Summary: Researchers have identified a molecule in the blood that is produced during exercise. The molecule, Lac-Phe, can effectively reduce food intake and obesity in mouse models.
Source: Baylor College of Medicine
Researchers from Baylor College of Medicine, Stanford School of Medicine, and collaborating institutions report today in the journal Nature who identified a molecule in the blood that is produced during exercise and can effectively reduce food intake and obesity in mice.
The findings improve our understanding of the physiological processes that underlie the interaction between exercise and hunger.
“Regular exercise has been shown to aid weight loss, regulate appetite and improve metabolic profile, especially for overweight and obese people,” said co-author Dr. Yong Xu, professor of pediatrics. – nutrition and molecular and cellular 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 to be able to reap some of its benefits,” said co-author Jonathan Long, MD, assistant professor of pathology at Stanford Medicine and Stanford’s Institute Scholar ChEM-H ( Chemistry, engineering and medicine for human health).
“For example, elderly or frail people who cannot exercise enough may someday benefit from taking a drug that can help slow osteoporosis, heart disease or other conditions.”
Xu, Long and their colleagues conducted comprehensive analyzes of the blood plasma compounds of the mice after an intense treadmill run. The most significantly induced molecule was a modified amino acid called Lac-Phe. It is synthesized from lactate (a byproduct of strenuous exercise 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 approximately 50% compared to control mice over a 12-hour period without affecting the their movements or energy expenditure. When given to mice for 10 days, Lac-Phe reduced cumulative food intake and body weight (due to the loss of body fat) and improved glucose tolerance.
The researchers also identified an enzyme called CNDP2 that is involved in the production of Lac-Phe and showed that mice lacking this enzyme did not lose as much weight during an exercise regimen as did a control group with the same exercise plan.
Interestingly, the team also found large increases in plasma Lac-Phe levels following physical activity in racehorses and humans. Data from a human exercise cohort showed that sprint exercise induced the most dramatic increase in plasma Lac-Phe, followed by resistance training and then resistance training.
“This suggests that Lac-Phe is an ancient and preserved system that regulates nutrition and is associated with physical activity in many animal species,” Long said.
“Our next steps include finding more details on how Lac-Phe mediates its effects in the body, including the brain,” Xu said. “Our goal is to learn how to modulate this exercise path for therapeutic interventions.”
About this exercise and neuroscientific research news
Author: Press office
Source: Baylor College of Medicine
Contact: Press Office – Baylor College of Medicine
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Original research: Closed access.
“An exercise-inducible metabolite that suppresses nutrition and obesity” by Jonathan Long et al. Nature
An exercise-inducible metabolite that suppresses nutrition and obesity
Exercise confers protection against obesity, type 2 diabetes and other cardiometabolic diseases. However, the molecular and cellular mechanisms that mediate the metabolic benefits of physical activity remain unclear.
Here we show that exercise stimulates the production of No.Lactoyl phenylalanine (Lac-Phe), a blood signaling metabolite that suppresses diet and obesity.
The biosynthesis of Lac-Phe from lactate and phenylalanine occurs in CNDP2+ cells, including macrophages, monocytes and other immune and epithelial cells located in different organs. In diet-induced obese mice, the pharmacological increases in Lac-Phe reduce food intake without affecting movement or energy expenditure.
Chronic administration of Lac-Phe reduces adiposity and body weight and improves glucose homeostasis. Conversely, genetic ablation of Lac-Phe biosynthesis in mice increases food intake and obesity after training.
Finally, large activity-inducible increases in circulating Lac-Phe are also observed in humans and racehorses, establishing this metabolite as a molecular effector associated with physical activity across multiple modes of activity and mammalian species.
These data define an exercise-inducible conserved metabolite that controls food intake and influences systemic energy balance.