31 10419651-0 1999 Interleukin 1beta mediates the effect of high D-glucose on the secretion of TNF-alpha by mouse uterine epithelial cells. Glucose 46-55 interleukin 1 beta Mus musculus 0-17 10419651-5 1999 Macrophages of the RAW 264.7 cell line were found to secrete more interleukin (IL)-1beta (but not TNF-alpha) when cultured in high D-glucose. Glucose 131-140 interleukin 1 beta Mus musculus 66-88 1451948-10 1992 Culture of islets obtained from NOD mice in the presence of the cytokine interleukin-1 beta induced a similar pattern of glucose metabolism as seen earlier in IgG or phosphate-buffered saline treated control NOD mice. Glucose 121-128 interleukin 1 beta Mus musculus 73-91 9629247-2 1998 The effect of interleukin-1 beta (IL-1 beta) on glucose blood levels serves as an example. Glucose 48-55 interleukin 1 beta Mus musculus 14-32 9629247-2 1998 The effect of interleukin-1 beta (IL-1 beta) on glucose blood levels serves as an example. Glucose 48-55 interleukin 1 beta Mus musculus 34-43 9195135-4 1997 S-methyl-L-thiocitrulline alone did not affect the islet glucose oxidation rate, but all concentrations of S-methyl-L-thiocitrulline prevented IL-1 beta induced suppression of the islet glucose metabolism. Glucose 186-193 interleukin 1 beta Mus musculus 143-152 8662965-0 1996 Long exposure to high glucose concentration impairs the responsive expression of gamma-glutamylcysteine synthetase by interleukin-1beta and tumor necrosis factor-alpha in mouse endothelial cells. Glucose 22-29 interleukin 1 beta Mus musculus 118-135 7948748-4 1994 In parallel with NO production, IL-1 beta+IFN-gamma+TNF-alpha impaired islet function, as judged by decreased islet DNA and insulin content, decreased glucose metabolism and decreased glucose-induced insulin release. Glucose 151-158 interleukin 1 beta Mus musculus 32-51 8987109-0 1996 Effects of a 33 residue interleukin-1 beta peptide and the antioxidant PQQ on interleukin-1 beta-mediated inhibition of glucose-stimulated insulin release from cultured mouse pancreatic islets. Glucose 120-127 interleukin 1 beta Mus musculus 24-42 8987109-0 1996 Effects of a 33 residue interleukin-1 beta peptide and the antioxidant PQQ on interleukin-1 beta-mediated inhibition of glucose-stimulated insulin release from cultured mouse pancreatic islets. Glucose 120-127 interleukin 1 beta Mus musculus 78-96 8987109-1 1996 Interleukin-1 beta (IL-1 beta) significantly inhibits insulin secretion from glucose stimulated islet cells. Glucose 77-84 interleukin 1 beta Mus musculus 0-18 8987109-1 1996 Interleukin-1 beta (IL-1 beta) significantly inhibits insulin secretion from glucose stimulated islet cells. Glucose 77-84 interleukin 1 beta Mus musculus 20-29 32945406-2 2020 The present study aimed to investigate the role of different MAPK signal transduction pathways in the interleukin-1beta (IL-1beta)-induced inhibition of glucose-stimulated insulin secretion (GSIS) in Min6 mouse pancreatic cells. Glucose 153-160 interleukin 1 beta Mus musculus 102-119 1535517-3 1992 The two test agents counteracted the initial stimulatory actions of IL-1 beta on both islet glucose-induced insulin release and glucose oxidation rates. Glucose 92-99 interleukin 1 beta Mus musculus 68-77 1535517-5 1992 When islets were exposed for 1 hr to IL-1 beta and studied after 12 hr, there was a 75% inhibition of glucose induced insulin release, a 50% decrease in glucose oxidation rates and a 30% decrease in (pro)insulin biosynthesis. Glucose 102-109 interleukin 1 beta Mus musculus 37-46 1535517-9 1992 Mouse islets exposed for 2 hr to IL-1 beta and studied after 12 hr presented a 50% decrease in the glucose-induced insulin release. Glucose 99-106 interleukin 1 beta Mus musculus 33-42 1832112-3 1991 Brief exposure (1-2 h) of rat and