Researchers at Baylor College of Medicine and Stanford School of Medicine have discovered a molecule in the blood that can be used to treat or prevent obesity and overeating in mice. This discovery contributes to the understanding of the biological systems involved in the relationship between physical exercise and hunger.
The results of the study, in its own way a milestone. were published on Wednesday 15 June in Nature, and I link them to you here.
The “exercise molecule”
It is now widely proven that regular exercise helps weight loss, regulates appetite and improves the metabolic profile. Especially in obese or overweight people. “If we can understand the mechanism by which exercise triggers these benefits,” says the Dr Yong Xu, molecular biologist, nutrition expert and co-author of the study, “we are closer to helping many people improve their health.”
“We wanted to understand how physical exercise works on a molecular level in order to exploit some of its advantages,” echoes another co-author, Jonathan Long, assistant professor of pathology at Stanford University School of Medicine.
Older or frail people who can't get enough exercise could take a drug that slows osteoporosis and counteracts heart disease and other conditions.
The research
Xu Long and colleagues conducted an in-depth study on the components of the blood plasma of mice after intense physical activity. The substance most significantly induced by exercise (a treadmill run) was Lac-Phe. It is an amino acid synthesized from lactate (a byproduct of intense exercise that causes muscle pain) and phenylalanine (an amino acid that is one of the building blocks of proteins).
A high amount of Lac-Phe has suppressed food intake by about 50% in obese mice over a 12-hour period compared to control animals. When given to mice for 10 days, Lac-Phe reduced cumulative food intake and body weight (due to fat loss). Glucose tolerance also improved significantly.
The researchers also identified an enzyme called CNDP2. This enzyme is involved in the production of Lac-Phe, and mice lacking this enzyme lost less weight than a control group.
And in humans?
We are getting there gradually, but faster than expected. The research team has already observed strong increases in plasma levels of Lac-Phe following physical activity in racehorses and humans. Sprint exercise induced the greatest increase in Lac-Phe. Followed by resistance and strength training. “This suggests that Lac-Phe is a system present in many animals to regulate feeding, and is associated with physical activity,” Long says.
The next steps? The search for more details on the effects of Lac-Phe in the body, including the brain. Modulating this path will lead to a drug. What will we call it? Gym in pills?
We'll see.
