News
The benefits of exercise in a pill? Science is closer to that goal

Researchers have identified a molecule in the blood that is produced during exercise and can effectively reduce food intake and obesity in mice.
This improves understanding of the physiological processes that underlie the interplay between exercise and hunger.
The study by Baylor College of Medicine, Stanford School of Medicine and collaborating institutions was published in the journal Nature on June 15.
“Regular exercise has been proven to help weight loss, regulate appetite and improve the metabolic profile, especially for people who are overweight and obese,” said co-corresponding author Dr. Yong Xu, professor of pediatrics – nutrition and molecular and cellular biology at Baylor.
“If we can understand the mechanism by which exercise triggers these benefits, then we are closer to helping many people improve their health.”
Exercise benefits
“We wanted to understand how exercise works at the molecular level to be able to capture some of its benefits,” said co-corresponding author Dr Jonathan Long, assistant professor of pathology at Stanford Medicine and an Institute Scholar of Stanford ChEM-H (Chemistry, Engineering and Medicine for Human Health).
“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.”
Xu, Long and their colleagues conducted comprehensive analyses of blood plasma compounds from mice following intense treadmill running.
The most significantly induced molecule was a modified amino acid called Lac-Phe.
It is synthesised from lactate (a byproduct of strenuous exercise that is responsible for the burning sensation in muscles) and phenylalanine (an amino acid that is one of the building blocks of proteins).
In mice with diet-induced obesity (fed a high-fat diet), a high dose of Lac-Phe suppressed food intake by about 50 per cent compared to control mice over a period of 12 hours without affecting their movement or energy expenditure.
When administered to the mice for 10 days, Lac-Phe reduced cumulative food intake and body weight (owing to loss of body fat) and improved glucose tolerance.
Enzyme
The researchers also identified an enzyme called CNDP2 that is involved in the production of Lac-Phe and showed that mice 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 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 training and then 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,” Long said.
“Our next steps include finding more details about how Lac-Phe mediates its effects in the body, including the brain,” Xu said. “Our goal is to learn to modulate this exercise pathway for therapeutic interventions.”
News
Shingles vaccine may slow biological ageing in older adults
News
Thousands of men in England to be offered life-extending prostate cancer drug
News
Blood sugar spike after meals may increase Alzheimer’s risk

Sharp rises in blood sugar after meals may raise Alzheimer’s risk, according to genetic analysis of more than 350,000 adults.
The findings point to after-meal glucose, rather than overall blood sugar, as a possible factor in long-term brain health.
Researchers examined genetic and health data from over 350,000 UK Biobank participants aged 40 to 69, focusing on fasting glucose, insulin, and blood sugar measured two hours after eating.
The team used Mendelian randomisation, a genetic method that helps test whether biological traits may play a direct role in disease risk.
People with higher after-meal glucose had a 69 per cent higher risk of Alzheimer’s disease.
This pattern, known as postprandial hyperglycaemia (elevated blood sugar after eating), stood out as a key factor.
The increased risk was not explained by overall brain shrinkage (atrophy) or white matter damage, suggesting after-meal glucose may affect the brain through other pathways not yet fully understood.
Dr Andrew Mason, lead author, said: “This finding could help shape future prevention strategies, highlighting the importance of managing blood sugar not just overall, but specifically after meals.”
Dr Vicky Garfield, senior author, added: “We first need to replicate these results in other populations and ancestries to confirm the link and better understand the underlying biology.
“If validated, the study could pave the way for new approaches to reduce dementia risk in people with diabetes.”
News2 weeks agoFDA clears automated brain fluid device
News2 weeks agoAgetech World’s latest innovation & investment round-up
News2 weeks agoInsilico signs US$888m oncology deal with Servier
News2 weeks agoFood preservatives linked to increased diabetes and cancer risk, study finds
News2 weeks agoUK bans junk food ads before 9pm to protect child health
News1 week agoCaptioning glasses win AARP pitch at CES
Insights2 weeks agoGlobal longevity initiative launches North American chapter
News6 days agoInterview: GlycanAge launch first hospital-based tests
















