Insulin Release from the Beta Cells in Acatalasemic Mice Is Highly Susceptible to Alloxan-Induced Oxidative Stress

Takemoto, Kazunori and Doi, Wakana and Kataoka, Ken and Ishihara, Kohji and Wang, Da-Hong and Sugiyama, Hitoshi and Masuoka, Noriyoshi (2015) Insulin Release from the Beta Cells in Acatalasemic Mice Is Highly Susceptible to Alloxan-Induced Oxidative Stress. Journal of Diabetes Mellitus, 05 (02). pp. 81-89. ISSN 2160-5831

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Abstract

Background: Catalase deficiency (acatalasemia) is sensitive to alloxan, and the administration to acatalasemic mice develops hyperglycemia under mild conditions. However, the mechanism is still poorly understood. Methods: Alloxan was used to induce the oxidative stress and intraperitoneally administered to acatalasemic and normal mice. The blood samples of these mice after 1, 3, 5 and 7 days were examined. The pancreatic islets 7 days after alloxan administration were isolated, and the insulin released under 3 mM and 20 mM glucose was examined. Results: After alloxan administration, increase of oxidative markers in blood and pancreatic apoptosis in acatalasemic mice were observed immediately. Insulin in blood was lowered after 3 days, and the insulin in acatalasemic mice was lower than that in normal mice. Hyperglycemia in the acatalasemic mice was observed after 3 days. The pancreatic islets after 7 days were isolated. A reduction of the insulin released from the islets under glucose stimulation was observed. The stimulation indexes of the normal and acatalasemic mice were 1.4 ± 0.6 and 0.7 ± 0.3, respectively. Conclusions: Alloxan induced a deterioration of glucose-dependent insulin secretion ability from the islets, and the deterioration mostly contributed to hyperglycemia, rather than apoptosis.

Item Type: Article
Subjects: Open Archive Press > Medical Science
Depositing User: Unnamed user with email support@openarchivepress.com
Date Deposited: 10 Mar 2023 07:33
Last Modified: 02 Oct 2024 08:21
URI: http://library.2pressrelease.co.in/id/eprint/657

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