An “anti-hunger” pill could be on the horizon, according to a new study. Researchers from Stanford Medicine and Baylor University have identified a molecule that keeps people from getting hungry after working out.
In experiments, the compound dramatically reduced food intake and obesity in mice. Study authors hope to turn it into a medication that may even replace the need to go to the gym.
“Regular exercise has been proven to help weight loss, regulate appetite and improve the metabolic profile, especially for people who are overweight and obese,” says lead author Professor Yong Xu from the Baylor College of Medicine in a statement, according to SWNS. “If we can understand the mechanism by which exercise triggers these benefits, then we are closer to helping many people improve their health.”
The findings in the journal Nature shed fresh light on the links between exercise and hunger. Physical activity protects against obesity and a host of diseases.
“We’re all generally aware that exercise is beneficial. It’s good for body weight and glucose control,” says Jonathan Long, PhD, a Standford Medicine assistant professor of pathology, in a university release. “But we wanted to take a look at that concept in more detail — we wanted to see if we could dissect exercise in terms of molecules and pathways.”
Workout byproduct lowers body fat and improves glucose tolerance
The team conducted comprehensive analyses of blood plasma from mice following intense treadmill running. They identified a modified amino acid called Lac-Phe as the most significantly induced molecule.
It is synthesized from lactate, a byproduct of strenuous exercise responsible for the burning sensation in muscles, and phenylalanine, a building block of proteins. In lab rodents fed a high-fat diet, a high dose of Lac-Phe halved food intake over a period of 12 hours compared to a control group. It also didn’t affect their movement or energy expenditure. When administered to the mice for 10 days, Lac-Phe reduced consumption and body fat and improved glucose tolerance.
The researchers also identified an enzyme called CNDP2 that is involved in the production of Lac-Phe. They showed mice lacking the enzyme did not lose as much weight on an exercise regime as a control group on the same 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 group showed that sprint exercise induced the most dramatic increase in plasma Lac-Phe – followed by resistance and endurance training.
“This suggests Lac-Phe is an ancient and conserved system that regulates feeding and is associated with physical activity in many animal species,” Dr. Long says, according to SWNS.
The metabolic effects of Lac-Phe were not investigated in the human participants. Further studies will be necessary to provide more insights into new therapeutic opportunities for human health.
“Our next steps include finding more details about how Lac-Phe mediates its effects in the body – including the brain,” Prof. Xu concludes. “Our goal is to learn to modulate this exercise pathway for therapeutic interventions.”