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Washington DC: Since 1975, the number of obese people has nearly tripled, creating a global epidemic.

Washington DC: Since 1975, the number of obese people has nearly tripled, creating a global epidemic. While lifestyle variables such as nutrition and exercise contribute to the development and progression of obesity, scientists have shown that obesity is also linked to intrinsic metabolic abnormalities. Researchers from the University of California, San Diego School of Medicine have thrown fresh light on how obesity affects our mitochondria, the vital energy-producing organelles in our cells.

In a study published in Nature Metabolism, the researchers found that when mice were fed a high-fat diet, mitochondria within their fat cells broke apart into smaller mitochondria with reduced capacity for burning fat. Further, they discovered that this process is controlled by a single gene. By deleting this gene from the mice, they were able to protect them from excess weight gain, even when they ate the same high-fat diet as other mice.

"Caloric overload from overeating can lead to weight gain and also triggers a metabolic cascade that reduces energy burning, making obesity even worse," said Alan Saltiel, PhD, professor in the Department of Medicine at UC San Diego School of Medicine. "The gene we identified is a critical part of that transition from healthy weight to obesity."

Obesity, which affects more than 40% of adults in the United States, occurs when the body accumulates too much fat, which is primarily stored in adipose tissue. Adipose tissue normally provides important mechanical benefits by cushioning vital organs and providing insulation. It also has important metabolic functions, such as releasing hormones and other cellular signaling molecules that instruct other tissues to burn or store energy.