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The Melanocortin Melanocyte-Stimulating Hormone/Adrenocorticotropin_4–10 Decreases Body Fat in Humans¹

Internal Medicine (H.L.F., R.S., W.K.), Department of Physiology (G.P.M., U.B.), University of Marburg, Marburg, Germany; and Clinical Neuroendocrinology, University of Lubeck (J.B.), 23538 Lubeck, Germany

Address all correspondence and requests for reprints to: Dr. J. Born, Clinical Neuroendocrinology, Ratzeburger Allee 160, Haus 23, 23538 Lubeck, Germany. E-mail: born{at}kfg.mu-luebeck.de

The control of body fat is a prominent factor in human health. Animal studies have indicated a homeostatic central nervous system regulation of body fat with particular involvement of the melanocortin receptor pathway. This study provides evidence for a similar role for melanocortins in the long-term control of fat stores in humans. Thirty-six normal weight humans were assigned to one of three experimental groups. After a 4-week baseline, one group was treated with MSH/ACTH_4–10 (MSH/ACTH_4–10) representing the core sequence of all melanocortins. Another group received desacetyl-MSH, a selective agonist of the brain melanocortin-4 receptor, which shares the 4–10 sequence with MSH/ACTH_4–10. The third group received placebo. Treatments were given intranasally twice daily for 6 weeks, at equimolar doses (MSH/ACTH_4–10, 0.5 mg; desacetyl-MSH, 0.84 mg). Body weight, body composition, and plasma hormone concentrations were measured before and after treatment. MSH/ACTH_4–10 reduced body fat, on the average, by 1.68 kg (P < 0.05) and body weight by 0.79 kg (P < 0.001). Concurrently, plasma leptin levels were decreased by 24% (P < 0.02), and insulin levels were decreased by 20% (P < 0.05) after MSH/ACTH_4–10. Changes after desacetyl-MSH remained nonsignificant. The finding of reduced body adiposity after MSH/ACTH_4–10 confirms and extends to the human the findings of animal models indicating an essential role of the hypothalamic melanocortin system in body weight control.

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