Diabetes is caused by progressive β cell dysfunction, insulin secretion deficiency and insulin resistance. Advanced glycation end products (AGEs) are nonenzymatically formed by reducing glucose, lipids, and/or certain amino acids on proteins, lipids, and nucleic acids. Nε-(carboxymethyl) lysine (CML) and carboxyethyl

insulin secretion by 55.9% ± 10.5% (p < 0.01), 13.9% ± 2.3% (p < 0.001), 69.1% ± 0.5% (p < 0.001) respectively. Furthermore, 12.4% ± 0.1% increased of UCP2 were found in the CML-BSA treated cells. The increased UCP might contribute the declined mitochondrial respiratory activity and mitochondrial membrane potential. These results suggest that CML could attenuate insulin secretion via mitochondrial dysfunction of β cells. CML-BSA might play an important role in the progressive β cells dysfunction and loss of β cells. Abstract