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This Article Full Text (Publish Ahead of Print[PDF]) All Versions of this Article: 89/3/973S    most recent ajcn.2008.26788Bv1 Purchase Article View Shopping Cart Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Friedman, J. M Search for Related Content PubMed PubMed Citation Articles by Friedman, J. M Agricola Articles by Friedman, J. M

Leptin at 14 y of age: an ongoing story^1,2,3,4

¹ From the Howard Hughes Medical Institute, The Rockefeller University, New York, NY.

² Presented at the symposium "Leptin: Weight Management and Beyond," held at Experimental Biology 2008, San Diego, CA, 6 April 2008.

³ Supported by NIH grant DK041096, the Picower Foundation, and the Howard Hughes Medical Institute.

⁴ Reprints not available. Address correspondence to JM Friedman, the Howard Hughes Medical Institute, The Rockefeller University, 1230 York Avenue, Campus Box 305, New York, NY 10065. E-mail: friedj{at}rockefeller.edu.

ABSTRACT

The cloning of the ob gene and its gene product leptin has led to the elucidation of a robust physiologic system that maintains constancy of fat stores. Leptin is a peptide hormone secreted by adipose tissue and regulates adipose tissue mass and energy balance. Recessive mutations in the leptin gene are associated with massive obesity in mice and in some humans, which establishes a genetic basis for obesity. Leptin circulates in blood and acts on the brain to regulate food intake and energy expenditure. When fat mass decreases, plasma leptin concentrations decrease, which stimulates appetite and suppresses energy expenditure until fat mass is restored. When fat mass increases, leptin concentrations increase, which suppresses appetite until weight is lost. This system maintains homeostatic control of adipose tissue mass.

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