Overview: Researchers have identified molecules in the blood that are produced during exercise. The molecule Lac-Phe can effectively reduce food intake and obesity in mouse models.
sauce: Baylor College of Medicine
Researchers at Baylor College of Medicine, Stanford University School of Medicine, and collaborating institutions report today in the journal. Nature They identified molecules in the blood that are produced during exercise and can effectively reduce food intake and obesity in mice.
The findings improve our understanding of the physiological processes underlying the interaction between exercise and hunger.
“Regular exercise has proven to help with weight loss, appetite regulation, and improved metabolic profile, especially for people who are overweight or obese,” said co-author, Dr. Yong Xu, a professor of pediatrics. Says. Baylor.
“Understanding the mechanisms by which exercise causes these benefits will help many people improve their health.”
“We wanted to understand how movement works at the molecular level so that we could get some of its benefits,” said Stanford ChEM-H, MD, Assistant Professor of Pathology, Stanford Medicine. Dr. Jonathan Long, MD, a collaborative author who is an institute scholar, said. Chemistry, engineering and medicine for human health).
“For example, older people and frail people who do not exercise well may one day benefit from taking medications that help delay osteoporosis, heart disease, or other conditions.”
Xu, Long et al. Performed a comprehensive analysis of mouse plasma compounds after intense treadmill running. The most significantly derived molecule was a modified amino acid called Lac-Phe. It is synthesized from lactic acid (a by-product of intense exercise that causes a burning sensation in muscles) and phenylalanine (an amino acid that is one of the constituents of protein).
In diet-induced obese (high-fat diet-fed) mice, high-dose Lac-Phe consumed approximately 50% of food intake over 12 hours compared to control mice without affecting exercise or energy expenditure. Suppressed. After 10 days of administration of Lac-Phe to mice, cumulative food intake and body weight decreased (due to decreased body fat) and glucose tolerance improved.
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 with exercise therapy as controls with the same exercise plan.
Interestingly, the team also found a strong increase in plasma Lac-Phe levels following racehorse and human physical activity. Data from the human exercise cohort showed that sprint exercise elicited the most dramatic increase in plasma Lac-Phe, followed by strength training and endurance training.
“This suggests that Lac-Phe is an old and conserved system that regulates feeding and is associated with physical activity in many animal species,” Long said.
“Our next step involves finding out more about how Lac-Phe mediates its effects in the body, including the brain,” Xu said. “Our goal is to learn to coordinate this motor pathway for therapeutic intervention.”
About this movement and neuroscience research news
author: Press office
sauce: Baylor College of Medicine
contact: Press Office – Baylor College of Medicine
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Independent research: Closed access.
Jonathan Longetal. “Exercise-induced metabolites that suppress feeding and obesity” by. Nature
See also
Overview
Exercise-induced metabolites that suppress feeding and obesity
Exercise provides protection against obesity, type 2 diabetes, and other cardiometabolic disorders. However, the molecular and cellular mechanisms that mediate the metabolic benefits of physical activity are unknown.
Here, exercise N-Lactyl-Phenylalanine (Lac-Phe), a blood-derived signal metabolite that suppresses feeding and obesity.
Biosynthesis of Lac-Phe from lactic acid and phenylalanine occurs in CNDP2+ + Cells that localize to various organs, including macrophages, monocytes, and other immune and epithelial cells. In diet-induced obese mice, pharmacologically mediated increases in Lac-Phe reduce food intake without affecting exercise or energy expenditure.
Chronic administration of Lac-Phe reduces obesity and weight and improves blood glucose homeostasis. Conversely, genetic elimination of Lac-Phe biosynthesis in mice increases food intake and obesity after exercise training.
Finally, a large activity-induced increase in circulating Lac-Phe has also been 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 conserved exercise-induced metabolites that control food intake and affect systemic energy balance.
