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Weight Gain May Not Be Based Just on What You Eat
Study suggests the brain chemical serotonin influences fat metabolism
By Alan Mozes
HealthDay Reporter
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THURSDAY, June 5 (HealthDay News) -- "You are what you eat" is a frustrating truism familiar to the diet-conscious choosing between carrots and carrot cake. But new research suggests that weight control isn't just a matter of what you put in your mouth, but also how the nervous system is genetically predisposed to process fat.
The theory is based on research with worms that suggests that the brain chemical serotonin -- long known for its appetite control properties -- relies on independent but coordinated nerve pathways to drive not only hunger, but also fat metabolism.
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"I want to be clear that there is absolutely nothing in our study that says that good nutrition and activity is not important or not good for you," said study lead author Kaveh Ashrafi, an assistant professor in the department of physiology and the Diabetes Center at the University of California, San Francisco. "But that said, I think that it is important to realize that there is a major contributing factor to body weight that is genetic."
The new findings, based on research with so-called C. elegans worms, is published in the June issue of the journal Cell Metabolism.
Ashrafi and his colleagues noted that, while the worms are obviously smaller and simpler organisms than humans, they are molecularly very close, having about 20,000 genes to a human's 25,000 genes. And both humans and worms have genetically evolved to protect and conserve energy depending on food availability, the researchers said.
Because of such similarities, the researchers attempted to partially deconstruct the worm's nervous system by tracking cell receptors that serotonin connects with when prompting feeding in worms. Then they tracked only those pathways that serotonin activates when regulating fat control.
The researchers were surprised to find that serotonin-directed feeding and fat-burning pathways are, in fact, two separate channels, each operating in a complementary but "molecularly disassociated" fashion.
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Copyright © 2008 ScoutNews, LLC. All rights reserved.
Last updated 6/5/2008
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SOURCES: Kaveh Ashrafi, Ph.D., assistant professor, department of physiology and Diabetes Center, University of California, San Francisco; Alice H. Lichtenstein, D.Sc., director, Cardiovascular Nutrition Lab, Gershoff Professor of Nutrition, USDA Human Nutrition Research Center, Tufts University, Boston, and immediate past chair, nutrition committee, American Heart Association; June 2008, Cell Metabolism
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