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Effects of Exogenous Leptin on Satiety and Satiation in Patients with Lipodystrophy and Leptin Insufficiency

Unit on Growth and Obesity, National Institute of Child Health and Human Development (J.R.M., R.J.F., J.A.Y.); Nutrition Department (P.A.R.) and Drug Information Service, Pharmacy Department (K.A.C.), Warren Grant Magnuson Clinical Center; National Institute of Diabetes, Digestive Disorders and Kidney Diseases (E.A.O.), National Institutes of Health, Bethesda, Maryland 20892; and Amgen, Inc. (A.M.D.), Thousand Oaks, California 91320

Address all correspondence and requests for reprints to: Dr. Jack A. Yanovski, Unit on Growth and Obesity, Developmental Endocrinology Branch, National Institute of Child Health and Human Development, National Institutes of Health, 10 Center Drive, Building 10, Room 10N262, MSC 1862, Bethesda, Maryland 20892-1862. E-mail: yanovskj{at}mail.nih.gov.

To examine leptin’s role in human appetite regulation, we studied recombinant methionyl human leptin’s effects on satiation and satiety in a model of leptin insufficiency, lipodystrophy. Eight females with hypoleptinemia and lipodystrophy were given sc injections of A-100 (maximal dose, 200% of that predicted to normalize serum leptin) for 4 months. Satiation and satiety were determined before and again during leptin treatment. Satiation was measured as the time to voluntary cessation of eating from a standardized food array after a 12-h fast. Satiety was determined as the time to hunger sufficient to consume a full meal after consumption of a standardized preload. During leptin treatment, satiation time decreased (41.2 ± 18.2 to 19.5 ± 10.6 min; P = 0.01), satiety time increased (62.9 ± 64.8 to 137.8 ± 91.6 min; P = 0.04), energy consumed to produce satiation decreased (2034 ± 405 to 1135 ± 432 kcal or 8.5 ± 1.7 to 4.7 ± 1.8 MJ; P < 0.01), and the amount of food desired in the postabsorptive state decreased (P < 0.02). Ghrelin concentrations also decreased during leptin administration (284.3 ± 127.9 to 140.6 ± 104.5 pmol/liter; P < 0.002). We conclude that increased leptin in patients with lipodystrophy results in less caloric, shorter, more satiating meals and longer-lived satiety. These data support the hypothesis that leptin plays an important, permissive role in human appetite regulation.

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