By Mark Waghorn via SWNS
An exercise pill for couch potatoes could be on the horizon, according to a new study.
It is based on a protein produced in the blood during work-outs, say scientists.
In experiments, the compound dramatically reduced food intake and obesity in mice.
The US team hopes to turn it into a medication that replaces going to the gym.
Lead author Professor Yong Xu, a nutritionist at Baylor College of Medicine, in Houston, Texas, said: "Regular exercise has been proven to help weight loss, regulate appetite and improve the metabolic profile, especially for people who are overweight and obese.
"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.
Co-lead author Dr. Jonathan Long, of Stanford University in California, said: "We wanted to understand how exercise works at the molecular level to be able to capture some of its benefits.
"For example, older or frail people who cannot exercise enough, may one day benefit from taking a medication that can help slow down osteoporosis, heart disease or other conditions."
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 by-product 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 cohort showed that sprint exercise induced the most dramatic increase in plasma Lac-Phe - followed by resistance and endurance training.
Dr. Long said: "This suggests Lac-Phe is an ancient and conserved system that regulates feeding and is associated with physical activity in many animal species."
The metabolic effects of Lac-Phe were not investigated in the human cohorts. Further studies are needed to provide more insights into new therapeutic opportunities for human health.
Added Prof Xu: "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."
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