Article citationsMore>>

Kikumoto, Y., Sugiyama, H., Inoue, T., Morinaga, H., Takiue, K., Kitagawa, M., Fukuoka, N., Saeki, M., Maeshima, Y., Wang, D.H., Ogino, K., Masuoka, N. and Makino, H. (2010) Sensitization to Alloxan-Induced Diabetes and Pancreatic Cell Apoptosis in Acatalasemic Mice. Biochimica et Biophysica Acta, 1802, 240-246. http://dx.doi.org/10.1016/j.bbadis.2009.10.009

has been cited by the following article:

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

  AUTHORS: Kazunori Takemoto, Wakana Doi, Ken Kataoka, Kohji Ishihara, Da-Hong Wang, Hitoshi Sugiyama, Noriyoshi Masuoka

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

  JOURNAL NAME: Journal of Diabetes Mellitus, Vol.5 No.2, May 5, 2015

  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.