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• W79658936 abstract "1) Abstract　The aim of this study was to determine the time course and mechanism of hypoxia‑induced pancreatic islet dysfunction. Islets isolated from Sprague Dawley rats were cultured in 1% O2 (hypoxia) . Glucose stimulated insulin secretion (GSIS) was then examined for islets in either static or perifused cultures followed by an evaluation of mitochondrial activity and islet cell death. Additionally we examined the eff ect of culturing previously hypoxic islets for an additional 24 h under normoxia to determine whether the hypoxic eff ects were reversible and to assess the eff ects of re‑oxygenation on GSIS. In the static islet culture insulin secretion declined signifi cantly after 24 h. In perifused islets the area under the curve (AUC) of fi rst‑phase GSIS declined signifi cantly after 6 h while the AUC of second‑phase GSIS decreased signifi cantly after 12 h. Mitochondrial activity dropped markedly after 48 h but cell death assays revealed that apoptosis did not increase in the time period from 6 h to 48 h. However necrosis increased signifi cantly after 24 h. In the re‑oxygenation study the return to normoxia signifi cantly worsened the decline in GSIS. In conclusion exposure to hypoxia fi rst causes functional disorder in the islets followed by cell death due to necrosis rather than apoptosis. Furthermore re‑oxygenation aggravated islet dysfunction." @default.
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• W79658936 date "2009-03-31" @default.
• W79658936 modified "2023-09-26" @default.
• W79658936 title "HYPOXIA INDUCES DYSFUNCTION AND CELL DEATH OF THE RAT PANCREATIC ISLET" @default.
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