FRIDAY, Aug. 3, 2007 (HealthDay News) --A genetic defect in the liver explains why some people become obese while others remain thin, a new study suggests.
The defect may prevent some people's liver enzymes from burning fat effectively and may actually cause people to eat more in an effort to create enough energy for their bodies, according to researchers at the Monell Chemical Senses Center, in Philadelphia. The finding could lead to a genetic test that would identify people at risk of becoming overweight.
"Results of this study help explain the interaction between genes and diet that underlies diet-induced obesity," senior author Mark Friedman said in a prepared statement. "They also point to a way to identify individuals at risk for dietary obesity, perhaps even during childhood before the development of unhealthy eating habits," he said.
Cells burn fat to provide energy for the body. This process, known as fat oxidation, takes place inside mitochondria, the cells' power plants for generating energy. If the ability to oxidize fat is impaired, the body's capacity to make energy is reduced. This leads to increased hunger and overeating, as the body tries to increase the amount of energy available to meet its needs.
Paradoxically, this means people and animals with the genetic inclination to become obese will actually consume more food despite their weight gain. The effect is not noticeable when people and animals are on a low-fat diet -- it is the presence of excess fat in the diet that triggers the problems with oxidation and fat storage, the researchers said.
Friedman's team compared weight gain in rats that were genetically inclined toward obesity with rats that were not. When both groups were fed low-fat diets, the rats all weighed the same, although the obesity-prone rats struggled to burn the same amount of fat. But, when the researchers switched the rats to a high-fat diet, the rats that were genetically inclined toward obesity ate more and gained 36 percent more weight than the slender rats.
The reduction in fat burning capacity is tied to a lack of two liver enzymes -- CD36 and acyl-coenzyme A dehydrogenase, the researchers said. CD36 is responsible for transferring fat into liver cells while the second enzyme begins the oxidation process. A third enzyme, CPT1A, which is responsible for transporting fat into mitochondria, is also less available in obesity-prone rats.
The increasing numbers of obese and overweight people are often thought to be a result of a diet high in calories and carbohydrates. The new study results, available in the August issue of Metabolism, suggest a genetic impact on oxidation at the cellular level as a culprit in weight gain.
"The present findings point to fat oxidation in the liver as a target for the development of drugs that suppress appetite and promote weight loss in obese individuals," Friedman said.
Learn more about obesity from the U.S. Centers for Disease Control and Prevention.