Researchers from Baylor College of Medicine, Stanford School of Medicine and collaborating institutions reported today in the journal nature that they have identified a molecule in the blood that is produced during exercise and can effectively reduce food intake and obesity in mice. The results improve our understanding of the physiological processes that underlie the interaction between exercise and hunger.
“Regular exercise has been shown to help lose weight, regulate appetite and improve the metabolic profile, especially in overweight and obese people,” said co-correspondent Dr. Yong Xu, professor of pediatrics – nutrition and molecular and cell biology in Baylor. “If we can understand the mechanism by which exercise causes 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 co-correspondent Jonathan Long, MD, assistant professor of pathology at Stanford Medicine and a Stanford ChEM-H Fellow. (Chemistry, Engineering and Medicine for Human Health). “For example, older or weak people who can’t exercise enough may one day benefit from taking a drug that can help slow osteoporosis, heart disease or other conditions.
Xu, Long, and their colleagues conducted comprehensive analyzes of compounds in the blood plasma of mice after intense treadmill running. The most significantly induced molecule is 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 building blocks of protein).
In mice with diet-induced obesity (fed a high-fat diet), a high dose of Lac-Phe suppressed food intake by about 50% compared to control mice over a 12-hour period without affecting their movement or energy consumption. When administered to mice for 10 days, Lac-Phe reduces cumulative food intake and body weight (due to weight loss) and improves glucose tolerance.
The researchers also identified an enzyme called CNDP2, which is involved in the production of Lac-Phe, and showed that mice without this enzyme did not lose as much weight on an exercise regimen as the control group on the same exercise plan.
Interestingly, the team also found a strong increase in Lac-Phe plasma levels after physical activity in racehorses and humans. Data from a cohort of human exercise showed that sprint exercise caused the most dramatic increase in Lac-Phe plasma, followed by resistance training and then endurance training. “This suggests that Lac-Phe is an ancient and well-preserved system that regulates nutrition and is associated with physical activity in many animal species,” Long said.
“Our next steps include finding more details about how Lac-Phe mediates its effects in the body, including the brain,” Sue said. “Our goal is to learn to modulate this path of therapeutic intervention exercises.”
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Jonathan Long, an exercise-induced metabolic that suppresses nutrition and obesity, nature (2022). DOI: 10.1038 / s41586-022-04828-5. www.nature.com/articles/s41586-022-04828-5
Provided by Baylor College of Medicine
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