J. Exp. Med.
Volume 185 January 1997 171-176

BRIEF DEFINITIVE REPORT:
Multiple Cytokines and Acute Inflammation Raise Mouse Leptin Levels: Potential Role in Inflammatory Anorexia

By Pasha Sarraf,^* Robert C. Frederich, Ewa M. Turner,^* Grace Ma,^* Nora T. Jaskowiak,^* Dennis J. Rivet III,^* Jeffrey S. Flier, Bradford B. Lowell, Douglas L. Fraker,^* and H. Richard Alexander^*

From ^* The Surgical Metabolism Section, Surgery Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892; and  Division of Endocrinology, Beth Israel Hospital, Boston, Massachusetts 02215

Several inflammatory cytokines, most notably tumor necrosis factor (TNF) and IL-1, induce anorexia and loss of lean body mass, common manifestations of acute and chronic inflammatory conditions. In C57BL/6 female mice, the administration of TNF, IL-1, and, to a lesser extent, leukemia inhibitory factor (LIF), produced a prompt and dose-dependent increase in serum leptin levels and leptin mRNA expression in fat. IL-10, IL-4, ciliary neurotrophic factor, and IL-2, cytokines not known to induce anorexia or decrease food intake, had no effect on leptin gene expression or serum leptin levels. After administration of Escherichia coli lipopolysaccharide (LPS), leptin gene expression and leptin levels were increased. These findings suggest that leptin levels may be one mechanism by which anorexia is induced during acute inflammatory conditions.

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