Sarraf P, Frederich R C, Turner E M, Ma G, Jaskowiak N T, Rivet D J, Flier J S, Lowell B B, Fraker D L, Alexander H R
Surgical Metabolism Section, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA.
J Exp Med. 1997 Jan 6;185(1):171-5. doi: 10.1084/jem.185.1.171.
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.
