Researchers at Baylor College of Medicine and Stanford College of Medicine and the Collaborating Institutions reported in a report published in the journal Nature that they were able to identify a molecule in the blood that is produced during exercise and can effectively reduce food intake and obesity in mice.
According to Neuroscience News, the new findings could contribute to improving scientists’ understanding of the physiological processes that underlie the interaction between exercise and reduced hunger.
“Regular exercise has been shown to aid weight loss, regulate appetite and improve the metabolic profile, especially for overweight and obese people,” said study co-author Dr. Yong Shu, professor of pediatrics, nutrition and molecular biology at Baylor College.
“If we (researchers) can understand the mechanism by which exercise leads to these benefits, we are closer to helping many people improve their health,” he added.
“Understanding how exercise works at the molecular level will allow us to be able to reap some of its benefits,” said co-author Professor Jonathan Long, assistant professor of pathology at Stanford Medicine and a researcher at the Stanford Chem-H Institute.
The elderly and the weak
“For example, elderly or frail people who can’t exercise enough may one day benefit from taking a drug that can help slow osteoporosis, heart disease or other conditions,” he added.
Xu, Long and their colleagues performed comprehensive analyzes of blood plasma compounds taken from mice after intense running on a treadmill. The most catalytic molecule was a modified amino acid called Lac-Phe. It’s made from lactate, a byproduct of strenuous exercise that causes muscle “burning”, and phenylalanine, an amino acid that is one of the building blocks of proteins.
Obese mice given a high-fat diet reduced food intake by approximately 50% compared to control mice over a 12-hour period, without affecting their movement or energy expenditure. When administered to mice for 10 days, Lac-Phe reduced accumulated food intake and body weight (due to the loss of body fat) and improved glucose tolerance.
CNDP2 enzyme deficiency
The researchers also found that an enzyme called CNDP2 is involved in the production of Lac-Phe and that the mice deficient in this enzyme did not lose as much weight on the exercise regime as they did with the control group on the same exercise plan.
Interestingly, the team of researchers also detected strong elevations in plasma Lac-Phe levels after physical activity in racehorses and humans. Data from a human group doing aerobic exercise such as jogging showed that there was the most dramatic increase in Lac-Phe levels, which appeared after sprinting followed by resistance training and then endurance training.
“Our (team of researchers) next steps include finding more details about how Lac-Phe mediates its effects in the body, including the brain,” said Dr. Shaw. “The goal is to learn to modify the exercise pathway for therapeutic purposes.”