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Phase III+: The University is open for expanded research operations; only authorized personnel will be admitted on campus. More info here.
Phase III+: The University is open for expanded research operations; only authorized personnel will be admitted on campus. More info here.
Phase III+: The University is open for expanded research operations; only authorized personnel will be admitted on campus. More info here.

Jeffrey M. Friedman receives Albert Lasker Award for discovery of leptin

This year’s Albert Lasker Award for Basic Medical Research, the most prestigious American prize in science, honors Rockefeller University’s Jeffrey M. Friedman, who discovered leptin, a hormone that regulates food intake and body weight. Friedman, who is the Marilyn M. Simpson Professor and head of the Laboratory of Molecular Genetics at Rockefeller University, shares the award with Douglas L. Coleman, emeritus scientist at
The Jackson Laboratory. The award will be presented at a luncheon ceremony on Friday, October 1, in New York City.

Jeffrey M. Friedman

Now in its 65th year, the Lasker Award is the nation’s most distinguished honor for outstanding contributions to basic and clinical medical research. Seventy-nine Lasker Laureates have received the Nobel Prize, including 30 in the last two decades. Twenty-one Lasker Award recipients are associated with The Rockefeller University.

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, including certain forms of diabetes, and for women with hypothalamic amenorrhea, infertility that is sometimes seen in extremely lean women.

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.

However, the majority of obese people have very high levels of leptin circulating in their blood. Friedman’s lab went on to show that high leptin levels are associated with resistance to leptin and provided evidence that suggests that animals destined to be obese increase their production of leptin to satisfy a higher set point for weight. These observations have reframed views on the pathogenesis of obesity and suggested that the development of approaches to improve leptin response in resistant individuals could provide new treatments for obesity.

The ob mouse was first discovered in 1950 by researchers at The Jackson Laboratory. Then in 1966, animal care technicians noticed some young mice that were much fatter than their siblings, with symptoms of diabetes. It was Friedman’s Lasker Award co-recipient, Coleman, who became interested in these mice, known as diabetes (db) mutant mice, for his studies of metabolic pathways.

Coleman conducted a series of experiments that led him, in 1973, to propose the existence of a “satiety factor” (later identified as leptin) that the obese mice fail to produce and that the diabetes mice produce but do not respond to. He later wrote that his work with the obese and diabetes mice “established that the severity of the diabetes was dependent on unknown modifying genes.”

Friedman graduated from Rensselaer Polytechnic Institute and, in 1977 at the age of 22, received his M.D. from Albany Medical College of Union University. After completing a medical and chief residency at Albany Medical Center Hospital, Friedman came to Rockefeller as a postgraduate fellow and associate physician in 1980. In 1986 he received his Ph.D., working in the lab of James E. Darnell Jr., and was appointed assistant professor. In 1991 he was named head of laboratory, and in 1995 he was promoted to professor. He was appointed the Marilyn M. Simpson Professor in 1999. He has been an investigator at the Howard Hughes Medical Institute since 1986.

In addition to the Lasker Award, Friedman’s many honors include the 2009 Shaw Prize in Life Science and Medicine (shared with Coleman), 14th annual Keio Medical Science Prize, the 2007 Jessie Stevenson Kovalenko Medal, the sixth Danone International Prize for Nutrition, the 2004 Gairdner Foundation International Award and the 2004 Passano Foundation Award. Friedman is a member of the U.S. National Academy of Sciences and its Institute of Medicine.

The Lasker Foundation