mouse pancreatic islets to 10 ng/ml recombinant interleukin-1 beta induced an 70-80% inhibition of insulin response to glucose after 12 h. These effects were completely counteracted by co-incubation with 100 ng/ml interleukin-1 receptor antagonist protein. Glucose 153-160 interleukin 1 beta Mus musculus 82-100 34749292-16 2021 GSDMD-/- attenuated interleukin-1beta (IL-1beta) level and peritoneal fibrosis induced by dextrose peritoneal dialysate treatment in pericytes in vivo. Glucose 90-98 interleukin 1 beta Mus musculus 20-37 33214151-3 2020 We now show that RBP4 primes the NLRP3 inflammasome for interleukin-1beta (IL1beta) release, in a glucose-dependent manner, through the TLR4/MD2 receptor complex and TLR2. Glucose 98-105 interleukin 1 beta Mus musculus 56-73 30710049-1 2019 LPS-activated macrophages require metabolic reprogramming and glucose uptake mediated by hypoxia-inducible factor (HIF)-1 alpha and glucose transporter 1 (Glut1) expression for proinflammatory cytokine production, especially IL-1beta. Glucose 62-69 interleukin 1 beta Mus musculus 225-233 30791996-6 2019 High glucose and palmitic acid treatment enhanced the expression of interleukin-1beta and interleukin-18; these enhancements were further increased after treatment with DsbA-L siRNA but alleviated by co-treatment with an AMPK activator. Glucose 5-12 interleukin 1 beta Mus musculus 68-85 31647995-8 2019 The CECs from Asah1fl/fl/ECcre mice had decreased MVB-lysosome interaction and increased IL-1beta-containing exosome release in response to high glucose stimulation. Glucose 145-152 interleukin 1 beta Mus musculus 89-97 30586442-0 2018 Tumor-secreted factors induce IL-1beta maturation via the glucose-mediated synergistic axis of mTOR and NF-kappaB pathways in mouse macrophages. Glucose 58-65 interleukin 1 beta Mus musculus 30-38 30586442-7 2018 TCM increased the levels of IL-1beta via glucose-mediated activation of the inflammasome. Glucose 41-48 interleukin 1 beta Mus musculus 28-36 30586442-11 2018 Finally, glucose inhibition by inoculation with 2-deoxy-D-glucose in vivo decreased the IL-1beta levels in both the blood and tumor region of B16F10-bearing C57BL/6 mice relative to those in PBS-injected tumor-bearing mice. Glucose 9-16 interleukin 1 beta Mus musculus 88-96 30586442-12 2018 These results suggest that glucose supplied from blood vessels might be important for IL-1beta production in tumor-associated macrophages via the integrated signals of the NF-kappaB and mTOR pathways in the tumor microenvironment. Glucose 27-34 interleukin 1 beta Mus musculus 86-94 30250027-11 2018 In addition, silencing Kcnq1ot1 promoted gasdermin D cleavage and the secretion of IL-1beta, thus repressing the TGF-beta1/smads pathway in high glucose-treated cardiac fibroblasts through miR-214-3p and caspase-1. Glucose 145-152 interleukin 1 beta Mus musculus 83-91 30555402-6 2018 Furthermore, an increased expression of pro-inflammatory cytokines, including IL-1beta, IL-6, IL-8, and TNF-alpha, was observed in brain endothelial cells in response to oxygen/glucose depletion/reoxygenation, which was decreased by the shRNA-mediated Atg7 knockdown. Glucose 177-184 interleukin 1 beta Mus musculus 78-86 30420491-9 2018 Moreover, glucose treatment promoted mRNA levels of TNF-alpha, IL-1beta, and IL-6 in mesangial cells. Glucose 10-17 interleukin 1 beta Mus musculus 63-71 29868580-13 2018 The findings showed the significant blood glucose levels regulation capacity and declination of IL-1beta concentration in all transplanted mice. Glucose 42-49 interleukin 1 beta Mus musculus 96-104 29753610-0 2018 Improvement of hyperglycemia in a murine model of insulin resistance and high glucose- and inflammasome-mediated IL-1beta expressions in macrophages by silymarin. Glucose 78-85 