Author(s)

Kazunori Takemoto¹, Wakana Doi², Ken Kataoka², Kohji Ishihara², Da-Hong Wang^3., Hitoshi Sugiyama⁴, Noriyoshi Masuoka^2*

¹Medical Science Education Center, Okayama University of Science, Okayama, Japan.
²Department of Life Science, Faculty of Science, Okayama University of Science, Okayama, Japan.
³Department of Biochemistry, Faculty of Science, Okayama University of Science, Okayama, Japan.
⁴Department of Medicine and Clinical Science, Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University, Okayama, Japan.

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.

Alloxan, Hyperglycemia, Acatalasemia, Insulin Release, Diabetes, Beta Cells

Takemoto, K. , Doi, W. , Kataoka, K. , Ishihara, K. , Wang, D. , Sugiyama, H. and Masuoka, N. (2015) Insulin Release from the Beta Cells in Acatalasemic Mice Is Highly Susceptible to Alloxan-Induced Oxidative Stress. Journal of Diabetes Mellitus, 5, 81-89. doi: 10.4236/jdm.2015.52010.