The effect of 1α,25(OH)2 D3 vitamin over oxidative stress and biochemical parameters in rats where Type 1 diabetes is formed by streptozotocin

• Published in: Journal of diabetes and its complications 2009-11, Vol.23 (6), p.401-408
• Main Authors: Çetinkalp, Şevki, Delen, Yasemin, Karadeniz, Muammer, Yüce, Gül, Yılmaz, Candeğer
• Format: Article
• Language: English
• Subjects: Endocrinology & Metabolism
• ISSN: 1056-8727
• DOI: 10.1016/j.jdiacomp.2008.09.005

Abstract Introduction The 1α,25-dihydroxyvitamin D3 [1α,25(OH)2 D3 ] plays an essential role in mineral balance but has also been recognized as a powerful modulator of immune response. We aimed to examine the effect of the 1α,25(OH)2 D3 treatment on insulin/c-peptide, catalase, superoxide dismutase (SOD), and blood glucose in rats that take streptozotocin (STZ). Methods Forty pieces of male rats of Albino family whose average weights were 261.00±07.62 g were used in the study. Rats were made diabetic by giving STZ of 40 mg/kg during 5 days through intraperitoneal path. Some of the diabetic group and nondiabetic group were received 1α,25(OH)2 D3 . The levels of SOD, insulin, c-peptide, glucose, SOD, and catalase were measured at the zero, second, fourth, and sixth weeks. Results Erythrocyte SOD levels didn't show a significant difference at the end of the sixth week in all groups when compared to the beginning. While erythrocyte catalase levels didn't show a significant difference in nondiabetic control and nondiabetic with vitamin D, and diabetic with vitamin D groups at the end of sixth week when compared to the beginning, a significant measurement was made in diabetic without vitamin D group. Maximal insulinitis scoring values were observed in diabetic without vitamin D that didn't receive 1α,25(OH)2 D3 treatment. Conclusion The highness of insulin and c-peptide levels in the group that received treatment when compared to other groups and the lowness of oxidative markers such as SOD, catalase in this study can be explained by the fact that 1α,25(OH)2 D3 treatment prevents the intervention of apoptosis mechanism.