Diabetes mellitus is a metabolic disease caused by absolute or relative lack of insulin, with disorders of glucose metabolism as the main manifestation. Although the etiology of diabetes is complex and the pathogenesis is not fully understood, the central role of pancreatic islet cells in the regulation of glucose homeostasis is indisputable. Previous studies have shown that the decline in the function and number of pancreatic islet β-cells is not only central to the development of all types of diabetes, but also an important target in the prevention and treatment of diabetes. Recent studies have found that type 2 diabetic patients also have inappropriate hyperglycemia, suggesting abnormal islet α-cell function. The newly released GLP-1 analogues and DPP-VI inhibitors have the biphasic effect of promoting insulin secretion from pancreatic β cells and inhibiting glucagon secretion from α cells. Therefore, comprehensive assessment of functional changes of pancreatic β and α cells in diabetic patients has become a key part of individualized treatment. By detecting the dynamic changes of blood glucose, insulin, C-peptide and glucagon, we can gain insight into the functional status of pancreatic β cells and α cells in diabetic patients and provide a basis for individualized treatment.