Leptin Researcher to Describe Its Role in Obesity

Jeffrey Friedman


The contribution of the relatively newly discovered hormone leptin to obesity will be the subject of the state-of-the-art lecture by Jeffrey M. Friedman, MD, PhD, on Thursday, November 10, beginning at 8 a.m.

Dr. Friedman is a professor at the Rockefeller University, an investigator at the Howard Hughes Medical Institute, and the director of the Starr Center for Human Genetics in New York City.

Dr. Friedman’s research received national attention in 1994 when he and his colleagues isolated a gene linked to mouse obesity and its human homologue. They subsequently found that injections of the protein leptin decrease body weight in mice by reducing food intake and increasing energy expenditure. In his lecture, “Leptin and the Biological Basis of Obesity,” Dr. Friedman will describe the current state of research in the area, including his approach to understanding the genetic basis of obesity in humans and the mechanisms by which leptin transmits its weight-reducing signal.

Leptin, a hormone made in fat tissue, plays a key role in regulating weight by modulating food intake relative to energy expenditure to maintain weight within a relatively narrow range. Defects in the leptin gene are associated with severe obesity in animals and humans. Leptin acts on neurons in brain centers that control energy balance, and it plays a general role in regulating many of the physiological responses observed with changes in nutritional states, with clear effects on female reproduction, immune function, and the function of other hormones, including insulin.

Dr. Friedman’s lab is active in elucidating the molecular mechanisms responsible for the regulation of gene expression associated with weight change. The amount of leptin expressed from fat is strongly regulated, which suggests that the fat cell knows how much fat it has. To address this question, the lab is using transgenic mice to identify DNA regulatory elements that change expression of a receptor gene controlled by the leptin gene in parallel with changes in adipose tissue mass.

Diet-induced weight loss in humans decreases leptin concentration, which may explain the high failure rate of dieting. Recent clinical studies at Rockefeller University Hospital explored the possibility that administering leptin to dieting patients can alter their response to weight.

Dr. Friedman received his PhD from the Rockefeller University in 1986. He was appointed assistant investigator with the Howard Hughes Medical Institute at Rockefeller in 1986, promoted to associate investigator in 1991, and investigator in 1997. He received his MD from Albany Medical College.

He was elected to the National Academy of Sciences and is a member of its Institute of Medicine. He has received numerous national and international awards, including the Albert Lasker Basic Medical Research Award and the Endocrinology Transatlantic Medal from the United Kingdom’s Society for Endocrinology.

October-November 2011 (Vol. 3, Number 10 & 11)