Jeffrey Friedman receives Shaw Prize for discovery of leptin

Published on June 16, 2009 at 4:55 PM · No Comments

Jeffrey M. Friedman, Marilyn M. Simpson Professor and head of the Laboratory of Molecular Genetics at Rockefeller University, has received the 2009 Shaw Prize in Life Science and Medicine. The prize was announced today by the Hong Kong-based Shaw Prize Foundation.

Friedman shares the $1 million award with Douglas L. Coleman, emeritus scientist at The Jackson Laboratory, for their work leading to the discovery of leptin, a hormone that regulates food intake and body weight.

Prior to Friedman's groundbreaking research, little was known about the components of the biologic system that controls weight, with many scientists questioning the very existence of such a homeostatic system. The discovery of leptin provided a genetic explanation of obesity and has challenged the popular belief that lack of willpower causes people to be obese.

With the discovery of leptin and Friedman's subsequent studies, the logic of an entirely new physiological system has been established with direct implications for the pathophysiology of human obesity. In addition to providing scientists with a new target for treating obesity, the discovery has helped scientists develop treatments for other metabolic conditions, such as diabetes, and for women with hypothalamic amenorrhea.

In December 1994, Friedman, who also is an investigator at the Howard Hughes Medical Institute, and his colleagues published a landmark paper in the journal Nature, in which they identified a gene in mice and humans called obese (ob) that codes for a hormone he later named leptin, after the Greek word leptos, for thin. Friedman and colleagues showed that leptin is a hormonal signal made by the body's fat cells that regulates food intake and energy expenditure. Leptin has powerful effects on reproduction, metabolism, other endocrine systems and even immune function.

Mice that lack ob, and thus do not produce leptin, are massively obese, weighing as much as three times the size of their normal littermates. Friedman showed that after normal and ob-deficient mice are injected with synthetic leptin, they are more active and lose weight. In addition, humans lacking leptin eat copious amounts and are massively obese. Leptin treatment of these individuals leads to massive weight loss. The dramatic effect of leptin in these patients establishes a key role for this hormone in human physiology.

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