SNAPIN Regulates Cell Cycle Progression to Promote Pancreatic β Cell Growth

In diabetes mellitus, death of beta cell in the pancreas occurs throughout the development of the disease, with loss of insulin production. The maintenance of beta cell number is essential to maintaining normoglycemia. SNAPIN has been found to regulate insulin secretion, but whether it induces beta cell proliferation remains to be elucidated. This study aimed to explore the physiological roles of SNAPIN in beta cell proliferation. SNAPIN expression increases with the age of mice and SNAPIN is down-regulated in diabetes. KEGG pathway and GO analysis showed that SNAPIN- interacting proteins were enriched in cell cycle regulation. B cell cycle was arrested in the S phase, and cell proliferation was inhibited after SNAPIN knockdown. The expression of CDK2, CDK4 and CCND1 proteins in the S phase of the cell cycle were reduced after SNAPIN knockdown, whereas they were increased after overexpression of SNAPIN. In addition, insulin protein and mRNA levels also increased or decreased after SNAPIN knockdown or overexpression, respectively. Conclusions: Our data indicate that SNAPIN mediates beta cells proliferation and insulin secretion, and provide evidences that SNAPIN might be a pharmacotherapeutic target for diabetes mellitus.

Automated summary

This study reveals that SNAPIN plays a crucial role in regulating insulin secretion and beta cell proliferation, with its expression influenced by age and diabetes. The function of SNAPIN is achieved through its impact on cell cycle regulation, suggesting it might be a potential pharmacotherapeutic target for diabetes mellitus.