Impaired brain protein drives fat cravings and obesity in mice
Obesity is a global health concern that can contribute to diabetes, cardiovascular disease and other metabolic disorders. While many health conditions can lead to obesity, an increasingly worrying cause is found on grocery shelves: high-fat foods. These foods are known to be hard to resist and can promote overeating.
A research team led by Professor Shigenobu Matsumura from Osaka Metropolitan University's Graduate School of Human Life and Ecology has discovered that a brain protein called optic atrophy-1 (OPA1) plays a key role in regulating appetite and body weight in mice. The study, published in The FASEB Journal, provides insight into the neural mechanisms behind obesity, which is a growing health concern worldwide.
The researchers compared wild-type mice with mice that had their OPA1 gene disabled specifically in MC4R neurons, which are involved in regulating appetite and energy metabolism. They found that the OPA1-deficient mice consumed more food, especially fat, and gained weight more quickly than their wild-type counterparts, particularly females. Additionally, when given access to both standard chow and soybean oil (a high-fat food source), the OPA1-deficient mice ate more fat and experienced greater weight gain.
The study also tested the effectiveness of setmelanotide, a drug that targets the MC4R receptor to suppress appetite, on both male and female OPA1-deficient mice. While the drug reduced appetite in male mice, its effectiveness was significantly diminished in female mice, suggesting that sex-specific differences may play a role in OPA1's impact on obesity.
Professor Matsumura concluded that these findings offer valuable insights into the molecular mechanisms underlying obesity, particularly from the perspective of neuronal energy metabolism. The sex differences observed in OPA1 responses and susceptibility to obesity could help inform the development of more targeted obesity treatments and personalized medicine approaches.
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