The mTORC2/PKC pathway sustains compensatory insulin secretion of pancreatic β cells in response to metabolic stress

• Published in: Biochimica et biophysica acta. General subjects Vol. 1861; no. 8; pp. 2039 - 2047
• Main Authors: Xie, Yun, Cui, Canqi, Nie, Aifang, Wang, Yan, Ni, Qicheng, Liu, Yun, Yin, Qinglei, Zhang, Hongli, Li, Yong, Wang, Qidi, Gu, Yanyun, Ning, Guang
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier B.V 01.08.2017
• Subjects: Animals; calcium; capacitance; Diabetes Mellitus, Type 2 - etiology; Diet, High-Fat; electrophysiology; glucose; High-fat diet; insulin; Insulin - metabolism; Insulin Secretion; Insulin-Secreting Cells - metabolism; islets of Langerhans; Mechanistic Target of Rapamycin Complex 2; Mice; Mice, Inbred C57BL; Mice, Knockout; mTORC2; Multiprotein Complexes - physiology; noninsulin-dependent diabetes mellitus; palmitates; pathogenesis; phosphorylation; PKC; protein kinase C; Protein Kinase C-alpha - physiology; proteins; Signal Transduction - physiology; Stress, Physiological - physiology; Tetradecanoylphorbol Acetate - pharmacology; TOR Serine-Threonine Kinases - physiology; Type 2 Diabetes; β cell; βRicKO; PMA; HM; Type 2 Diabetes; HFD; T2D; Rictor; PKC; β cell; GIIS; NCD; Insulin secretion; High-fat diet; mTOR; TM; mTORC2

Compensation of the pancreatic β cell functional mass in response to metabolic stress is key to the pathogenesis of Type 2 Diabetes. The mTORC2 pathway governs fuel metabolism and β cell functional mass. It is unknown whether mTORC2 is required for regulating metabolic stress-induced β cell compensa...