Rats prone to obesity had decreased expression of fat oxidation molecules.

Researchers at the Monell Chemical Senses Center identified a genetically transmitted metabolic defect that can lead to obesity in some individuals. The defect involves decreased production of liver enzymes needed to burn fat.

If the ability to oxidize fat is impaired, the body’s capacity to make energy is reduced, which leads to increased hunger and overeating. To determine whether preexisting differences in fat oxidation might contribute to individual susceptibility to diet-induced obesity, researchers used rats that differ in their genetic predisposition to gain weight and become obese when fed a high-fat diet.

The closely-related rat strains weigh the same and eat the same amount of calories when fed a low-fat diet. However, the team found that when switched to a high-fat diet, the strain that is obesity-prone overeats and becomes obese, while the obesity-resistant strain does not.

The scientists also discovered that even when eating a low-fat diet and still lean, the obesity-prone rats were less able to burn fat than were the obesity-resistant rats.

This intrinsic deficit in fat oxidation was associated with a decrease in the capacity to make two liver enzymes. CD36 is responsible for transferring fat fuels into liver cells, while acyl-coenzyme A dehydrogenase begins the oxidation process in mitochondria.

When fed a high-fat diet, the obesity-prone rats overate and became obese, gaining 36% more than resistant animals. Fat oxidation was further compromised due to the rats’ decreased ability to make CPT1A, the liver enzyme responsible for transporting fat into mitochondria.

The study will be published in the August issue of Metabolism.

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