PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 17035503-4 2006 This effect was largely antagonized by blockade of IL-1 receptors in the brain; and (iv) when animals with an advanced Type II diabetes were treated with IL-1 and challenged with glucose, they died in hypoglycemia. Glucose 179-186 interleukin 1 complex Mus musculus 51-55 19236331-2 2009 There is a peripheral component in the hypoglycemia that the cytokine induces resulting from an increased glucose uptake, an effect that can be exerted in a paracrine fashion at the site where IL-1 is locally produced. Glucose 106-113 interleukin 1 complex Mus musculus 193-197 19236331-5 2009 Here we report that administration of IL-1 or long-lasting insulin results in different changes in food intake and in neuroendocrine mechanisms 8 h following induction of the same degree of hypoglycemia (40-45% decrease in glucose blood levels). Glucose 223-230 interleukin 1 complex Mus musculus 38-42 17035503-5 2006 However, when IL-1 receptors in the brains of these diabetic mice were blocked, they survived, and glucose blood levels approached those that these mice had before IL-1 administration. Glucose 99-106 interleukin 1 complex Mus musculus 14-18 9452447-2 1998 We observe that hyperglycemic levels of D-glucose (8-20 mM) inhibit the release of IL-1 by lipopolysaccharide-stimulated RAW 264.7 murine macrophage cells. Glucose 40-49 interleukin 1 complex Mus musculus 83-87 9629247-5 1998 Even after a glucose load, IL-1-treated animals remain hypoglycemic, suggesting that central mechanisms that control the set point of glucose homeostasis are affected. Glucose 13-20 interleukin 1 complex Mus musculus 27-31 9629247-10 1998 IL-1-mediated effects on glucose levels might be directed at providing more energy supply to tissues during processes with high metabolic demands. Glucose 25-32 interleukin 1 complex Mus musculus 0-4 17035503-0 2006 IL-1 resets glucose homeostasis at central levels. Glucose 12-19 interleukin 1 complex Mus musculus 0-4 17035503-2 2006 Here, we show that this effect can be elicited by endogenous IL-1 and is related to not only the capacity of the cytokine to increase glucose uptake in peripheral tissues but also to mechanisms integrated in the brain. Glucose 134-141 interleukin 1 complex Mus musculus 61-65 9452447-3 1998 An inhibitor of glucose transport and metabolism, 2-deoxyglucose, prevents this inhibition of IL-1 release. Glucose 16-23 interleukin 1 complex Mus musculus 94-98 9452447-5 1998 Immunoprecipitation and activity measurements demonstrate that high glucose levels block the release of IL-1 but do not inhibit IL-1 production. Glucose 68-75 interleukin 1 complex Mus musculus 104-108 9452447-7 1998 Phorbol 12-myristate 13-acetate, an agonist of PKC, mimics glucose-induced inhibition of IL-1 release. Glucose 59-66 interleukin 1 complex Mus musculus 89-93 9452447-8 1998 These results demonstrate that high glucose levels inhibit IL-1 release (but not production) by RAW 264. Glucose 36-43 interleukin 1 complex Mus musculus 59-63 2691218-4 1989 However, glucose-stimulated insulin release was significantly impaired after 3 days of in vivo administration of IL-1, either 3 micrograms/animal/day or 0.3 micrograms/animal/day. Glucose 9-16 interleukin 1 complex Mus musculus 113-117 7948065-4 1994 When the islets of NOD mice were incubated with the IL-1 (10, 100 U/ml) under condition of high glucose, IAP and endogenous retrovirus type C frequently appeared in the beta-cells. Glucose 96-103 interleukin 1 complex Mus musculus 52-56 7948065-7 1994 When the islets of NON mice were incubated with or without IL-1 (10 U/ml) in the presence of high glucose, IAP was rarely found in beta-cells and retrovirus type C was undetectable in beta-cells. Glucose 98-105 interleukin 1 complex Mus musculus 59-63 7509141-6 1993 A protective effect of IL-1 via effects on glucose homeostasis during the acute-phase response was investigated by comparing plasma glucose levels in IL-1-treated mice and control mice before and during infection. Glucose 43-50 interleukin 1 complex Mus musculus 23-27 7509141-7 1993 Although glucose levels in IL-1-pretreated mice were somewhat higher in the later stages of infection, no significant differences from levels in control mice were present, and the glucose levels in control-treated animals never fell to hypoglycemic values. Glucose 9-16 interleukin 1 complex Mus musculus 27-31 7509141-7 1993 Although glucose levels in IL-1-pretreated mice were somewhat higher in the later stages of infection, no significant differences from levels in control mice were present, and the glucose levels in control-treated animals never fell to hypoglycemic values. Glucose 180-187 interleukin 1 complex Mus musculus 27-31 1510786-7 1992 Thus, IL-1 treatment could clinically be an effective immunotherapeutic modality for autoimmune diabetes mellitus by suppressing early disease progression or normalize plasma glucose levels when insulin is present. Glucose 175-182 interleukin 1 complex Mus musculus 6-10 1999179-5 1991 We investigated the possible roles of changes in serum corticosterone and glucose in the effects of LPS, TNF and IL-1. Glucose 74-81 interleukin 1 complex Mus musculus 113-117 2691218-5 1989 The administration of IL-1 inhibited an acute phase of glucose-induced insulin release, whereas neither basal insulin secretion nor insulin release from 10-30 min of perifusion with glucose was