Summary: Researchers have identified a molecule in the blood that is produced during exercise. The molecule, Lac-Phe, can effectively reduce food intake and obesity in mouse models.
source: Baylor College of Medicine
Researchers at Baylor College of Medicine, Stanford School of Medicine and their collaborating institutions published today in the journal temper nature They identified a molecule in the blood produced during exercise that could effectively reduce food intake and obesity in mice.
The findings improve our understanding of the physiological processes that underlie the interaction between exercise and starvation.
“Regular exercise has been shown to help with weight loss, appetite regulation, and improved metabolic profile, especially for people who are overweight and obese,” said co-author Dr. Yong Shu, MD, professor of pediatrics – nutrition and molecular and cellular biology at Baylor.
“If we can understand the mechanism by which exercise leads to these benefits, we are closer to helping many more people improve their health.”
“We wanted to understand how exercise works at the molecular level so that we can reap some of its benefits,” said co-author Jonathan Long, MD, assistant professor of pathology at Stanford Medicine and a researcher at Stanford Chem-H. Chemistry, engineering and medicine for human health).
“For example, elderly or frail people who cannot exercise enough, may one day benefit from taking a medication that can help slow osteoporosis, heart disease, or other conditions.”
Xu, Long and their colleagues performed comprehensive analyzes of blood plasma compounds from mice after intense running on a treadmill. The most catalytic molecule was a modified amino acid called Lac-Phe. It’s made from lactate (a byproduct of strenuous exercise responsible for the burning sensation in the muscles) and phenylalanine (an amino acid that is one of the building blocks of proteins).
In diet-induced obese mice (fed a high-fat diet), a high dose of Lac-Phe reduced food intake by approximately 50% compared to control mice over a 12-hour period without affecting their locomotion or energy expenditure. When administered to rats for 10 days, Lac-Phe reduced accumulated food intake and body weight (due to loss of body fat) and improved glucose tolerance.
The researchers also identified an enzyme called CNDP2 involved in Lac-Phe production and showed that mice lacking this enzyme didn’t lose as much weight on the exercise regime as the control group on the same exercise plan.
Interestingly, the team also found strong elevations in plasma Lac-Phe levels after physical activity in racehorses and humans. Data from a human exercise group showed that sprint exercise produced the most dramatic increase in plasma Lac-Phe, followed by resistance training and then endurance training.
“This indicates that Lac-Phe is an ancient, protected system that regulates nutrition and is associated with physical activity in many animal species,” Long said.
“Our next steps include finding more details about how Lac-Phe mediates its effects in the body, including the brain,” Shaw said. “Our goal is to learn to modify this exercise pathway for therapeutic interventions.”
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“Exercise-stimulated metabolite inhibiting lactation and obesityWritten by Jonathan Long et al. temper nature
Exercise-stimulated metabolite inhibiting lactation and obesity
Exercise confers protection against obesity, type 2 diabetes, and other cardiovascular diseases. However, the molecular and cellular mechanisms that mediate the metabolic benefits of physical activity remain unclear.
Here we show that exercise stimulates the production of n-Lactoyl-phenylalanine (Lac-V), a blood-borne signaling metabolite that inhibits nutrition and obesity.
Biosynthesis of Lac-Phe from lactate and phenylalanine occurs in CNDP2+ Cells, including macrophages, monocytes, immune cells, and other epithelial cells localized to diverse organs. In diet-induced obese mice, pharmacological increases in Lac-Phe reduce food intake without affecting locomotion or energy expenditure.
Chronic use of Lac-Phe reduces obesity and body weight and improves glucose homeostasis. Conversely, gene ablation of Lac-Phe biosynthesis in mice increases food intake and adiposity after exercise training.
Finally, significant inducible increases in activity in circulating Lac-Phe have also been observed in humans and racehorses, leading to the establishment of this metabolite as a molecular effector associated with physical activity across multiple activity modalities and mammalian species.
These data identify a conserved, exercise-stimulated metabolite that controls food intake and influences systemic energy balance.