{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,22]],"date-time":"2026-09-22T18:21:35Z","timestamp":1790101295947,"version":"4.0.1"},"reference-count":29,"publisher":"The Endocrine Society","issue":"9","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2004,9,1]]},"abstract":"<jats:p>To examine leptin\u2019s role in human appetite regulation, we studied recombinant methionyl human leptin\u2019s 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 \u00b1 18.2 to 19.5 \u00b1 10.6 min; P = 0.01), satiety time increased (62.9 \u00b1 64.8 to 137.8 \u00b1 91.6 min; P = 0.04), energy consumed to produce satiation decreased (2034 \u00b1 405 to 1135 \u00b1 432 kcal or 8.5 \u00b1 1.7 to 4.7 \u00b1 1.8 MJ; P &amp;lt; 0.01), and the amount of food desired in the postabsorptive state decreased (P &amp;lt; 0.02). Ghrelin concentrations also decreased during leptin administration (284.3 \u00b1 127.9 to 140.6 \u00b1 104.5 pmol\/liter; P &amp;lt; 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.<\/jats:p>","DOI":"10.1210\/jc.2003-031868","type":"journal-article","created":{"date-parts":[[2004,9,8]],"date-time":"2004-09-08T03:32:28Z","timestamp":1094614348000},"page":"4258-4263","source":"Crossref","is-referenced-by-count":111,"title":["Effects of Exogenous Leptin on Satiety and Satiation in Patients with Lipodystrophy and Leptin Insufficiency"],"prefix":"10.1210","volume":"89","author":[{"given":"Jennifer R.","family":"McDuffie","sequence":"first","affiliation":[{"name":"Unit on Growth and Obesity, National Institute of Child Health and Human Development (J.R.M., R.J.F., J.A.Y.), Maryland 20892"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Patti A.","family":"Riggs","sequence":"additional","affiliation":[{"name":"Nutrition Department (P.A.R.), Maryland 20892"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Karim A.","family":"Calis","sequence":"additional","affiliation":[{"name":"Drug Information Service, Pharmacy Department (K.A.C.), Warren Grant Magnuson Clinical Center"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Renee J.","family":"Freedman","sequence":"additional","affiliation":[{"name":"Unit on Growth and Obesity, National Institute of Child Health and Human Development (J.R.M., R.J.F., J.A.Y.), Maryland 20892"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Elif A.","family":"Oral","sequence":"additional","affiliation":[{"name":"National Institute of Diabetes, Digestive Disorders and Kidney Diseases (E.A.O.), National Institutes of Health, Bethesda, Maryland 20892"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alex M.","family":"DePaoli","sequence":"additional","affiliation":[{"name":"Amgen, Inc. 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