Hypoxia induces Dysfunction and Cell Death of the Rat Pancreatic Isle
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概要
- 論文の詳細を見る
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.
- 弘前大学の論文
著者
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Ogawa Yoshiji
Diabetes Unit Aomori Prefectural Central Hospital
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Suda Toshihiro
Department Of Endocrinology And Metabolism Hirosaki University Graduate School Of Medicine
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Suda Toshihiro
Department Of Endocrinology And Metabolism Hirosaki University Graduated School Of Medicine
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Tomotsune Ken
Department of Endocrinology and Metabolism, Hirosaki University Graduated School of Medicine
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Hasegawa Noriyuki
Department of Internal Medicine, Itayanagi Central Hospital
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Kudo Takanori
Department of Endocrinology and Metabolism, Hirosaki University Graduated School of Medicine
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Naraoka Maki
Department of Endocrinology and Metabolism, Hirosaki University Graduated School of Medicine
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Chikazawa Shinji
Department of Endocrinology and Metabolism, Hirosaki University Graduated School of Medicine
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Tamasawa Naoki
Department of Endocrinology and Metabolism, Hirosaki University Graduated School of Medicine
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Kudo Takanori
Department Of Endocrinology And Metabolism Hirosaki University Graduated School Of Medicine
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Hasegawa Noriyuki
Department Of Internal Medicine Itayanagi Central Hospital
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Naraoka Maki
Department Of Endocrinology And Metabolism Hirosaki University Graduate School Of Medicine
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Naraoka Maki
Department Of Endocrinology And Metabolism Hirosaki University Graduated School Of Medicine
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Tomotsune Ken
Department Of Endocrinology And Metabolism Hirosaki University Graduated School Of Medicine
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Tamasawa Naoki
Department Of Endocrinology And Metabolism Hirosaki University Graduate School Of Medicine
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Tamasawa Naoki
Department Of Endocrinology And Metabolism Hirosaki University Graduated School Of Medicine
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Chikazawa Shinji
Department Of Endocrinology And Metabolism Hirosaki University Graduated School Of Medicine
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友常 健
Department of Endocrinology and Metabolism, Hirosaki University Graduated School of Medicine
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小川 吉司
Diabetes Unit, Aomori Prefectural Central Hospital
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長谷川 範幸
Department of Internal Medicine, Itayanagi Central Hospital
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Kudo Takanori
Department of Applied Chemistry, Graduate School of Engineering, The University of Tokyo
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