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AJP - Regulatory, Integrative and Comparative Physiology, Vol 253, Issue 5 794-R798, Copyright © 1987 by American Physiological Society
ARTICLES |
A. del Rey and H. Besedovsky
Medizinische Abteilung, Schweizerisches Forschungsinstitut, Davos-Platz, Switzerland.
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.
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