Studies over the years have conclusively shown the numerous benefits to the body from regular exercises, including in regulating appetite, helping in weight loss, and improving the metabolic profile of individuals, especially for those who are overweight or obese.
Scientists have for long been attempting to understand the mechanism by which exercise triggers these benefits at the molecular level, as it could help many people improve their health. It could prove especially beneficial to those who cannot engage in regular physical exercise due to age or health restrictions.
Now researchers at Baylor College of Medicine and at Stanford College of Medicine in the United States say their studies on mice have led to the discovery of a molecule in blood that is produced during exercise, which can effectively reduce food intake and obesity.
The new findings could help improve understanding of the physiological processes governing the interplay between exercise and hunger. The development of medications based on the latest finding could assist older or frail people to obtain the benefits of exercise regimens, including in slowing down osteoporosis, heart diseases or other conditions.
Researchers behind the study conducted a comprehensive analysis of blood plasma compounds from mice following intense treadmill running. 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 proteins).
The study found that in mice with diet induced obesity (fed a high-fat diet), a high dose of Lac-Phe suppressed food intake by about 50 percent compared to control mice over a period of 12 hours without affecting their movement or energy expenditure. When administered to the mice for 10 days, Lac-Phe reduced cumulative food intake and body weight (owing 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 regime as a control group on the same exercise plan.
Interestingly, the team also found robust 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 most dramatic increase in plasma Lac-Phe, followed by resistance training and then endurance training.
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