interleukin 1 beta Mus musculus 113-121 29108965-7 2018 Indeed, exposure of mouse tracheal epithelial cells to IL-1beta or IL-1alpha resulted in increased glycolytic flux, glucose use, expression of glycolysis genes, and lactate production. Glucose 116-123 interleukin 1 beta Mus musculus 55-63 28711598-6 2017 Further investigation showed that high glucose induced KLF5 nitration by iNOS-mediated peroxynitrite generation, and nitrated KLF5 increased its interaction with NF-kappaB p50 and thus cooperatively activated the expression of inflammatory cytokines TNF-alpha and IL-1beta. Glucose 39-46 interleukin 1 beta Mus musculus 264-272 29155303-0 2018 Therapeutic vaccine against IL-1beta improved glucose control in a mouse model of type 2 diabetes. Glucose 46-53 interleukin 1 beta Mus musculus 28-36 29732438-7 2018 Comparisons of pro-inflammatory cytokine concentrations among central and peripheral metabolic tissues indicate that patterns of liver interleukin-1beta concentrations best reflects observed changes in glucose tolerance. Glucose 202-209 interleukin 1 beta Mus musculus 135-152 28972154-4 2017 We found that when incubated in buffer with up to 20 mm glucose, human and murine neutrophils, but not monocytes, generate progressively more MPs with high interleukin (IL)-1beta content. Glucose 56-63 interleukin 1 beta Mus musculus 156-178 29018785-7 2017 Lipopolysaccharide and glucose-induced nitric oxide production, protein expression of inducible nitric oxide synthase, COX-2, and superoxide dismutase 2, and mRNA expression levels of interleukin (IL)-1beta and IL-18 were significantly suppressed by turanose treatment. Glucose 23-30 interleukin 1 beta Mus musculus 184-206 28947919-0 2017 Glucagon-like peptide-1 receptor agonist exendin-4 protects against interleukin-1beta-mediated inhibition of glucose-stimulated insulin secretion by mouse insulinoma beta cells. Glucose 109-116 interleukin 1 beta Mus musculus 68-85 28092375-0 2017 Postprandial macrophage-derived IL-1beta stimulates insulin, and both synergistically promote glucose disposal and inflammation. Glucose 94-101 interleukin 1 beta Mus musculus 32-40 28433068-0 2017 The role of interleukin-1beta and extracellular signal-regulated kinase 1/2 in glucose-stimulated insulin secretion. Glucose 79-86 interleukin 1 beta Mus musculus 12-29 28433068-9 2017 After intervention by 0.15 ng/mL, 1.5 ng/mL, and 15 ng/mL IL-1beta, the level of ERK1/2 phosphorylation induced by 1.38mM glucose stimulation decreased in a dose-dependent manner, and the insulin level correspondingly decreased. Glucose 122-129 interleukin 1 beta Mus musculus 58-66 28092375-2 2017 However, a possible physiological role for IL-1beta in glucose metabolism has remained unexplored. Glucose 55-62 interleukin 1 beta Mus musculus 43-51 28092375-3 2017 Here we found that feeding induced a physiological increase in the number of peritoneal macrophages that secreted IL-1beta, in a glucose-dependent manner. Glucose 129-136 interleukin 1 beta Mus musculus 114-122 28092375-6 2017 IL-1beta and insulin increased the uptake of glucose into macrophages, and insulin reinforced a pro-inflammatory pattern via the insulin receptor, glucose metabolism, production of reactive oxygen species, and secretion of IL-1beta mediated by the NLRP3 inflammasome. Glucose 45-52 interleukin 1 beta Mus musculus 0-8 28092375-6 2017 IL-1beta and insulin increased the uptake of glucose into macrophages, and insulin reinforced a pro-inflammatory pattern via the insulin receptor, glucose metabolism, production of reactive oxygen species, and secretion of IL-1beta mediated by the NLRP3 inflammasome. Glucose 45-52 interleukin 1 beta Mus musculus 223-231 28092375-6 2017 IL-1beta and insulin increased the uptake of glucose into macrophages, and