AJP - Regu Fuel your research with LabChart
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


Am J Physiol Regul Integr Comp Physiol 253: R794-R798, 1987;
0363-6119/87 $5.00
This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by del Rey, A.
Right arrow Articles by Besedovsky, H.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by del Rey, A.
Right arrow Articles by Besedovsky, H.

AJP - Regulatory, Integrative and Comparative Physiology, Vol 253, Issue 5 794-R798, Copyright © 1987 by American Physiological Society


ARTICLES

Interleukin 1 affects glucose homeostasis

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.


This article has been cited by other articles:


Home page
CVIHome page
S. Oguri, K. Motegi, Y. Iwakura, and Y. Endo
Primary Role of Interleukin-1{alpha} and Interleukin-1{beta} in Lipopolysaccharide-Induced Hypoglycemia in Mice
Clin. Vaccine Immunol., November 1, 2002; 9(6): 1307 - 1312.
[Abstract] [Full Text] [PDF]


Home page
J. Immunol.Home page
A. R. Shikhman, D. C. Brinson, J. Valbracht, and M. K. Lotz
Cytokine Regulation of Facilitated Glucose Transport in Human Articular Chondrocytes
J. Immunol., December 15, 2001; 167(12): 7001 - 7008.
[Abstract] [Full Text] [PDF]


Home page
GutHome page
J Hardin, K Kroeker, B Chung, and D G Gall
Effect of proinflammatory interleukins on jejunal nutrient transport
Gut, August 1, 2000; 47(2): 184 - 191.
[Abstract] [Full Text] [PDF]


Home page
Proc. Natl. Acad. Sci. USAHome page
H. Schneider, F. Pitossi, D. Balschun, A. Wagner, A. del Rey, and H. O. Besedovsky
A neuromodulatory role of interleukin-1beta in the hippocampus
PNAS, June 23, 1998; 95(13): 7778 - 7783.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online