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GLP-1 receptor agonism promotes insulin secretion in a glucose-dependent manner, reduces appetite, and slows gastric emptying
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[1] Selectivity testing indicated the scaffold did not inhibit related SAM-dependent methyltransferases or NAD+ salvage enzymes
In C2C12 myotubes, NNMT inhibitor treatment produces concentration-dependent increases in NADH levels (50% higher at 30 M) and reduces NAD+/NADH ratios by 25-40%
