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identifier PRJEB31793
type bioproject
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title Diabetes causes marked inhibition of mitochondrial metabolism in pancreatic β-cells
description Diabetes is a global health problem caused primarily by the inability of pancreatic β-cells to secrete adequate levels of insulin. The molecular mechanisms underlying the progressive failure of β-cells to respond to glucose in type-2 diabetes remain unresolved. Using a combination of transcriptomics and proteomics, we find significant dysregulation of major metabolic pathways in islets of diabetic βV59M mice, a non-obese, eulipidaemic diabetes model. Multiple genes/proteins involved in glycolysis/gluconeogenesis are upregulated, whereas those involved in oxidative phosphorylation are downregulated. In isolated islets, glucose-induced increases in NADH and ATP are impaired and both oxidative and glycolytic glucose metabolism are reduced. INS-1 β-cells cultured chronically at high glucose show similar changes in protein expression and reduced glucose-stimulated oxygen consumption: targeted metabolomics reveals impaired metabolism. These data indicate hyperglycaemia induces metabolic changes in β-cells that markedly reduce mitochondrial metabolism and ATP synthesis. We propose this underlies the progressive failure of β-cells in diabetes.
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dbXrefs
sra-run  ERR3238076ERR3238077ERR3238078ERR3238079ERR3238080ERR3238081ERR3238082
sra-submission  ERA1782188
biosample  SAMEA5523462SAMEA5523463SAMEA5523464SAMEA5523465SAMEA5523466SAMEA5523467SAMEA5523468
sra-study  ERP114395
sra-sample  ERS3325545ERS3325546ERS3325547ERS3325548ERS3325549ERS3325550ERS3325551
sra-experiment  ERX3265454ERX3265455ERX3265456ERX3265457ERX3265458ERX3265459ERX3265460
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status public
visibility unrestricted-access
dateCreated 2019-04-12T00:00:00Z
dateModified 2019-04-12T00:00:00Z
datePublished