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This inhibition reduces intracellular 1-methylnicotinamide (1-MNA) production (EC50 = 2.3 M) and preserves nicotinamide availability for the NAD+ salvage pathway

Since growth hormone signaling drives cellular proliferation and protein synthesis in fibroblasts, this amplification creates a stronger repair response

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This contraindication stems from observations in rodent studies where semaglutide and other GLP-1 receptor agonists caused dose-dependent and treatment-duration-dependent thyroid C-cell tumors

It does not transform that hypothesis into an authorised human claim

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