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 that they identified a molecule in the blood that is produced during exercise that 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 with weight loss, appetite regulation and improved metabolic profile, especially for overweight and obese people,” said co-corresponding 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 one step closer to helping many people improve their health.”
“We wanted to understand how exercise works at the molecular level so we could capture some of its benefits,” said co-corresponding author Jonathan Long, MD, assistant professor of pathology at Stanford Medicine and Stanford Institute ChEM researcher. -H ( Chemistry, Engineering & Medicine for Human Health).
“For example, elderly or frail people who can’t exercise enough could one day benefit from taking a drug that can help slow osteoporosis, heart disease or other conditions.”
Xu, Long and their colleagues performed comprehensive compound analyzes of mouse blood plasma after strenuous treadmill running. The most significant induced molecule was 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 approximately 50% compared to control mice over a period of 12 hours without affecting their movement or energy expenditure. When given 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 which is involved in the production of Lac-Phe and showed that mice lacking this enzyme did not lose as much weight with an exercise regimen as a control group with the same plan. of exercise.
Interestingly, the team also found robust elevations in plasma Lac-Phe levels after 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 endurance training.
“This suggests that Lac-Phe is an ancient and conserved system that regulates feeding and is associated with physical activity in many animal species,” Long said.
“Our next steps are to find more details about how Lac-Phe mediates its effects in the body, including the brain,” Xu said. “Our goal is to learn how to modulate this exercise pathway for therapeutic interventions.”
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Author: Press office
Source: Baylor College of Medicine
Contact: Press Office – Baylor College of Medicine
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“An exercise-inducible metabolite that suppresses diet and obesityby Jonathan Long et al. Nature
An exercise-inducible metabolite that suppresses diet 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.
We show here that exercise stimulates the production of NOT-lactoyl-phenylalanine (Lac-Phe), a blood-borne signaling metabolite that suppresses diet and obesity.
Lac-Phe biosynthesis from lactate and phenylalanine occurs in CNDP2+ cells, including macrophages, monocytes and other immune and epithelial cells located in various organs. In diet-induced obese mice, pharmacological increases in Lac-Phe reduce food intake without affecting movement or energy expenditure.
Chronic administration of Lac-Phe decreases adiposity and body weight and improves glucose homeostasis. Conversely, genetic ablation of Lac-Phe biosynthesis in mice increases food intake and obesity after exercise training.
Finally, strong 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 in multiple activity modalities and mammal species.
These data define a conserved exercise-inducible metabolite that controls food intake and influences systemic energy balance.
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