Gene Deletion Shields Mice from Obesity Despite High-Fat Diet

Researchers discover a gene linked to mitochondrial dysfunction and metabolic disruption in obesity, offering potential new therapeutic target.

Researchers at the University of California San Diego School of Medicine discovered that a high-fat diet causes fat cell mitochondria in mice to fragment into smaller, less efficient units, a process controlled by a single gene.
By deleting this gene, associated with the molecule RaIA, the mice were protected from weight gain despite consuming the same high-fat diet.
The study revealed that this mitochondrial fragmentation leads to reduced ability to burn fat, contributing to metabolic disruption in obesity.
The researchers found that some of the proteins affected by RaIA in mice are analogous to human proteins that are associated with obesity and insulin resistance, suggesting that similar mechanisms may be driving human obesity.
The findings suggest a new therapeutic target for obesity treatment in humans, by targeting the RaIA pathway with new therapies.