@article{oai:hirosaki.repo.nii.ac.jp:00003661,
 author = {Tomotsune, Ken and Ogawa, Yoshiji and Hasegawa, Noriyuki and Kudo, Takanori and Naraoka, Maki and Chikazawa, Shinji and Tamasawa, Naoki and Suda, Toshihiro},
 issue = {1/2/3/4},
 journal = {弘前医学},
 month = {Mar},
 note = {application/pdf, The aim of this study was to determine the time course and mechanism of hypoxia-induced pancreaticislet dysfunction. Islets isolated from Sprague Dawley rats were cultured in 1％ O2（ hypoxia）. Glucose stimulatedinsulin secretion（ GSIS） was then examined for islets in either static or perifused cultures, followed by an evaluation ofmitochondrial activity and islet cell death. Additionally, we examined the eff ect of culturing previously hypoxic islets foran additional 24 h under normoxia to determine whether the hypoxic eff ects were reversible and to assess the eff ects ofre-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 GSISdecreased signifi cantly after 12 h. Mitochondrial activity dropped markedly after 48 h, but cell death assays revealedthat 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, exposureto 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., 弘前医学. 60(1/2/3/4), 2009, p.54-62},
 pages = {54--62},
 title = {Hypoxia induces Dysfunction and Cell Death of the Rat Pancreatic Isle},
 volume = {60},
 year = {2009}
}