[Interleukin-1 and regulation of glucose homeostasis]

Cells involved in immune responses, inflammation, and development are sensitive to interleukin-1 (IL-1). In recent years, many studies have addressed the effects of IL-1 on carbohydrate metabolism. In vivo studies in rats and mice have shown that IL-1 induces hypoglycemia, with or without changes in serum insulin levels according to the species. The genesis of this effect has been investigated by studying central nervous system, liver (hepatocyte), and peripheral tissue responses to IL-1. In vitro, beta-islet cells incubated briefly with IL-1 produced insulin; incubation for longer periods of time or with high levels of IL-1 induced cytotoxic effects for which suggested mechanisms include production of free radicals, alterations in mitochondrial function, increased production of phosphoinositide second messenger, accumulation of prostaglandins, alterations in ion fluxes or changes in gene transcription. Studies of links between IL-1 and diabetes mellitus have focused on animal models of genetic diabetes including the non obese diabetic (NOD) mouse and the biobreeding (BB) rat. Although currently available data suggest that IL-1 modulates the incidence of diabetes mellitus, they are not adequate to determine whether or not IL-1 has a potential for preventing development of the disease.