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These results indicate that the increased amount of non-12-OH FXR-antagonistic BAs consequent to the decrease in CYP8B1 expression after T3 treatment potentiates GLP-1 production by deactivating the intestinal FXR, thereby improving glucose homeostasis via the augmentation of insulin secretion
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They are then excreted from the body
Retatrutide adds glucagon receptor activity, making it a triple agonist rather than a dual agonist
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