2014
DOI: 10.18632/aging.100647
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Abstract: Hyperglycemia impairs insulin secretion as well as insulin action, being recognized as the glucotoxicity that accelerates diabetes. However, the mechanism underlying the glucotoxicity in pancreatic β-cells is not thoroughly understood. Hyperglycemia alters glucose metabolism within β-cells and interstitial conditions around β-cells, including elevated osmolarity and increased concentrations of insulin and ATP released from overstimulated β-cells. In this study, to explore direct effects of these alterations on… Show more

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Cited by 8 publications
(3 citation statements)
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References 19 publications
(26 reference statements)
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“…During development and progression of diabetes, many pathways are upregulated in an attempt to handle the overflow of glucose in the body. These pathways include the polyol pathway, the glycation pathway, the protein kinase c pathway, the hexosamine pathway, and the enediol/alpha‐ketoaldehyde pathway . It is now believed that all the pathways converge on elevation of reactive oxygen species (ROS) by a variety of ROS generation systems …”
Section: Introductionmentioning
confidence: 99%
“…During development and progression of diabetes, many pathways are upregulated in an attempt to handle the overflow of glucose in the body. These pathways include the polyol pathway, the glycation pathway, the protein kinase c pathway, the hexosamine pathway, and the enediol/alpha‐ketoaldehyde pathway . It is now believed that all the pathways converge on elevation of reactive oxygen species (ROS) by a variety of ROS generation systems …”
Section: Introductionmentioning
confidence: 99%
“…However, chronic exposure to hyperglycemia leads to accumulation of ROS due to incomplete reduction of oxygen during glucose metabolism [ 200 , 201 ]. In addition, aberrant glucose metabolism generates ROS through activation of protein kinase C, glucose auto-oxidation, generation of excessive superoxide, increased hexosamine metabolism, and increased islet amyloid deposition [ 202 , 203 , 204 ]. A major factor contributing to pancreatic β-cell dysfunction is oxidative stress-mediated mitochondrial damage [ 205 ].…”
Section: Nrf2 Agonism In Diabetes and Its Complicationsmentioning
confidence: 99%
“…Apart from the protein O-GlcNAc modification, activation of HBP produces H 2 O 2 , and may independently induce cellular dysfunction in pancreatic β-cells [ 6 ]. This pathway was also implicated in interfering with the required influx of Ca +2 into β-cells that is required for insulin secretion [ 11 ].…”
Section: Hyperglycemia and Glucose Metabolismmentioning
confidence: 99%