Columbia University

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Leibel was known in his younger years, practicing at Harvard and Cambridge City Hospital, as an outstanding pediatric endocrinologist who specialized in hormone disorders. When one of his young patients' frustrated parents made him realize how little he really knew about obesity, he took up a position in Jules Hirsch's laboratory at Rockefeller University in 1978.

Leibel was particularly interested in finding out how the body controlled its weight: altering the "set point". Sometimes thought of as the "Holy Grail" of obesity research, the idea of the set point comes from Jean Mayer (Harvard psychologist), who hypothesized that the body contains a "lipostat" that keeps the amount of fat in the body constant. If researchers learned how to adjust the set point, they could literally control the amount of fat in the body. Leibel threw himself into this work, examining the records of severely obese patients and normal controls at Rockefeller who had lost weight by consuming a special liquid formula as part of clinical studies. Leibel found that the important variable in comparing energy requirements was fat-free body mass—no matter the amount of fat, people with a similar fat-free body mass would require a similar amount of calories. What this meant in practice was that after patients had lost fat below their standard homeostatic point, they would literally require fewer calories to maintain their weight than people who had weighed the same amount as they now weighed and not dieted. Otherwise, they would gain weight.

Leibel realized that some of this body-weight regulation must be genetic, so in i986 he turned his attention with his collaborator Jeff Friedman (then an assistant professor at Rockefeller) to cloning the ob gene, which was thought to be the cause of obesity in rodents. Graduate student Nathan Bahary, lab technician Ricardo Proenca, and postdoctoral fellows Yiying Zhang and Margherita Maffei did painstaking work over the course of six years in the lab to find the mutation, which resulted in the rodent's fat cells producing a nonfunctional version of a protein that would ordinarily function as a hormone that signaled satiety, a hormone called leptin. Their work was published in Nature in 1994, but Bahari and Leibel were left off the author list by Friedman (Shell 2001: 77-104). When the gene was sold by Rockefeller to Amgen for a staggering 20 million dollars up front (the largest sum at the time a patent had ever been sold for) plus promised future payments as the drug based on lep-tin got closer to market, Leibel was not eligible for a cut of this money because he was not on the author list. As a result, he left Rockefeller for Columbia University with Zhang to set up his own laboratory.

According to Leibel's website, the lab's current research in the Genetics of Complex Disorders training program at Columbia includes identifying genes in both rodents and humans related to obesity and Type 2 diabetes, particularly those that regulate homeostasis, leptin, and the glucose/insulin cycle at the molecular level.

SLG/Katharine Mancuso

See also Friedman; Genetics; Homeostasis; Hormone; Metabolism

References and Further Reading

Anon. "Rudy Leibel, MD," Genetics of Complex Disorders Training Program, available online at < Preceptors/Leibel.html> (accessed April 20, 2006). Kolata, Gina (2007) Rethinking Thin: The New Science of Weight Loss—and the Myths and Realities of Dieting, New York: Farrar, Straus and Giroux.

Shell, Ellen Ruppel (2001) The Hungry Gene: The Science of Fat and the Future of Thin, New York: Atlantic Monthly Press.

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