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The glucagon agonism is designed to boost hepatic energy expenditure and reduce fat storage, potentially offering a different efficacy and side effect profile compared to GIP/GLP-1 targets

Furthermore, GIPR antagonism in combination with GLP-1R agonism synergistically reduced BW in DIO mice and obese cynomolgus monkeys 33 , suggesting the potential for a GIPR/GLP-1R bispecific molecule for improving the efficacy of obesity treatment

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219 The transition to fasting enhances both the cellular NAD + level and the SIRT3 expression, which, in turn, catalyzes the deacetylation of LCAD to promote fatty-acid oxidation