impaired. Glucose 55-62 interleukin 1 complex Mus musculus 22-26 2691218-6 1989 There was an only partial (27%) and non-significant restoration of the insulin secretory response to glucose stimulation 4 days after discontinuation of IL-1 treatment. Glucose 101-108 interleukin 1 complex Mus musculus 153-157 2691218-7 1989 We conclude that IL-1 administered in vivo is capable of adversely affecting pancreatic islet response to glucose stimulation. Glucose 106-113 interleukin 1 complex Mus musculus 17-21 3297891-3 1987 Inhibition of glucose-induced insulin secretion was observed after a 15-h treatment of islets with either purified IL-1, murine recombinant IL-1 (rIL-1), or human rIL-1, rIL-1 inhibition of glucose-induced insulin secretion was dose dependent with half-maximal inhibition observed at 25 pM human rIL-1. Glucose 14-21 interleukin 1 complex Mus musculus 115-119 2785952-6 1989 Furthermore, IL-1 seems to adjust the "set point" for glucose regulation to a lower level. Glucose 54-61 interleukin 1 complex Mus musculus 13-17 3297891-3 1987 Inhibition of glucose-induced insulin secretion was observed after a 15-h treatment of islets with either purified IL-1, murine recombinant IL-1 (rIL-1), or human rIL-1, rIL-1 inhibition of glucose-induced insulin secretion was dose dependent with half-maximal inhibition observed at 25 pM human rIL-1. Glucose 14-21 interleukin 1 complex Mus musculus 140-144 2824799-5 1987 Another in vivo activity of IL-1 relates to its capacity to induce a reduction in blood glucose levels. Glucose 88-95 interleukin 1 complex Mus musculus 28-32 2824799-12 1987 After 2 hr and for at least another 6 hr, glucose levels of alloxan-treated mice injected with IL-1 remained within the normal range. Glucose 42-49 interleukin 1 complex Mus musculus 95-99 33285301-8 2021 This observation was consistent with our finding that glucose-stimulated insulin secretion was reduced in islets isolated from IL-1alphaPdx1-/- mice. Glucose 54-61 interleukin 1 complex Mus musculus 127-140 3487590-6 1986 In adrenalectomized mice, IL 1 (5 PU) treatment produced similar results in steroid binding (66% of control) and plasma glucose (71% of control). Glucose 120-127 interleukin 1 complex Mus musculus 26-30 3487590-9 1986 IL 1 treatment inhibited the induction of PEPCK in fasted animals (13.4 +/- 2.0 U/mg) and caused a significant decrease in steroid binding (78% of fasted control) and plasma glucose (82% of fasted control). Glucose 174-181 interleukin 1 complex Mus musculus 0-4 3487590-11 1986 These data indicate that IL 1 decreases intracellular steroid receptors, resulting in decreased induction of PEPCK and subsequent reduced gluconeogenesis and plasma glucose. Glucose 165-172 interleukin 1 complex Mus musculus 25-29 26599867-6 2015 Thus, our findings confirm that the locally-increased IL-1 elicited by masticatory behavior, although present small in amounts, contributes to supporting MM activity by maintaining normal glucose homeostasis in these muscles. Glucose 188-195 interleukin 1 complex Mus musculus 54-58 26643538-9 2016 The results showed that, in an activity-dependent and paracrine/autocrine manner, endogenous IL-1 produced by neurons and astrocytes facilitates glucose uptake by these cells. Glucose 145-152 interleukin 1 complex Mus musculus 93-97 24013028-5 2013 Therefore, we hypothesized that hypothalamic IL-1 gene expression is regulated by glucose and glucose-induced feeding suppression is mediated via hypothalamic IL-1 signaling. Glucose 82-89 interleukin 1 complex Mus musculus 45-49 24013028-5 2013 Therefore, we hypothesized that hypothalamic IL-1 gene expression is regulated by glucose and glucose-induced feeding suppression is mediated via hypothalamic IL-1 signaling. Glucose 94-101 interleukin 1 complex Mus musculus 45-49 24013028-5 2013 Therefore, we hypothesized that hypothalamic IL-1 gene expression is regulated by glucose and glucose-induced feeding suppression is mediated via hypothalamic IL-1 signaling. Glucose 94-101 interleukin 1 complex Mus musculus 159-163 24013028-11 2013 These findings support the role for hypothalamic IL-1 signaling in the mediation of the anorectic effect of glucose. Glucose 108-115 interleukin 1 complex Mus musculus 49-53 24351180-8 2013 These data also suggest that local delivery of IL-1Ra genes or recombinant proteins (anakinra) or other IL-1 antagonists such as antibodies or soluble IL-1 receptors would suppress sensor-induced tissue reactions and likely enhance glucose sensor function by inhibiting inflammation and wound healing at sensor implantation sites. Glucose 232-239 interleukin 1 complex Mus musculus 47-51 24351180-8 2013 These data also suggest that local delivery of IL-1Ra genes or recombinant proteins (anakinra) or other IL-1 antagonists such as antibodies or soluble IL-1 receptors would suppress sensor-induced tissue reactions and likely enhance glucose sensor function by inhibiting inflammation and wound healing at sensor implantation sites. Glucose 232-239 interleukin 1 complex Mus musculus 104-108 24351180-0 2013 Role of interleukin-1/interleukin-1 receptor antagonist family of cytokines in long-term continuous glucose monitoring in vivo. Glucose 100-107 interleukin 1 complex Mus musculus 8-21 24351180-0 2013 Role of interleukin-1/interleukin-1 receptor antagonist family of cytokines in long-term continuous glucose monitoring in vivo. Glucose 100-107 interleukin 1 complex Mus musculus 22-35