Faculty Information |
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Article types | Original article |
Language | English |
Refereed paper | Refereed |
Title | Interleukin-18 Reduces Blood Glucose and Modulates Plasma Corticosterone in a Septic Mouse Model. |
Journal | Formal name:Shock (Augusta, Ga.) Abbreviation:Shock ISSN code:1540-0514(Electronic)1073-2322(Linking) |
Domestic / Foregin | Foregin |
Volume, Number, Page | 47(4),pp.455-462 |
Papers・Author | ◎Yamashita Hayato, Ishikawa Michiko, Inoue Taketo, Usami Makoto, Usami Yu, Kotani Joji |
Publication date | 2017/04 |
Papers・Description | BACKGROUND:Dysregulation of glucose metabolism, including hyperglycemia with insulin resistance, is commonly observed in critically ill patients. Interleukin-18 (IL-18) improves the insulin resistance associated with obesity, but the relationship between IL-18 and glucose metabolism in sepsis was unclear. The purpose of this study was to investigate the influence of IL-18 on hyperglycemia during sepsis.METHODS:Sepsis was induced using cecal ligation and puncture (CLP) in wild-type (WT) mice, IL-18 knockout (KO) mice, and IL-18 KO mice pretreated with recombinant IL-18. Blood glucose and plasma insulin, glucagon, and corticosterone were measured. The mRNAs for gluconeogenic enzymes (g6pc, pck1) and activation of insulin signaling were also analyzed.RESULTS:In both WT and IL-18 KO mice, CLP operation led to hyperglycemia that lasted longer (18 h) than after sham operation (6 h). Blood glucose levels in IL-18 KO mice were significantly higher than in WT mice, without alteration of insulin or glucagon levels. In IL-18 KO mice, insulin signaling in the liver and skeletal muscle was decreased during hyperglycemia as compared with WT mice without suppression of hepatic glucose production enzymes. Pretreatment with recombinant IL-18 reduced blood glucose levels after CLP. Additionally, corticosterone levels were higher after CLP in the presence of either endogenous or exogenous IL-18.CONCLUSION:IL-18 may reduce blood glucose by modulating insulin signaling in the liver during sepsis-induced hyperglycemia. IL-18 is an important factor associated with alterations in blood glucose during sepsis. |
DOI | 10.1097/SHK.0000000000000747 |
PMID | 27648697 |