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Patients were grouped according to background medication (metformin, sulphonylurea, thiazolidinedione, sodium-glucose cotransporter-2 inhibitor, insulin, or combinations thereof)

Therefore, whether the occurrence of a pro-oxidant state caused by an altered intracellular redox status, which might increase homocysteinylation, is one of the molecular bases of the potential atherogenicity of moderate hyperhomocysteinemia remains to be determined