( CPT1c must play a role in feeding beh...)Eat less, weigh more? Enzyme makes lean mice 'susceptible' to dietary fat

And when fed a high-fat diet (mouse chow laced with lard) for 10 weeks, mice lacking CPT1c still ate less than their normal littermates, but they were much heavier.

What scientists already know about the regulation of body weight helps explain why the absence of CPT1c may have its seemingly paradoxical effect.

Under normal circumstances, says Wolfgang, body weight is maintained by a combination of food intake and energy expenditure, how hungry the body is, and how much energy cells need. Many cells in the body use a sugar called glucose as a source of energy. When the body is starved, the body literally feeds on itself, breaking down fat to form fatty acids that fuel energy needs. When the cells of the body are well fed and energy is in ample supply, molecular signals from the brain tell cells in the body to store the excess energy by converting it to fat. Weight gain results when food intake greatly exceeds energy expenditure. But when the brain's appetite/energy regulator is out of whack, so are the rules for gaining and losing weight.

"How do you know when to stop eating?" asks M. Daniel Lane, Ph.D., senior author of the study and a professor of biological chemistry in the Institute for Basic Biomedical Sciences at Hopkins. "The liver sure isn't going to tell you, it just keeps storing fat as long as the body is well fed." Instead, he notes, it is the control regions of the brain, namely the hypothalamus, that governs eating behavior.

Previously, the same researchers showed that a molecule called malonyl-CoA is critical for fat metabolism. And as it turns out, malonyl-CoA interacts with CPT1c, according to Lane.

Increasing the amount of malonyl-CoA in the liver causes those cells to synthesize fat, which is stored. Increasing malonyl-CoA in the hypothalamus somehow tells the cells in the body to break down fats for energy and the muscle cells t
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Source:Johns Hopkins Medical Institutions