Scientists have identified a molecule in the blood, created during exercise, that can effectively reduce food intake and obesity in mice.
The Benefits of Exercise on a Pill? Science is now closer to that goal.
Researchers have identified a molecule in the blood that occurs during exercise that can effectively reduce food intake and obesity in mice. The discovery enhances our understanding of the physiological processes underlying the interaction between exercise and appetite. Scientists at Baylor College of Medicine, the Stanford School of Medicine and collaborating institutions reported the findings on June 15 in the journal Nature.
“Regular exercise has been shown to help with weight loss, regulate appetite and improve the metabolic profile, especially for overweight and obese people,” said co-author Dr. Yong Xu, professor of pediatrics. – nutrition and molecular and cell biology at Baylor. “If we can understand the mechanism by which exercise triggers these benefits, then we are closer to helping many people improve their health.”
“We wanted to understand how exercise works at the molecular level so we can capture some of its benefits,” said lead author Jonathan Long, MD, an adjunct professor of pathology at Stanford Medicine and a researcher at the Stanford ChEM-H Institute. Chemistry, Engineering and Medicine for Human Health). “For example, elderly or frail people who can’t get enough exercise may one day benefit from taking a medication that can help curb osteoporosis, heart disease, or other conditions.”
Xu, Long, and their colleagues performed thorough analyzes of mouse blood plasma compounds after an intense tape run. The most significantly induced molecule was a modified amino acid called Lac-Phe. It is synthesized from lactate (a byproduct of intense exercise that is responsible for the burning sensation in the muscles) and phenylalanine (an amino acid that is one of the basic components of proteins).
In diet-induced obese mice (fed a high-fat diet), a high dose of Lac-Phe suppressed food intake by 50% compared to control mice for an unaffected 12-hour period. its movement or energy expenditure. When administered to mice for 10 days, Lac-Phe 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 involved in the production of Lac-Phe and showed that mice that did not have this enzyme did not lose as much weight in an exercise regimen as a control group in the same plan. exercise.
Interestingly, the team also found robust elevations in Lac-Phe plasma levels after physical activity in racehorses and humans. Data from a cohort of human exercises showed that sprint exercise induced the most dramatic increase in plasma Lac-Phe, followed by a resistance workout and then a resistance workout. “This suggests that Lac-Phe is an ancient and preserved system that regulates feeding and 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 on the body, including the brain,” Xu said. “Our goal is to learn how to modulate this exercise pathway for therapeutic interventions.”
Reference: “An exercise-inducible metabolite that suppresses diet and obesity” by Veronica L. Li, Yang He, Kevin Contrepois, Hailan Liu, Joon T. Kim, Amanda L. Wiggenhorn, Julia T. Tanzo, Alan Sheng-Hwa Tung, Xuchao Lyu, Peter-James H. Zushin, Robert S. Jansen, Basil Michael, Kang Yong Loh, Andrew C. Yang, Christian S. Carl, Christian T. Voldstedlund, Wei Wei, Stephanie M. Terrell , Benjamin C. Moeller, Rick M. Arthur, Gareth A. Wallis, Koen van de Wetering, Andreas Stahl, Bente Kiens, Erik A. Richter, Steven M. Banik, Michael P. Snyder, Yong Xu and Jonathan Z. Long, June 15, 2022, Nature. DOI: 10.1038 / s41586-022-04828-5