Stamford, CA – A new study suggests a “hunger-fighting” pill may be on the way. Researchers at Stanford School of Medicine and Baylor University have discovered a molecule that prevents people from feeling hungry after a workout.
In experiments, the compound significantly reduced food intake and obesity in mice. The study authors hope to turn it into a drug that could even replace the need to go to the gym.
“Regular exercise has been shown to aid weight loss, regulate appetite and improve metabolic status, especially in overweight and obese individuals,” lead author Professor Yong Xu from Baylor College of Medicine said in a statement, according to SWNS. “If we can understand the mechanisms by which exercise triggers these benefits, we’re one step closer to helping many people improve their health.”
finds in magazines nature Links between exercise and hunger revealed. Physical activity can prevent obesity and many diseases.
“We generally know that exercise is good. It’s good for weight and blood sugar control,” Dr. Jonathan Lang, an assistant professor of pathology at Stanford University, said in a press release issued by the university. “But we wanted to study the concept in more detail — we wanted to see if we could dissect motion from a molecular and pathway perspective.”
Exercise byproducts reduce body fat and improve glucose tolerance
The team performed a comprehensive analysis of mouse plasma following strenuous treadmill runs. They identified a modified amino acid called Lac-Phe as the most prominent inducing molecule.
It is synthesized from lactic acid (a byproduct of vigorous exercise) and phenylalanine (a building block of protein). In laboratory rodents fed a high-fat diet, high doses of Lac-Phe halved food intake over 12 hours compared to controls. It also doesn’t affect their movement or energy expenditure. When administered to mice for 10 days, Lac-Phe reduced consumption and body fat, and improved glucose tolerance.
The researchers also discovered an enzyme called CNDP2, which is involved in the production of Lac-Phe. They showed that mice lacking the enzyme did not lose as much weight during the exercise regimen as the controls in the same program.
Interestingly, the team also found that plasma Lac-Phe levels were significantly elevated after horse racing and physical activity in humans. Data from the human exercise group showed that sprinting caused the most significant increase in plasma Lac-Phe – followed by resistance and endurance training.
“This suggests that Lac-Phe is an ancient and conserved system that regulates feeding and is associated with physical activity in many animal species,” said Dr Long, as reported by SWNS.
The metabolic effects of Lac-Phe have not been studied in human participants. Further research is needed to provide more insights into new therapeutic opportunities in human health.
“Our next steps include finding more details about how Lac-Phe mediates its effects in the body, including the brain,” concluded Prof. Xu. “Our goal is to learn to modulate this exercise pathway for therapeutic intervention.”
Southwest News Service writer Mark Waghorn contributed to this report.