Physical exercise reduces feeling of hunger: Study
Researchers from Baylor College of Medicine, the Jan and Dan Duncan Neurological Research Institute (Duncan NRI) at Texas Children’s Hospital, Stanford University School of Medicine, and partner institutions have uncovered a new explanation for how exercise promotes weight loss, WAM reports.
Their research revealed that Lac-Phe, a compound generated during physical activity, decreases appetite in mice and contributes to weight reduction. The results were published in Nature Metabolism.
“Regular exercise is considered a powerful way to lose weight and to protect from obesity-associated diseases, such as diabetes or heart conditions,” said co-corresponding author Dr. Yang He, assistant professor of pediatrics–neurology at Baylor and investigator at the Duncan NRI. “Exercise helps lose weight by increasing the amount of energy the body uses; however, it is likely that other mechanisms are also involved.”
Earlier research showed that Lac-Phe is the metabolite that rises the most in the bloodstream after vigorous exercise, a pattern observed not only in mice but also in humans and racehorses. The same team previously demonstrated that giving Lac-Phe to obese mice reduced their food intake and promoted weight loss without harmful side effects. However, the mechanism by which Lac-Phe suppresses appetite was not well understood until now.
To investigate further, the researchers examined two types of neurons in the mouse brain: AgRP neurons, located in the arcuate nucleus of the hypothalamus, which stimulate hunger; and PVH neurons in the paraventricular nucleus, which help suppress hunger.
Under normal conditions, AgRP neurons send inhibitory signals to PVH neurons, creating a sensation of hunger. When AgRP neurons are silenced, PVH neurons become more active, reducing appetite.
The team found that Lac-Phe acts directly on AgRP neurons, suppressing their activity and thereby allowing PVH neurons to become more active. As a result, the mice consumed less food. Importantly, their overall behaviour remained unchanged, suggesting that Lac-Phe reduces appetite without causing negative side effects.
In addition, the team investigated how Lac-Phe inhibits AgRP neurons. “We found that Lac-Phe acts on a protein on AgRP neurons called KATP channel, which helps regulate cell activity. “When Lac-Phe activates these channels in AgRP neurons, the cells become less active,” He said. “When we blocked the KATP channels using drugs or genetic tools, Lac-Phe no longer suppressed appetite. This confirmed that the KATP channel is essential for Lac-Phe’s effects.”
Although the study focused on mice, the researchers described the findings as promising for humans. Future research will explore how Lac-Phe functions in different metabolic states, such as obesity and leanness, how it travels to the brain, and whether it can be developed into a safe and effective therapy.
As earlier reported, Australian research highlights lifestyle role in reducing dementia, Alzheimer’s.
