Physical exercise produces a substance that decreases hunger in mice

“Fulanito doesn't get fat and I do, although we eat the same; It's because of my metabolism." This well-known excuse, debatable from the scientific point of view, could contain a certain truth (although not surely the one that those who resort to it would want). Metabolism is the set of bodily processes, such as digestion and exercise –or the mere existence, in the case of basal metabolism– that use and transform energy. Those processes sometimes involve the body making certain substances called metabolites. Now, An investigation published this Wednesday in Nature relates a specific metabolite produced during physical exercise with a reduction in the sensation of hunger and, therefore, with a lower intake of food and the reduction of obesity in mice.

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That physical activity protects against obesity and associated diseases is well known. The increased demand for energy forces our body to burn more calories. What this new study also indicates is that physical exercise could contribute to having less desire to eat, which would be a great incentive to get up from the sofa.

Stanford University biochemist and pathologist Jonathan Long and his collaborators have performed extensive analyzes of metabolites in the blood plasma of mice after intense running on a treadmill (like the ones in the gym, but adapted to them). As they report in a press release, the most significantly induced metabolite was a modified amino acid called Lac-Phe that 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).

A high dose of Lac-Phe suppressed food intake in mice with diet-induced obesity (fed a high-fat diet) by approximately 50%, compared to control mice, over a 12-hour period. without affecting their movement or energy expenditure, the statement indicates.

Administration of Lac-Phe to mice for 10 days reduced cumulative food intake, decreased body weight (due to loss of body fat), and improved glucose tolerance. The authors also identified an enzyme 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 exercise plan. However – and this is important and perhaps somewhat discouraging – the appetite-suppressing effect of Lac-Phe only existed after exercise, not in the sedentary state, and was only seen in mice rendered obese by a high-fat diet.

In horses and in humans

Strong elevations of plasma Lac-Phe level were also observed after physical activity in racehorses and in humans. Human exercise data showed that sprinting induced the most dramatic increase in plasma Lac-Phe, followed by aerobic exercise and weight lifting. In humans, however, it has not yet been studied whether Lac-Phe suppresses hunger. The authors conclude that more studies are needed.

“It is possible to speculate that there are people who do not want to exercise but benefit from the reducing effect of Lac-Phe intake. It must be remembered that the work does not analyze the secondary effects that can be derived from taking this compound, and above all the adequate concentration to inject in humans without toxic effects. This is another important avenue of research that is also necessary", says Nabil Djouder, head of the Growth Factors, Nutrients and Cancer Group at the National Cancer Research Center (CNIO), in statements to SMC Spain. And he adds: "It would be relevant to analyze the relationship between the secretion of Lac-Phe and inflammation, which is a process that has to do with physical exercise and is, in fact, involved in muscle regeneration."

“The results of this study are of great interest and describe a specialized and almost unknown metabolite until now. However, where it is produced, what cells it targets and how it exerts its appetite-suppressing effects will require further characterization”, point out Francesc Villarroya and Marta Giralt Oms, professors at the Department of Biochemistry and Molecular Biomedicine at the University of Barcelona and principal investigators of the IBUB and CIBEROBN, also in statements to the SMC Spain.

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