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Evidence has recently revealed that GLP-1RAs inhibit cardiac hypertrophy by upregulating GLP-1R expression and activating the AMPK/mechanistic target of the rapamycin (mTOR) signaling pathway [78]

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This is associated with reduced capacity to utilize fatty acids and glucose, and this impairment promotes lipid accumulation within muscle, aggravating IR and muscle dysfunction

doi: 10.1016/j.mayocp.2017.12.003 50 MagnussonIRothmanDLKatzLDShulmanRGShulmanGI

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A separate set of enzymes and transporters also plays a buffering role by eliminating acetyl-CoA from inside mitochondria created by the pyruvate dehydrogenase complex that is in excess of its utilization by the Krebs cycle