The accumulation of advanced glycation end products (AGEs), as an important mechanism in the pathogenesis of diabetes, can cause oxidative stress damage and lead to cell dysfunction or even death, which eventually leads to multiple histiocytic damage in diabetes [2] When enteroendocrine cells distributed in the intestinal epithelium are continuously exposed to high concentrations of AGEs, the secretion function of incretin is impaired. This evidence concerns the gene GCG and diabetes mellitus.