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Cambridge researchers show activating GIPR in the brainstem and blocking it in the hypothalamus both drive weight loss in mice
Cambridge researchers discovered that activating the GIP receptor in the brainstem reduces appetite, while blocking the same receptor in the hypothalamus releases a brake on fullness signals, with both paths leading to weight loss in mice.
This explains why obesity drugs with opposite effects on the GIP receptor can achieve similar results. It also suggests that combining GIP-targeting treatments with GLP-1 drugs or amylin receptor medicines could produce stronger weight loss effects.
Written by elseif from the cluster below · every claim links back to a sourceThe three things worth knowing
Cambridge researchers found that GIPR agonists reduce appetite by acting on the brainstem in mice.
GIPR antagonists promote weight loss by blocking a brake on fullness signals in the hypothalamus.
Combining GIPR antagonists with GLP-1 drugs or amylin receptor medicines may enhance weight loss effects.
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