Prior to his 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. With leptin and Friedman's subsequent studies, the logic of an entirely new physiologic system has been established with direct implications for the pathophysiology of human obesity.
Friedman, Marilyn M. Simpson Professor and head of the Laboratory of Molecular Genetics at Rockefeller and an investigator at the Howard Hughes Medical Institute, received the Gairdner Award and gave a talk on the genetic roots of obesity on Tues., April 5 in Toronto, Canada. On Tues., April 19, he will receive the Passano Award at the Center Club in Baltimore, Md., and give the Passsano Foundation Award lecture at Johns Hopkins University School of Medicine.
Discovery of leptin and its role in regulating body weight
In December 1994, Friedman 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 as their normal littermates. Friedman showed that after normal and ob mice are injected
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