US researchers have identified a molecule in the blood that is produced during exercise that can effectively reduce food intake and obesity in rats. These findings, published in “Nature,” not only improve the understanding of the physiological processes that underlie the interaction between exercise and appetite, but also suggest a way to design the long-awaited anti-obesity pill.
“Regular exercise has been shown to help with weight loss, controls appetite and especially in overweight and obese people,” says study co-author Yong Xu and professor of pediatrics-nutrition and molecular and cell biology at Baylor College of Medicine. If we can understand the mechanism by which exercise triggers these benefits, we will be closer to helping many people improve their health.”
“We wanted to understand how exercise works at the molecular level so that we can capture some of its benefits,” says co-author Jonathan Long, professor of pathology at Stanford Medicine and associate professor of Stanford Chem-H (Chemistry, Engineering and ” Institute of Medicine for Human Health. “For example, elderly or frail people who cannot exercise enough may one day benefit from taking a drug that can help prevent osteoporosis, heart disease, or other conditions.”
Xu, Long and their colleagues conducted a comprehensive analysis of the compounds in the blood plasma of rats.s after a race, The most significantly inspired molecule was a modified amino acid called Lac-Phe. It is synthesized from lactate (a byproduct of vigorous exercise that is responsible for muscle burning) and phenylalanine (an amino acid that is one of the building blocks of protein).
In rats with diet-induced obesity (fed a high-fat diet), a high dose of Lac-Phe produced approximately 50 percent compared to control rats over a 12-hour period, without affecting your movement or energy expenditure. Suppressed food intake by %. When administered to rats for 10 days, Lac-Fe reduced cumulative food intake and body weight (due to loss of body fat) and improved glucose tolerance.
The researchers also identified an enzyme called CNDP2, which is involved in the production of Lac-Phe, and showed that mice lacking this enzyme did not lose as much weight on an exercise regimen as a control group on the same exercise plan. did.
Interestingly, the team also observed a strong increase in plasma Lac-Phe levels after physical activity in horses. race and humans,
Data from the human exercise group showed that sprint exercise induced the most dramatic increase in plasma Lac-Phe, followed by resistance training.” This suggests that Lac-Phe is an ancient and conserved system that regulates feeding. ” And it is associated with physical activity in many animal species,” Long said.
“Our next steps include finding out more about how Lac-Phe mediates its effects in the body, including the brain,” Xu said. “Our goal is to learn how to modify this practice pathway for therapeutic intervention.”