Benefits of Exercise on Pills? Science is closer to that goal

Summary: Scientists have identified a molecule formed in the blood during exercise. The molecule, Lac-Phe, can effectively reduce nutrition and obesity in mouse models.

A source: Baylor Medical College

Researchers from Baylor College of Medicine, Stanford School of Medicine and Collaborative Institutes will report to the journal today. nature they have identified a molecule in the blood that is formed during exercise and can effectively reduce nutrition and obesity in mice.

The results improve understanding of the physiological processes underlying the interaction between exercise and starvation.

“Regular exercise has been shown to help lose weight, regulate appetite and improve the metabolic profile, especially for overweight and obese people,” said Dr. Co-Correspondent. Yong Xu, Professor of Pediatrics and Nutrition and Molecular and Cell Biology at Baylor.

“If we can understand the mechanism by which exercise benefits these benefits, we will be able to help more people improve their health.”

“We want to understand how exercise works at the molecular level and see some of its benefits,” said correspondent Jonathan Long, a doctor of medical sciences, assistant professor of pathology at Stanford Medicine, and a scientist at the Stanford ChEM-H Institute. Chemistry, engineering and medicine for human health).

“For example, older or weaker people who can’t get enough exercise may one day benefit from medications that can help slow osteoporosis, heart disease, or other conditions.”

Xu, Long, and their colleagues performed a comprehensive analysis of blood plasma compounds after intense mouse running. The most important induced molecule was a modified amino acid called Lac-Phe. It is synthesized from lactate (a by-product of strenuous exercise responsible for muscle burning sensation) and phenylalanine (an amino acid that is one of the building blocks of proteins).

In diet-derived obese mice (fed a high-fat diet), high doses of Lac-Phe reduced food intake by 12% over 12 hours without affecting their movement or energy expenditure compared to control mice. When administered to mice for 10 days, Lac-Phe reduced concentrated food intake and body weight (due to body fat loss) and improved glucose tolerance.

Researchers have identified a molecule in the blood that is formed during exercise and can effectively reduce malnutrition and obesity in mice. Image in public domain

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 in the same exercise regimen as the control group on the same exercise plan.

Interestingly, the team also observed a strong increase in plasma Lac-Phe levels after the physical activity of racehorses and humans. Data from the human exercise cohort showed that sprint exercise stimulated the sharpest increase in plasma Lac-Phe, followed by resistance and endurance training.

“This shows that Lac-Phe regulates nutrition and is an ancient and preserved system associated with the physical activity of many animal species,” Long said.

“Our next steps include finding out more about how Lac-Phe mediated its effects on the body, including the brain,” Sue said. “Our goal is to learn how to modulate this exercise pathway for therapeutic interventions.”

It’s about exercise and neuroscience research news

Author: Press service
A source: Baylor Medical College
The connection: Press Service – Baylor Medical College
Photo: Image in public domain

Original study: Closed access.
Jonathan Long nature

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Abstract

An exercise-inducing metabolite that suppresses nutrition and obesity

Exercise protects against overweight, type 2 diabetes and other cardiovascular diseases. However, the molecular and cellular mechanisms that mediate the metabolic benefits of physical activity remain unknown.

Here we show that exercise stimulates production Do not-lactoil-phenylalanine (Lac-Phe), a signal metabolite that passes through the blood, suppresses nutrition and obesity.

Lac-Phe biosynthesis from lactate and phenylalanine occurs in CNDP2.+ cells, including macrophages, monocytes, and other immune and epithelial cells localized to various organs. Pharmacological increases in Lac-Phe in diet-derived obese mice reduce food intake without affecting movement or energy expenditure.

Chronic administration of Lac-Phe reduces fat and body weight and improves glucose homeostasis. In contrast, genetic ablation of Lac-Phe biosynthesis in mice increases nutrition and obesity after exercise.

Finally, significant increases in circulating Lac-Phe activity are also observed in humans and runners, marking the metabolite as a molecular effector associated with physical activity across several activity modes and mammalian species.

These data identify stored exercise-induced metabolites that control the effects of food and systemic energy balance.

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