What if you might enjoy the health benefits of exercise without having to exercise? This idea might soon become a reality thanks to researchers from Baylor College of Medicine and Stanford School of Medicine.
Like the team in the specialist magazine Nature reported identifying a molecule in the blood produced during exercise that can reduce food intake and obesity in mice.
“Regular exercise has been shown to help with weight loss, regulate appetite, and improve metabolic profile, especially in overweight and obese people,” said co-author Yong Xu, professor of pediatrics, nutrition, and molecular and cell biology at Baylor University. “If we can understand the mechanism by which exercise triggers these benefits, we’ll be closer to helping many people improve their health.”
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“We wanted to understand how movement works at the molecular level in order to be able to reap some of its benefits,” said co-author Jonathan Long, assistant professor of pathology at Stanford Medicine. “For example, elderly or frail people who are unable to exercise adequately might one day benefit from taking a drug that may help slow osteoporosis, heart disease or other diseases.”
Xu, Long and their colleagues performed comprehensive analyzes of blood plasma compounds in mice following intense treadmill exercise. The molecule that was most affected 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).
In mice with dietary obesity (fed a high-fat diet), a high dose of Lac-Phe suppressed food intake by regarding 50 percent over a 12-hour period compared to control mice, without affecting their movement or energy expenditure. When given to the mice for ten days, Lac-Phe decreased 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 regimen.
The team also found that plasma levels of Lac-Phe increased sharply following exercise in both racehorses and humans. Data from a human exercise cohort showed that sprint training caused the largest increases in plasma Lac-Phe levels, followed by resistance training and endurance training. “This suggests that Lac-Phe is an ancient and conserved system that regulates nutrition and is associated with physical activity in many animal species,” Long said.
“Our next steps are to find more details on how Lac-Phe mediates its effects in the body, including the brain,” Xu said. “Our goal is to learn how to adapt this movement path for therapeutic interventions.”
