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Obesity, which affects more than 40 percent of U.S. adults, arises when the body stores excess fat, primarily in adipose tissue. While adipose tissue is an important source of energy, its capacity to produce energy in the setting of obesity diminishes, complicating weight loss efforts. A recent study demonstrates that obesity promotes fragmentation of the mitochondria in adipose cells, resulting in smaller and less effective mitochondria with reduced fat-burning capacity.

Researchers fed mice an obesogenic diet and assessed its effects on their fat cells' mitochondrial function. Then, they analyzed gene activity in fat samples collected from people with obesity.

They found that after eating a high-fat diet, mitochondria in the animals' adipose cells underwent fragmentation, forming smaller, less efficient mitochondria with diminished fat-burning capabilities. This metabolic alteration was orchestrated by the activity of RaIA, a molecule that serves various roles, one of which involves assisting in the breakdown of dysfunctional mitochondria. Deleting this gene in the mice prevented excessive weight gain despite consuming an obesogenic diet, highlighting RaIA’s crucial role in transitioning from a healthy weight to obesity. They also found evidence of increased gene activity in people with obesity that corresponded with persistent elevation in RalA.

These findings suggest that obesity induces fragmentation of mitochondria, compromising their function and driving a vicious cycle of diminished fat-burning capability and increased body fat gain. Evidence suggests cold exposure and fasting promote weight loss. Learn more in this episode featuring Dr. Ray Cronise.

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