Based on the analysis presented, we propose the following scientific hypothesis: FFA metabolism reduces NAD+ levels, inhibiting AMPK and SIRT1 expression, leading to hypoxia-induced HIF-1α protein activation and β-cell dysfunction, thereby disrupting glucose homeostasis and β-cell pathophysiology, ultimately contributing to the development of T2DM; NMN intervention may delay β-cell dysfunction induced by FFA via modulating NAD+/AMPK/SIRT1/HIF-1α pathway, thereby improving T2DM. The gene discussed is PRKAA1; the disease is type 2 diabetes mellitus.