Researchers at a leading U.S. institute have successfully targeted a specific gene in mice brains. By deactivating it, they reduced the animals' food intake and increased their drive to exercise. This breakthrough paves the way for potential new obesity treatments in humans.
A team from the Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD) aimed to alter eating and activity behaviors in mice. Their study, published in JCI Insight on November 3, 2020, details how they deactivated a gene in the mice's brains. This led to diminished food attraction paired with heightened exercise motivation. The researchers now explore adapting this approach for human therapies.
Obesity poses a major public health challenge, influenced by genetics, environment, and lifestyle. It raises risks for cardiovascular diseases like heart attacks and strokes, type 2 diabetes, musculoskeletal issues such as osteoarthritis, and cancers including breast and colon. These findings highlight genetics' role in developing innovative treatments.
The habenula resides in the epithalamus, the dorsal part of the diencephalon, alongside the pineal gland and stria medullaris. Though not fully understood, the habenular neural circuit draws growing interest for its links to addiction, motivation, depression, and reward processing. It's modulated by the Prkar2a gene.
A 2012 French study showed that disrupting the habenular circuit prevented obesity in mice fed a high-fat diet. Similarly, the NICHD research reduced appeal for rewarding foods while promoting physical activity.
Could this combat human obesity? It's promising, but therapies must undergo extensive long-term animal testing to ensure safety and minimize side effects before human trials.
