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In hyperglycemic Glp1r KO mice fed HFD for 5 weeks or longer, p.o

methylmalonyl CoA mutase converts methylmalonyl CoA to succinyl CoA, with 5-deoxy adenosyl cobalamin required as a cofactor

Paradoxically, in an environment where metabolic dysfunction is being actively corrected (e.g., through improved insulin sensitivity, reduced inflammation, or calorie deficit), the net effect of improved glucose handling might facilitate more efficient fuel partitioning, thereby reducing ectopic fat accumulation in the liver

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