Acute pancreatic beta cell apoptosis by IL-1β is responsible for postburn hyperglycemia: Evidence from humans and mice

ConclusionsOur findings reveal a novel mechanism of acute hyperglycemia postburn in which impaired insulin secretory capacity mediated by IL-1β leads to acute hyperglycemia. These data suggest that targeting IL-1β to restore endogenous insulin secretory function may be a novel glycemic control strategy to improve outcomes for burn patients.Graphical abstract
Source: Biochimica et Biophysica Acta (BBA) Molecular Basis of Disease - Category: Molecular Biology Source Type: research
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