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Interleukin 1 Increases Serum Leptin Concentrations in Humans

Medicine Branch (J.E.J., B.D.C. B.L.G.), Division of Clinical Sciences, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892-1906; Indiana University School of Medicine (R.V.C.), Indianapolis, Indiana 46202; Clinical Services Program (H.C.R., G.C.P., W.C.K.), SAIC Frederick, National Cancer Institute-Frederick Cancer Research and Development Center, Frederick, Maryland 21702-1201; Earle Chiles Research Institute (J.W.S.), Providence Medical Center, Portland, Oregon 97213; and Data Management Services, Inc. (W.G.A.), SAIC Frederick, National Cancer Institute-Frederick Cancer Research and Development Center, Frederick, Maryland 21702-1201

Address all correspondence and requests for reprints to: Dr. Janik, Medicine Branch, Division of Clinical Sciences, National Cancer Institute, National Institutes of Health, Building 10, Room 12N226, 9000 Rockville Pike, Bethesda, Maryland 20892-1906.

Leptin, the protein product of the ob gene, regulates appetite and body weight in animals. Endotoxin and cytokines, induced by endotoxin, interleukin (IL) 1 and tumor necrosis factor, increase expression of leptin in mice and hamsters. We measured serum leptin concentrations in patients with cancer before and after administration of recombinant human IL-1. Fourteen patients received IL-1 at one of three dose levels (0.03, 0.1, or 0.3 µg/kg·day) for 5 days. Serum leptin concentrations increased in all but two patients within 24 h after the first dose. The increase in leptin was correlated directly with IL-1 dose (P = 0.0030). Despite continued administration of IL-1, serum leptin concentrations returned to pretreatment levels by day 5 of therapy. An increase in serum leptin concentrations may be one mechanism by which anorexia is induced by IL-1. However, tachyphylaxis of the leptin response suggests that other mechanisms also are involved.

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