This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Reprints and Permissions Copyright Information Books from ASM Press MicrobeWorld Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Oguri, S. Articles by Endo, Y. Search for Related Content PubMed PubMed Citation Articles by Oguri, S. Articles by Endo, Y.

Primary Role of Interleukin-1 and Interleukin-1ß in Lipopolysaccharide-Induced Hypoglycemia in Mice

Departments of Pharmacology,¹ Maxillofacial and Plastic Surgery, Graduate School of Dentistry, Tohoku University, 4-1 Seiryo-Machi, Aoba-Ku, Sendai 980-8575,² Center for Experimental Medicine, Institute of Medical Science, University of Tokyo, Minato-Ku, Tokyo 108-8639, Japan³

Received 9 October 2001/ Returned for modification 23 April 2002/ Accepted 5 July 2002

Within a few hours of its injection into mice, lipopolysaccharide (LPS) induces hypoglycemia and the production of various cytokines. We previously found that interleukin-1 (IL-1), IL-1ß, and tumor necrosis factor alpha (TNF-) induce hypoglycemia and that the minimum effective dose of IL-1 or IL-1ß is about 1/1,000 that of TNF-. In the present study, we examined the contribution made by IL-1 to the hypoglycemic action of LPS. Nine other cytokines tested were all inactive at inducing hypoglycemia. LPS produced hypoglycemia in mice deficient in either IL-1 or IL-1ß but not in mice deficient in both cytokines (IL-1 and -1ß knockout [IL-1/ß KO] mice). IL-1, IL-1ß, and TNF- induced hypoglycemia in IL-1/ß KO mice, as they did in normal control mice. The LPS-induced elevation of serum cortisol was weaker in IL-1/ß KO mice than in control mice, and, in the latter, serum cortisol was markedly raised while blood glucose was declining. IL-1 decreased blood glucose both in NOD mice (which have impaired insulin production) and in KK-Ay mice (insulin resistant). These results suggest that (i) cortisol may not be involved in mediating the resistance of IL-1/ß KO mice to the hypoglycemic action of LPS, (ii) as a mediator, IL-1 is a prerequisite for the hypoglycemic action of LPS, (iii) IL-1 and IL-1ß perform mutual compensation, and (iv) IL-1 plays a role as the primary stimulator of the many anabolic reactions required for the elaboration of immune responses against infection.

This article has been cited by other articles:

• Metzger, S., Nusair, S., Planer, D., Barash, V., Pappo, O., Shilyansky, J., Chajek-Shaul, T. (2004). Inhibition of Hepatic Gluconeogenesis and Enhanced Glucose Uptake Contribute to the Development of Hypoglycemia in Mice Bearing Interleukin-1{beta}- Secreting Tumor. Endocrinology 145: 5150-5156 [Abstract] [Full Text]