Jeffrey M. Friedman
Jeffrey Friedman, MD, PhD (born July 20, 1954) is a molecular geneticist at New York City's Rockefeller University and an Investigator of the Howard Hughes Medical Institute. His discovery of the hormone leptin and its role in regulating body weight has had a major role in the area of human obesity. Friedman is a physician scientist studying the genetic mechanisms that regulate body weight. His research on various aspects of obesity received national attention in late 1994, when it was announced that he and his colleagues had isolated the mouse ob gene and its human homologue. They subsequently found that injections of the encoded protein, leptin, decreases body weight of mice by reducing food intake and increasing energy expenditure. Current research is aimed at understanding the genetic basis of obesity in human and the mechanisms by which leptin transmits its weight-reducing signal.
Friedman was born in Orlando, Florida on July 20, 1954, and grew up in North Woodmere, New York, graduating from Hewlett High School in the Class of 1971. As a young man he aspired to becoming a physician. He entered a six-year medical program out of high school and received his M.D. at the age of 22. But after a year-long fellowship working in the laboratory of Mary Jane Kreek, he fell in love with the science life. "As a doctor, you're trained to absorb the facts you're given and accept them," says Friedman. "Science is almost the opposite. It's a frontier of discovery that's always moving. And I decided I wanted to do research." Friedman started his affiliation with the Rockefeller University began in 1980, where he was awarded a Ph.D. degree in 1986. He was appointed Assistant Investigator with the Howard Hughes Medical Institute at The Rockefeller University in 1986, promoted to Associate Investigator in 1991, and Investigator in 1996 and received the Marilyn M. Simpson professorship in 1998. Friedman received an M.D. degree from Albany Medical College in 1977 and completed a medical residency at Albany Medical College in 1980.
When Friedman started his own laboratory at The Rockefeller University, he turned his attention to the question of weight regulation. Working with a special strain of mice, he set out to identify the hormone that normal animals use to control their appetite - a molecular that was missing in the plump rodents. After eight years—on May 8, 1994, at 5:30 a.m.—he found what he was looking for: evidence that he'd located the gene that produces the hormone he later dubbed "leptin", after the Greek word for "thin" (λεπτός leptos). It was astonishingly beautiful, he says of the x-ray film that nailed the gene, a piece of data that now hangs on his office wall.
Numerous lines of evidence have suggested that energy balance in animals and humans is tightly controlled. With the identification of leptin and its receptors by our laboratory, two of the molecular components of a system that maintains constant weight have been identified. Leptin is a hormone secreted by the adipose (fat) tissue in proportion to its mass that in turn modulates food intake relative to energy expenditure. Increased fat mass increases leptin levels, which in turn reduces body weight; decreased fat mass leads to a decrease in leptin] levels and an increase in body weight. By this mechanism, weight is maintained within a relatively narrow range. Defects in the leptin gene are associated with severe obesity in animals and in humans. Leptin acts on sets of neurons in brain centers that control energy balance. Leptin also plays a general role in regulating many of the physiologic responses that are observed with changes in nutritional state, with clear effects on female reproduction, immune function and the function of many other hormones, including insulin.
Leptin feeds into the circuit of neurons in the brain that controls eating and energy expenditure. When an animal loses weight, leptin concentrations fall. This dip in leptin levels instructs the body to search for food. In studies of obese mice, Friedman has found that leptin actually restructures the brain, rewiring the neural circuit that controls feeding. The hormone reinforces the nerve cells that encourage the body to slenderize and prunes the neurons that compel eating.
Friedman has published over one hundred and fifty publications and over ten book chapters.
His work in the area of obesity and the leptin gene has led to Friedman receiving many prestigious awards: Time Magaziness Best of Science section in 1994 and 1996; Popular Sciences Best of Science Award, 1995; The Heinrich Wieland Prize, 1996; The Jacobaeus Prize, 1997, the Steven C. Beering Award, 1999; The Endocrinology Transatlantic Medal, 2000; the Rolf Luft Award, Karolinska Hospital, 2000; elected to the National Academy of Science, 2001, the Bristol-Myers Squibb Award for Distinguished Achievement in Metabolic Research, 2001; the Passano Award, 2005; elected to The Royal Swedish Academy of Sciences, Foreign Member, 2005; the Gairdner International Award, 2005; Kovalenko Medal, 2006; the Danone International Prize, 2007; Keio Medical Science Prize, 2009; the Shaw Prize for Life Sciences and Medicine, 2009; Hamdan Award for Medical Research Excellence, 2009; the Thomson Reuters Citation Laureate, 2010; the Robert J. and Claire Passano Foundation Award, 2010; the Albert Lasker Basic Medical Research Award, 2010; The Foundation IPSEN 11th Endocrine Regulation Prize, 2012; the UCL Prize Lecture in Clinical Science, 2012; the BBVA Frontier of Knowledge Award, 2013; the King Faisal International Prize in Medicine, 2013; and elected to the American Academy of Arts and Sciences, 2013. His work on leptin also garnered him much television time, including an appearance on the PBS show Scientific American Frontiers in a long interview with host Alan Alda.
- Zhang, Y, Proenca, R, Maffei, M, Barone, M, Leopold, L, and Friedman, JM. Positional cloning of the mouse obese gene and its human homologue. Nature, 1994, 372: 425-432.