Dataset on acute hyperglycemia in extensively burned patients and mice.

A single center, prospective cohort study recruiting 107 burn patients and 62 control patients was conducted to characterize the early phase of acute hyperglycemia in patients with burns. A total of 1643 blood samples were collected, and blood glucose and serum proinflammatory cytokines were detected and analyzed. A mouse severe burn model was used to study the underlying mechanisms of acute hyperglycemia postburn. An expression profile of IL-1 receptor, serum IL-1β and pancreatic islet function were detected in both control mice and burned mice. The data in this article is associated with the research article published in Biochim Biophys Acta “Acute pancreatic beta cell apoptosis by IL-1β is responsible for postburn hyperglycemia: evidence from humans and mice” [1].