1. Academic Validation
  2. Glibenclamide-Induced Autophagy Inhibits Its Insulin Secretion-Improving Function in β Cells

Glibenclamide-Induced Autophagy Inhibits Its Insulin Secretion-Improving Function in β Cells

  • Int J Endocrinol. 2019 Aug 15;2019:1265175. doi: 10.1155/2019/1265175.
Jiali Zhou 1 2 Xincong Kang 1 2 Yushuang Luo 1 2 Yuju Yuan 3 Yanyang Wu 3 Meijun Wang 1 Dongbo Liu 1 2 4 5
Affiliations

Affiliations

  • 1 Horticulture and Landscape College, Hunan Agricultural University, Changsha 410128, China.
  • 2 State Key Laboratory of Subhealth Intervention Technology, Changsha 410128, China.
  • 3 College of Food Science and Technology, Hunan Agricultural University, Changsha 410128, China.
  • 4 Hunan Provincial Key Laboratory of Crop Germplasm Innovation and Utilization, Hunan Agricultural University, Changsha 410128, China.
  • 5 Hunan Co-Innovation Center for Utilization of Botanical Functional Ingredients, Changsha 410128, China.
Abstract

Diabetes is a Metabolic Disease, partly due to hypoinsulinism, which affects ∼8% of the world's adult population. Glibenclamide is known to promote Insulin secretion by targeting β cells. Autophagy as a self-protective mechanism of cells has been widely studied and has particular physiological effects in different tissues or cells. However, the interaction between Autophagy and glibenclamide is unclear. In this study, we investigated the role of Autophagy in glibenclamide-induced Insulin secretion in pancreatic β cells. Herein, we showed that glibenclamide promoted Insulin release and further activated Autophagy through the adenosine 5'-monophosphate (AMP) activated protein kinase (AMPK) pathway in MIN-6 cells. Inhibition of Autophagy with Autophagy Inhibitor 3-methyladenine (3-MA) potentiated the secretory function of glibenclamide further. These results suggest that glibenclamide-induced Autophagy plays an inhibitory role in promoting Insulin secretion by activating the AMPK pathway instead of altering the mammalian target of rapamycin (mTOR).

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