Hypoxia Induces Dysfunction and Cell Death of the Rat Pancreatic Islet
Year: 2009
Type: article
Abstract: The aim of this study was to determine the time course and mechanism of hypoxia-induced pancreatic\nislet dysfunction. Islets isolated from Sprague Dawley rats were cultured in 1％ O2（ hypoxia）. Glucose stimulated\ninsulin secretion（ GSIS） was then examined for islets in either static or perifused cultures, followed by an evaluation of\nmitochondrial activity and islet cell death. Additionally, we examined the eff ect of culturing previously hypoxic islets for\nan additional 24 h under normoxia to determine whether the hypoxic eff ects were reversible and to assess the eff ects of\nre-oxygenation on GSIS. In the static islet culture, insulin secretion declined signifi cantly after 24 h. In perifused islets,\nthe area under the curve（ AUC） of fi rst-phase GSIS declined signifi cantly after 6 h, while the AUC of second-phase GSIS\ndecreased signifi cantly after 12 h. Mitochondrial activity dropped markedly after 48 h, but cell death assays revealed\nthat apoptosis did not increase in the time period from 6 h to 48 h. However, necrosis increased signifi cantly after 24 h.\nIn the re-oxygenation study, the return to normoxia signifi cantly worsened the decline in GSIS. In conclusion, exposure\nto hypoxia fi rst causes functional disorder in the islets, followed by cell death due to necrosis rather than apoptosis.\nFurthermore, re-oxygenation aggravated islet dysfunction.
Language: English
Subfield: Endocrinology, Diabetes and Metabolism
Field: Medicine
Domain: Health Sciences
Open Access status: green
OpenAlex ID: W79658936