Interleukin 1 affects glucose homeostasis

Am J Physiol. 1987 Nov;253(5 Pt 2):R794-8. doi: 10.1152/ajpregu.1987.253.5.R794.


Alterations in glucose metabolism are known to occur during certain types of inflammation and infectious diseases. Interleukin 1 (IL 1), an immune-derived cytokine released during these processes, is proposed to function as a mediator of such alterations, since administration of low subpyrogenic doses of human rIL 1 to mice and rats produced hypoglycemia. In mice this effect was paralleled by increased insulin, glucagon, and corticosterone blood levels. When IL 1 was repeatedly injected, mice remained hypoglycemic for at least 14 h after the last injection. Furthermore, these animals responded normally to a challenge with glucose, thus suggesting that the proper function of the pancreas was preserved. A moderate hypoglycemia, paralleled by increased glucagon and corticosterone blood levels, was also observed in IL 1-injected rats, but no increase in insulin levels was detected. IL 1 administration to adrenalectomized rats resulted in a more marked hypoglycemia and in a profound hypoinsulinemia. The results suggest that IL 1 causes hypoglycemia by increasing insulin blood levels and probably also by mechanisms independent of the insulin secretagogue action of this cytokine.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adrenalectomy
  • Animals
  • Blood Glucose / metabolism
  • Corticosterone / blood
  • Glucagon / blood
  • Glucose / metabolism*
  • Homeostasis / drug effects*
  • Insulin / blood
  • Interleukin-1 / pharmacology*
  • Male
  • Mice
  • Mice, Inbred C3H


  • Blood Glucose
  • Insulin
  • Interleukin-1
  • Glucagon
  • Glucose
  • Corticosterone