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T2D is thought to be a complication of metabolic syndrome caused by disorders of energy utilization and storage [1] and characterized by insulin resistance and deficiency of insulin secretion [2]

This enzymatic process results in the depletion of NAM, a precursor of nicotinamide adenine dinucleotide (NAD + ), and the generation of SAH, a precursor of homocysteine (Hcy)

The reactions that consume NAD are mediated by enzymes involved in the non-oxidative roles of NAD [1-4]