A Defect in Mitochondrial Complex III but Not in Complexes I or IV Causes Early β-Cell Dysfunction and Hyperglycemia in Mice
Overview
Authors
Affiliations
Article Highlights: Mitochondrial metabolism is critical for β-cell insulin secretion, and mitochondrial dysfunction is involved in type 2 diabetes pathogenesis. We determined whether individual oxidative phosphorylation complexes contribute uniquely to β-cell function. Compared with loss of complex I and IV, loss of complex III resulted in severe in vivo hyperglycemia and altered β-cell redox status. Loss of complex III altered cytosolic and mitochondrial Ca2+ signaling and increased expression of glycolytic enzymes. Individual complexes contribute differently to β-cell function. This underscores the role of mitochondrial oxidative phosphorylation complex defects in diabetes pathogenesis.
HADHA Regulates Respiratory Complex Assembly and Couples FAO and OXPHOS.
Qin C, Gong S, Liang T, Zhang Z, Thomas J, Deng J Adv Sci (Weinh). 2024; 11(47):e2405147.
PMID: 39488787 PMC: 11653673. DOI: 10.1002/advs.202405147.
Glucose Regulation of β-Cell KATP Channels: It Is Time for a New Model!.
Merrins M, Kibbey R Diabetes. 2024; 73(6):856-863.
PMID: 38768366 PMC: 11109790. DOI: 10.2337/dbi23-0032.
Mitochondrial bioenergetics, metabolism, and beyond in pancreatic β-cells and diabetes.
Rivera Nieves A, Wauford B, Fu A Front Mol Biosci. 2024; 11:1354199.
PMID: 38404962 PMC: 10884328. DOI: 10.3389/fmolb.2024.1354199.