Nicholson Lecture 2017 by Dr. Jeffrey M. Friedman

Nicholson Lecture 2017

Titel: Leptin Physiology, Pathophysiology and the Neural Control of Feeding Behavior by Dr. Jeffrey M. Friedman. 



Leptin is an adipose tissue hormone that maintains homeostatic control of adipose tissue mass. This endocrine system thus serves a critical evolutionary function by protecting individuals from the risks associated with being too thin (starvation) or too obese (predation). Mutations in leptin or its receptor cause massive obesity in mice and humans, and leptin can effectively treat obesity in leptin deficient patients. The identification of leptin has thus provided a framework for studying the regulation of feeding behavior and the pathogenesis of obesity.

While most obese patients have high endogenous levels of leptin indicating that they are leptin resistant , obese patients with low endogenous levels show robust weight loss with leptin treatment. Leptin also links changes in nutrition to adaptive responses in other physiologic systems with effects on insulin sensitivity, fertility, immune function and neuroendocrine function (among others). Leptin is an approved treatment for generalized lipodystrophy, a condition associated with severe diabetes, and has also shown promise for the treatment of other types of diabetes and for hypothalamic amenorrhea, an infertility syndrome in females.

The identification of leptin has also advanced our understanding of the neural mechanisms that control feeding. Current research focuses on the function of specific neural populations in the hypothalamus and other brain regions. The role of these neural subtypes is being evaluated by identifying molecular markers for specific subpopulations modulating their activity.


Lecturer Dr. Jeffrey M. Friedman

Dr. Jeffrey Friedman is a physician scientist studying the molecular mechanisms that regulate body weight. Dr. Friedman's 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 on leptin is aimed at understanding the genetic basis of obesity in human and the neural mechanisms by which leptin transmits its weight reducing signal.

Dr. Friedman is currently a Professor at the Rockefeller University and an Investigator at the Howard Hughes Medical Institute. Friedman's affiliation with The Rockefeller University began in 1980, where he was awarded a Ph.D. degree in 1986. He. Also received an MD. degree from Albany Medial College in 1977 and completed a medical residency at Albany Medical College in 1980.

His many awards and honors include the 2010 Albert Lasker Basic Medical Research Award, the BBVA Foundation Frontiers of Knowledge Award, the Shaw Prize for Life Sciences and Medicine, and the Gairdner Foundation International Award. His work was referred to in Time Magazine's Best of Science Section in 1995 and 1996 and in 1995 he also received Popular Science's, Best of Science Award. He has received honorary degrees from Yale University, LSU, Bilkent University and the University of Maastricht.