The prevalence of obesity has nearly tripled globally since 1975, emerging as a significant health concern. While lifestyle factors such as diet and exercise contribute to obesity, researchers from the University of California San Diego School of Medicine have uncovered new insights into how obesity affects mitochondria, the cellular structures responsible for energy production.
In a study published in Nature Metabolism on January 29, 2023, the researchers observed that mice fed a high-fat diet experienced the fragmentation of mitochondria within their fat cells, resulting in smaller mitochondria with reduced fat-burning capacity. They identified a single gene, RaIA, that controls this process. When this gene was deleted in the mice, it protected them from excessive weight gain, even when consuming the same high-fat diet.
Obesity affects over 40% of adults in the United States, leading to an accumulation of excess fat primarily stored in adipose tissue. The researchers focused on understanding how obesity-induced metabolic abnormalities begin, particularly within fat cells. Mice fed a high-fat diet exhibited mitochondrial fragmentation in their adipose tissue, indicating reduced fat-burning efficiency.
The study revealed that RaIA, when overactive, interferes with normal mitochondrial functioning, contributing to the metabolic issues associated with obesity. By deleting the RaIA-associated gene, the researchers protected the mice from diet-induced weight gain. Further analysis indicated that some proteins affected by RaIA in mice are analogous to human proteins associated with obesity and insulin resistance.
The findings suggest potential avenues for developing therapies that target the RaIA pathway to address obesity and associated metabolic issues, offering exciting possibilities for future treatments.