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Central and peripheral mechanisms contribute to the hypoglycemia induced by interleukin-1.

Authors
Type
Published Article
Journal
Annals of the New York Academy of Sciences
Publication Date
Volume
840
Pages
153–161
Identifiers
PMID: 9629247
Source
Medline
License
Unknown

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-1 beta (IL-1 beta) on glucose blood levels serves as an example. Although IL-1 beta 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-1 beta 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-1 beta. 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.

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