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Serotonin the Answer for Anti-Obesity Treatment

complications, Dr. Elmquist said.

The drug was removed from the market in 1997.But the mechanisms of how it caused weight loss were never fully determined, he said. So a few years ago, Dr. Elmquist and his research team set out to detail how fenfluramine affected the brain's molecular pathways to reduce appetite. In 2002, they examined the region of the brain's hypothalamus containing the arcuate nucleus, or ARC. In the ARC, drug-induced serotonin activates brain cells called pro-opiomelanocortin neurons, or POMC, which in turn release a hormone that acts on the MC4R to reduce appetite. The team's new study shows how serotonin also simultaneously blocks other neurons, known as NPY/AgRP, from being able to inhibit activity of MC4Rs. By blocking this inhibitory activity, serotonin prevents an increase in appetite.

Researchers studied the effect of Fen-phen and other serotonin-inciting drugs on both normal and genetically engineered lean and obese mice. They found that serotonin's dual regulation of POMC and AgRP neurons is necessary to promote weight loss. ‘The finding increases the understanding of the molecular circuitry that controls body weight in response to changing levels of serotonin,’ Dr. Elmquist said.

‘An overarching goal of this understanding, for humans, is to design specific, safe drugs to fight obesity.’ Dr. Elmquist, who recently left Harvard Medical School, directs the newly formed Center for Hypothalamic Research at UT Southwestern. The center, along with the Taskforce for Obesity Research, a National Institutes of Health Interdisciplinary Research Center, is part of the institution's effort to investigate the causes of obesity, metabolic syndrome and diabetes.

Source: Eurekaert
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