For many battling obesity, semaglutide has become a lifeline.
This drug, commonly used for treating both obesity and type 2 diabetes, helps people eat less and lose weight fast.
But it comes at a cost. Users often report nausea, loss of muscle mass, and fatigue.
Until now, researchers weren’t sure which parts of the brain triggered the benefits – and which caused the drawbacks. That has changed.
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Rewiring the brain without the drug
A team of scientists at the University of Gothenburg took a closer look at how semaglutide affects the brain.
Using mice, they traced the exact nerve cells activated by the drug.
But then they went a step further: they stimulated those same nerve cells without administering the drug at all.
The mice ate less and lost weight – just as they would with the medication.
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Yet when those specific nerve cells were destroyed, semaglutide’s appetite-suppressing effects almost vanished.
Interestingly, side effects like nausea and muscle loss continued even after these “weight loss” cells were removed.
A new path to side-effect-free slimming
The researchers identified a precise group of nerve cells in the dorsal vagal complex – a region in the brainstem tied to energy balance.
These cells seem responsible for the weight loss effects but not for the negative symptoms.
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This discovery opens the door to future treatments that only target the beneficial brain signals – without triggering the unpleasant ones.
And that could mean an entirely new generation of weight-loss therapies: as effective as semaglutide, but safer and easier to tolerate.
The implications don’t stop there.
As GLP-1 receptor agonists like semaglutide are increasingly explored for other conditions – from addiction to neurodegenerative diseases – understanding exactly how they work is more important than ever.
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This study could mark the beginning of a shift in how we treat obesity, making side effects a thing of the past.
The article is based on information from Medicalxpress.com.
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