Anti-obesity hormone: already present in the body?
Researchers confirm that the hormone GDF15 (heart hormone, appetite suppressant, marker of neurodegenerative disease) is released in response to intense exercise, but probably not in a sufficient amount to affect behavior or appetite. These findings add nuanced information to a hormone that is currently being analyzed for its potential as an anti-obesity drug.
A drug that helps us eat less could help more than 650 million people worldwide who suffer from obesity. One of the candidates that attracts the attention of researchers is the hormone GDF15 which, when administered to rodents, decreases their appetite and body weight. New research from the University of Copenhagen finds that the body produces large amounts of GDF15 during prolonged periods of intense exercise, probably as a signal of physiological stress.
This finding highlights important differences between GDF15 administered as a drug (pharmacology) and GDF15 released naturally in response to vigorous exercise (physiology). This is an important distinction in understanding the role of GDF15 in appetite regulation and energy balance, with implications for its role as a possible anti-obesity drug.
“If there are physiological conditions involving GDF15 as a regulator of energy metabolism, it is still an unsolved mystery,” says Associate Professor Christoffer Clemmensen of the Novo Nordisk Foundation’s Center for Basic Metabolic Research, at the University of Copenhagen. Christoffer Clemmensen, PhD student Trine Sand Nicolaisen and assistant Anders Bue Klein led the research in collaboration with the Department of Nutrition, Exercise and Sports at the University of Copenhagen, and the results were recently published on February 15, 2021, in Nature Communications.
The aim of their research was to better understand the physiological role of the hormone GDF15 in energy metabolism and behavior towards physical activity. Recent findings in rodents and monkeys suggest that the hormone, when administered pharmacologically, decreases appetite, but also has side effects, such as nausea.
Because little is known about how GDF15 works when released naturally by the body, the researchers set out to fill this knowledge gap with a series of experiments on humans and mice. Among their main findings was that more than two hours of exercise in humans resulted in a four- to five-fold increase in the hormone GDF15, suggesting that GDF15 functions as a signal of exercise-induced stress.
To test this idea, the researchers used animal models. They found that taking GDF15 in mice as a medicine clearly reduced their motivation to exercise and reduced their appetite. But when mice were trained vigorously to stimulate the physiological release of GDF15, it induced the same response to physical activity behavior as food consumption. These findings highlight a difference between physiological GDF15 and pharmacological GDF15. Christoffer Clemmensen points out that more studies are needed to understand this different action and especially to verify whether GDF15 also has behavioral effects in humans. He and his team will now focus on clarifying the effects of the hormone GDF15 when it is produced by the human body.
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