The benefits of exercise on a pill? Science is closer to that goal

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Baylor College of Medicine, Stanford School of Medicine and collaborating institutions reported today in the journal Nature they have identified a molecule in the blood that can be used to effectively reduce food intake and obesity in mice. The findings improve understanding of the physiological processes underlying the interaction between exercise and hunger.

“Regular exercise has been shown to help lose weight, regulate appetite, and improve metabolic profile, especially for people who are overweight and obese,” said Dr. Yong Xu, professor of pediatrics, nutrition and molecular and cellular biology. Baylor. “If we 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 that we can reap some of its benefits,” said Dr. Jonathan Long, an assistant professor of pathology at Stanford Medicine and an Institute Scholar at Stanford ChEM-H. Human Health Chemistry, Engineering and Medicine). “For example, it may be beneficial to take a medication that can help slow down osteoporosis, heart disease, or other conditions that may not be enough to help you get enough exercise.”

Xu, Long, and their colleagues performed a comprehensive analysis of the blood-plasma compounds of the mice after running on the tape. The most significant induced molecule was a modified amino acid called Lac-Phe. It is synthesized from lactate (a byproduct of a strenuous exercise responsible for burning sensation in the muscles) and phenylalanine (an amino acid that is one of the components of proteins).

In diet-induced obese mice (fed a high-fat diet), a high dose of Lac-Phe reduced food intake by about 50% compared to control mice within 12 hours without affecting their movement or energy expenditure. 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 that enzyme did not lose as much weight in an exercise regimen as a control group in the same exercise plan.

Interestingly, the team also found strong increases in Lac-Phe plasma levels after physical activity in racehorses and humans. Data from a human exercise cohort showed that the sprint exercise resulted in a significant increase in Lac-Phe plasma, followed by resistance training, and then resistance training. “This suggests that Lac-Phe is an old and well-preserved system that regulates feeding and is associated with physical activity in many animal species,” Long said.

“Our next step is to find out more about how Lac-Phe focuses its effects on the body, including the brain,” Xuk said. “Our goal is to learn how to modulate this exercise pathway for therapeutic interventions.”


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More information:
Jonathan Long, a metabolite that causes exercises that eliminate nutrition and obesity, Nature (2022). DOI: 10.1038 / s41586-022-04828-5. www.nature.com/articles/s41586-022-04828-5

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