insulin reinforced a pro-inflammatory pattern via the insulin receptor, glucose metabolism, production of reactive oxygen species, and secretion of IL-1beta mediated by the NLRP3 inflammasome. Glucose 147-154 interleukin 1 beta Mus musculus 0-8 28210097-7 2017 RESULTS: Data showed that high glucose increased the TNF-alpha and IL-1beta levels in the RECs, which were reduced cells treated with the Epac1 agonist. Glucose 31-38 interleukin 1 beta Mus musculus 67-75 28182085-12 2017 On the contrary, the expression of procaspase-1 and pro-IL-1beta protein was restrained by high glucose and enhanced by maresin 1 in a dose-dependent manner (P < 0.05). Glucose 96-103 interleukin 1 beta Mus musculus 56-64 28817808-13 2017 In addition, fenofibrate inhibited IL-1beta expression caused by combination use of high glucose and lipopolysaccharide. Glucose 89-96 interleukin 1 beta Mus musculus 35-43 27152706-0 2016 Interleukin-1beta-Targeted Vaccine Improves Glucose Control and beta-Cell Function in a Diabetic KK-Ay Mouse Model. Glucose 44-51 interleukin 1 beta Mus musculus 0-17 28348460-8 2017 Epac1 effectively reduced high glucose-induced increases in TLR4, HMGB1, cleaved caspase-1, and IL-1beta in REC. Glucose 31-38 interleukin 1 beta Mus musculus 96-104 26987023-8 2016 Attenuated IL-1beta secretion may improve glucose metabolism in the HFD-fed insulin resistance mouse model. Glucose 42-49 interleukin 1 beta Mus musculus 11-19 26051275-9 2015 These findings indicate that IL-1beta strongly and irreversibly impairs tenogenic potential and alters glucose metabolism in tendon progenitors appearing in injured tendons. Glucose 103-110 interleukin 1 beta Mus musculus 29-37 26987023-10 2016 Collectively, our data showed that CI inhibits IL-1beta secretion through attenuation of NLRP3 inflammasome activation, leading to an antidiabetic effect by improving glucose metabolism and inhibiting metainflammation. Glucose 167-174 interleukin 1 beta Mus musculus 47-55 26468333-9 2015 The expression of IL-1beta by endothelial cells from TLR4 deficient mice under high glucose condition was decreased. Glucose 84-91 interleukin 1 beta Mus musculus 18-26 26166692-6 2015 We also found that insulin receptor substrate-1 (IRS-1), a component of insulin signaling, was negatively regulated by NLRP3 and IL-1beta, and that IL-1beta inhibited insulin-induced glucose uptake in myoblasts. Glucose 183-190 interleukin 1 beta Mus musculus 148-156 26166692-7 2015 These results suggest that PLIN2 inhibits insulin-induced glucose uptake by activating NLRP3, caspase-1 and IL-1beta, leading to a decreased IRS-1 expression. Glucose 58-65 interleukin 1 beta Mus musculus 108-116 25793995-5 2015 Here we demonstrate that high glucose significantly downregulates both the mRNA and protein levels of SIRT1 and upregulates the mRNA level and the release of two pro-inflammatory cytokines, IL-1beta and TNF-alpha, in RAW264.7 macrophages. Glucose 30-37 interleukin 1 beta Mus musculus 190-198 25793995-7 2015 However, when the function of SIRT1 is inhibited by EX527 or its expression is suppressed by RNAi, the upregulated level and release of IL-1beta and TNF-alpha by high glucose are further increased. Glucose 167-174 interleukin 1 beta Mus musculus 136-144 25530164-11 2015 Lipopolysaccharides markedly increased the expression and secretion of IL-1beta, IL-6, IL-8, and TNF-alpha in the GECs cultured in high glucose medium, which was also partly blocked in the presence of RSV. Glucose 136-143 interleukin 1 beta Mus musculus 71-79 25405767-3 2014 ER stress, oxidative stress and high glucose concentrations may also activate the NLRP3 inflammasome leading to interleukin (IL)-1beta production and caspase-1 dependent pyroptosis. Glucose 37-44 interleukin 1 beta Mus musculus 112-134