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• W2948917215 abstract "Glucotoxicity-induced β-cell dysfunction in type 2 diabetes is associated with alterations of mitochondria and the endoplasmic reticulum (ER). Both organelles interact at contact sites, defined as mitochondria-associated membranes (MAMs), which were recently implicated in the regulation of glucose homeostasis. The role of MAMs in β-cells is still largely unknown, and their implication in glucotoxicity-associated β-cell dysfunction remains to be defined. Here, we report that acute glucose treatment stimulated ER-mitochondria interactions and calcium (Ca2+) exchange in INS-1E cells, whereas disruption of MAMs altered glucose-stimulated insulin secretion (GSIS). Conversely, chronic incubations with high glucose of either INS-1E cells or human pancreatic islets altered GSIS and concomitantly reduced ER Ca2+ store, increased basal mitochondrial Ca2+, and reduced ATP-stimulated ER-mitochondria Ca2+ exchanges, despite an increase of organelle interactions. Furthermore, glucotoxicity-induced perturbations of Ca2+ signaling are associated with ER stress, altered mitochondrial respiration, and mitochondria fragmentation, and these organelle stresses may participate in increased organelle tethering as a protective mechanism. Last, sustained induction of ER-mitochondria interactions using a linker reduced organelle Ca2+ exchange, induced mitochondrial fission, and altered GSIS. Therefore, dynamic organelle coupling participates in GSIS in β-cells, and over time, disruption of organelle Ca2+ exchange might be a novel mechanism contributing to glucotoxicity-induced β-cell dysfunction." @default.
• W2948917215 created "2019-06-14" @default.
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• W2948917215 date "2019-06-07" @default.
• W2948917215 modified "2023-10-17" @default.
• W2948917215 title "Differential Effect of Glucose on ER-Mitochondria Ca2+ Exchange Participates in Insulin Secretion and Glucotoxicity-Mediated Dysfunction of β-Cells" @default.
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• W2948917215 doi "https://doi.org/10.2337/db18-1112" @default.
• W2948917215 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/31175102" @default.
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