부산대학교 도서관

Pancreatic beta cells are insulin-producing cells that are structurally and functionally polarized in the islets of Langerhans. The organization and position of the Golgi complex play a key role in maintaining a polarized cell state, but the factors and molecular mechanisms determining the Golgi polarization of pancreatic beta cells are still unknown. In the current study, using pancreatic beta cell-specific Atg5 knockout mice, we found that Atg5 , an essential gene for autophagy, plays a pivotal role in regulating Golgi integrity and polarization by affecting the expression of genes involved in vesicle transport. Deletion of Atg5 led to endoplasmic reticulum (ER) stress and impaired the distribution of proinsulin and insulin secretion of pancreatic beta cells, which further exacerbates diabetes. These results contribute to a comprehensive understanding of autophagy-mediated Golgi polarization and its regulation of the function of pancreatic beta cells. • Knockout of pancreatic beta cell-specific Atg5 in mice leads to diabetes mellitus. • ATG5 regulates gene expression profiling associated with ER-Golgi and Golgi-ER vesicle trafficking. • ATG5 plays an important role in maintaining Golgi polarization in pancreatic beta cells. [ABSTRACT FROM AUTHOR]