Researchers have discovered why certain drugs, whether they activate or block the GIP receptor, can both help with weight loss. These substances act differently on the brain, influencing the circuits that control hunger and energy.
The study, published in
Nature Metabolism, shows that the brain plays a key role in the effects of these treatments. Drugs that activate GIP act on a specific type of neuron, while those that block it work through another pathway linked to a related hormone, GLP-1.
GIP and GLP-1 hormones are produced by the gut after a meal. They help regulate blood sugar but also send signals to the brain to suppress hunger.
Drugs like semaglutide, which mimic GLP-1, are already used to aid weight loss. Combining this type of drug with another that activates GIP, like tirzepatide, enhances the effect. Surprisingly, blocking GIP can also lead to weight loss.
To understand this, researchers conducted experiments on genetically modified mice. They found that blocking GIP activates the same brain regions as GLP-1 drugs.
These findings could lead to more effective obesity treatments with fewer side effects. A better understanding of how these drugs work could improve treatment targeting.
How do the gut and brain communicate?
After a meal, hormones like GLP-1 and GIP are released by the gut. They then send signals to the brain to indicate satiety.
GLP-1 acts on brain regions that reduce hunger sensations. GIP influences other circuits, though its exact mechanism is still not fully understood.
This gut-brain dialogue is essential for maintaining a healthy balance between food intake and energy expenditure. When this system is disrupted, it can contribute to obesity or diabetes.
This is why scientists are working to better understand it, aiming to develop more precise treatments.