This work was supported by the Volkswagen Stiftung and the Swiss National Research Council.
Central and Peripheral Mechanisms Contribute to the Hypoglycemia Induced by Interleukin-1a
Version of Record online: 7 FEB 2006
Annals of the New York Academy of Sciences
Volume 840, NEUROIMMUNOMODULATION: MOLECULAR ASPECTS, INTEGRATIVE SYSTEMS, AND CLINICAL ADVANCES pages 153–161, May 1998
How to Cite
DEL REY, A., MONGE-ARDITI, G. and BESEDOVSKY, H. O. (1998), Central and Peripheral Mechanisms Contribute to the Hypoglycemia Induced by Interleukin-1. Annals of the New York Academy of Sciences, 840: 153–161. doi: 10.1111/j.1749-6632.1998.tb09559.x
- Issue online: 7 FEB 2006
- Version of Record online: 7 FEB 2006
Abstract: The impact that neuroendocrine effects of cytokines have on general host homeostasis is reflected by the profound metabolic changes observed in parallel. The effect of interleukin-1β (IL-1β) on glucose blood levels serves as an example. Although IL-1β stimulates glucocorticoid output and decreases hepatic glycogen content, hypoglycemia is concomitantly detected in adult and newborn mice. This effect is observed even during fasting and is probably due to increased glucose transport into tissues. Even after a glucose load, IL-1-treated animals remain hypoglycemic, suggesting that central mechanisms that control the set point of glucose homeostasis are affected. Low doses of IL-1β injected i.c.v. can also induce hypoglycemia. Furthermore, central blockade of IL-1 receptors partially inhibits the hypoglycemia induced by peripheral administration of IL-1β. On the other hand, central depletion of catecholamines exacerbates IL-1-induced hypoglycemia. IL-1-mediated effects on glucose levels might be directed at providing more energy supply to tissues during processes with high metabolic demands.