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PARIS (AFP) - To the dismay of people who seem never to be able to lose weight no matter how hard they diet, genetic scientists have found that the body's fat-control mechanisms are much more complex than previously thought.
A leading target for obesity is how stored fat is converted into a form of energy known as triglycerides. Researchers from the Gladstone Institute of California and the University of Colorado Health Sciences Center have discovered that this process is more complicated than thought.
In May's issue of the US specialist journal Nature Genetics, they describe how they tested mice, which had been engineered to be deficient in a gene that controls a key enzyme called DGAT. According to conventional thinking, DGAT is what converts triglyceride. If its controlling gene can be switched on or off, a person could put on weight or burn it off accordingly.
But the researchers were surprised to find that the modified mice remained skinny, even when fed on high-fat food that made normal mice become chubby. For some reason, the DGAT-deficient mice developed a higher metabolic rate that caused them to use more energy, they found. This can only mean there are "multiple mechanisms" for synthesizing triglycerides, they conclude.
In an adjoining commentary, Ronald Kahn of Harvard Medical School says the discovery is the latest piece to add to the intricate puzzle of how fat is regulated. "The genetic discoveries made over the past decade indicate that the regulation of adipose tissue mass is not as simple as we used to think - and that staying thin is even harder than it used to be," he writes.
Thinking about fat has changed enormously over the past few decades. Previously, doctors thought that people gained weight if they ate too much or failed to exercise enough or had a low metabolic rate.
That simplistic view is being replaced by a tableau of complex molecular pathways - the hormones and enzymes, controlled by genes, which determine our appetite and whether fat is used or stored
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