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Previous Volume 341:879-884 September 16, 1999 Number 12 Next

	Since this article has no abstract, we have provided an extract of the first 100 words of the full text and any section headings.

	Full Text PDF Editorial by Rosenbaum, M. Add to Personal Archive Add to Citation Manager Notify a Friend E-mail When Cited PubMed Citation

Severely obese (ob/ob) mice are deficient in the adipocyte-derived hormone leptin, which acts on the hypothalamus to control appetite and energy expenditure.¹ The administration of leptin to these mice corrects their obesity by reducing their food intake and increasing their energy expenditure.^2,3,4 These mice also have hyperinsulinemia, corticosterone excess, and infertility, which also are reversed by treatment with leptin.⁵ In humans, serum leptin concentrations, in general, correlate positively with indexes of obesity.^6,7 We previously described two cousins with severe, early-onset obesity and undetectable serum leptin concentrations who were homozygous for a frame-shift mutation in the leptin gene.⁸ In . . . [Full Text of this Article]

Case Report

Methods

Results

Clinical and Anthropometric Features

Body Composition

Energy Intake

Energy Expenditure

Metabolic and Endocrine Status

Pharmacokinetics of Leptin

Discussion

Source Information

From the Departments of Medicine and Clinical Biochemistry (I.S.F., G.L., S.O.) and Paediatrics (I.A.H.), Addenbrooke's Hospital, Cambridge, United Kingdom; the Medical Research Council Dunn Clinical Nutrition Unit, Cambridge, United Kingdom (S.A.J., A.M.P.); Amgen, Thousand Oaks, Calif. (E.L., M.A.M.); and the Department of Paediatrics, Wycombe Hospital, High Wycombe, United Kingdom (C.H.C.).

Address reprint requests to Dr. O'Rahilly at the Departments of Medicine and Clinical Biochemistry, Box 157, Addenbrooke's Hospital, Cambridge CB2 2QQ, United Kingdom, or at sorahill@hgmp.mrc.ac.uk.

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