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doi: 10.1111/dom.14166

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Overexpression of METTL3 alleviates Cd-induced steatosis, fibrosis, and hepatic stellate cell activation

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Overall, our results suggest that the AP is responsible for the appetite-suppressing effects of GIPR agonism but that GIP receptors in the hypothalamus underlie the ability of GIPR antagonism to enhance the weight loss effects of GLP-1R and amylin receptor agonists