Researchers have identified a molecule in the blood that can effectively reduce food intake and obesity
The modified amino acid, called Lac-Phe, is produced during exercise
This could lead to the development of medication simulating exercise
The study was led by staff at Baylor College of Medicine and Stanford Medicine
understands researchers are moving closer to creating a pill to mimic some of the key benefits of exercise.
New studies have identified a molecule in the blood – produced during exercise – that can effectively prompt the reduction of food intake and help with the control of obesity.
The findings, published in the journal Nature
, improve the current understanding of the physiological processes and relationship between exercise and the feeling of hunger.
According to the study's co-corresponding author, Dr Yong Xu of Baylor College of Medicine, the research will help decode how exercise works at the molecular level, allowing scientists to "capture" some of its benefits.
This could lead to the development of medication simulating exercise – aimed at people who cannot exercise enough – helping to slow down osteoporosis, heart disease or other conditions.
“Regular exercise has been proven to help weight loss, regulate appetite and improve the metabolic profile, especially for people who are overweight and obese,” Xu said.
“If we can understand the mechanism by which exercise triggers these benefits, then we are closer to helping many people improve their health.”
The team led by Xu and Dr Jonathan Long, assistant professor of pathology at Stanford Medicine, conducted comprehensive analyses of blood plasma compounds following intense treadmill running.
The most significantly induced molecule was a modified amino acid called Lac-Phe.
It is synthesized from lactate (the byproduct of strenuous exercise responsible for the burning sensation in muscles) and phenylalanine (an amino acid that's one of the building blocks of proteins).
In those suffering from obesity, a high dose of Lac-Phe suppressed food intake by about 50 per cent, compared to a control group, over a period of 12 hours without affecting their movement or energy expenditure.
The researchers also identified an enzyme called CNDP2 that is involved in the production of Lac-Phe and showed that people lacking this enzyme did not lose as much weight on an exercise regime as a control group on the same exercise plan.
Interestingly, the team also found robust elevations in plasma Lac-Phe levels following physical activity in both racehorses and humans.
“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 Long.
Data from a human exercise cohort showed that sprint exercise resulted in the most dramatic increase in plasma Lac-Phe, followed by resistance training and then endurance training.
Xu added: “Our next steps include finding more details about how Lac-Phe mediates its effects in the body, including the brain.
“Our goal is to learn to modulate this exercise pathway for therapeutic interventions.”
To read the full research in Nature
, click here