Chronic central nervous system exposure to interleukin-1[beta]
causes catabolism in the rat.
Hill, Andrew G., Lauren Jacobson, Jorge Gonzalez, Jan Rounds, Joseph
A. Majzoub, Douglas W. Wilmore.
Laboratory for Surgical Metabolism and Nutrition, Department of
Surgery, Brigham and Women's Hospital
APStracts 3:0182R, 1996.
Interleukin-1 (IL-1) and Interleukin-6 (IL-6) are thought to play a
role in mediating weight loss, net protein catabolism, anorexia and
fever following infection or injury. Because IL-1 and IL-6 can be
synthesized in the brain, and have been shown to be increased in
central nervous system (CNS) infections, we investigated the
metabolic consequences of prolonged CNS exposure to these cytokines.
At equivalent doses, intracerebroventricular (icv) infusion of IL-1,
but not IL-6, caused negative nitrogen balance, weight loss, and
anorexia. Infusion of IL-1 icv also caused adrenocortical activation,
as indicated by increased adrenal weight and plasma corticosterone,
and decreased thymus weight. However, clamping plasma glucocorticoids
at low levels by adrenalectomy and corticosterone pellet replacement
did not attenuate IL-1-induced losses of body weight and nitrogen. We
conclude that centrally produced IL-1 could play an important role in
the metabolic alterations associated with CNS injury or infection,
and that these effects may not be solely attributable to increased
secretion of glucocorticoids.
Received 28 November 1995; accepted in final form 1 May 1996.
APS Manuscript Number R748-5.
Article publication pending Am. J. Physiol. (Regulatory Integrative
Comp. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 28 May 96