The physiological processes underlying the interaction between exercise and hunger are still poorly understood. Now, a scientific team has identified in mice a molecule in the blood that is produced during sports and that can effectively reduce food intake and obesity.
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Researchers from Baylor College of Medicine, the Stanford School of Medicine and collaborating institutions report this Wednesday in the journal Nature of the finding of this metabolite.
“Regular exercise has been shown to aid weight loss, regulate appetite and improve metabolic profile, especially in overweight and obese people,” says Yong Xu, a co-author of the study and a professor at Baylor. “If we can understand the mechanism by which exercise triggers these benefits, then we will be closer to helping many people improve their health.”
Stanford’s Jonathan Long explains that the team’s goal was to understand how exercise works at the molecular level so they might capture some of its benefits; “for instance, Older or frail people who can’t get enough exercise may one day benefit from taking a drug that can help slow down osteoporosis. heart disease or other conditions.
To reach their conclusions, the scientists carried out a comprehensive analysis of the compounds in the blood plasma of mice following 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 that is responsible for the burning sensation in muscles) and phenylalanine (an amino acid that is one of the building blocks of protein), explains a Boulder note.
In mice with diet-induced obesity (fed a high-fat diet), a high dose of Lac-Phe suppressed food intake by regarding 50% compared to control mice over a 12-hour period, without affecting their movement or energy expenditure.
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When 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 that is involved in the production of Lac-Phe and showed that mice lacking this enzyme did not lose as much weight on an exercise regimen as a control group on the same exercise plan.
The team also found strong elevations in plasma Lac-Phe levels following physical activity in racehorses and humans. Data from a human exercise cohort showed that sprint exercise induced the strongest increase in plasma Lac-Phe, followed by resistance training.
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“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 concludes. The team’s next steps include finding more details regarding how this molecule mediates its effects in the body, including the brain: “Our goal is to learn how to modulate this exercise pathway for therapeutic interventions,” Xu stresses.
EFE
