Effects of the interaction of diabetes and iron supplementation on hepatic and pancreatic tissues, oxidative stress markers, and liver peroxisome proliferatoractivated receptorα expression.

Abstract
This study evaluated the effects of the interaction of diabetes and Copyright © 2011 JCBN 2011 This is an open access article distributed under the terms of the a carbonyl iron supplemented on hepatic and pancreatic tissues, oxidative stress markers and liver peroxisome proliferatoractivated receptorα expressions. Hamsters were divided: Control which received a standard AIN 93 diet; Control Iron, composed of control animals that received a diet with 0.83% carbonyl iron; Diabetic, composed of animals that received a injection of streptozotocin (50 mg/kg, intraperitoneal) on day 35; and Diabetic Iron composed of streptozotocin treated animals that received a diet supple mented with carbonyl iron. Diabetes increased the glucose level and reduced triglycerides. Diabetic Iron group showed higher levels of glucose and serum triglycerides as compared to the Diabetic group. Diabetes decreased mRNA levels of peroxisome proliferator activated receptorα. Iron attenuated the diabetes induced down regulation of peroxisome proliferatoractivated receptorα mRNA. Moreover, diabetes increased carbonyl protein and decreased glutathione levels and catalase activity, while iron attenuated the increase in levels of carbonyl protein and attenuated the decrease in those of glutathione level and catalase activity. Histological analysis shows that supplementation iron caused an increase in the size of the islets in Control Iron. The results show that iron does not aggravated liver oxidant/antioxidant status and per oxisome proliferatoractivated receptorα expression in diabetic hamsters.
Description
Keywords
Carbonyl iron, Streptozotocin, Hamsters, Oxidative stress
Citation
SILVA, M. et al. Effects of the interaction of diabetes and iron supplementation on hepatic and pancreatic tissues, oxidative stress markers, and liver peroxisome proliferatoractivated receptorα expression. Journal of Clinical Biochemistry and Nutrition, v. 49, p. 102-108, 2011. Disponível em: <https://www.jstage.jst.go.jp/article/jcbn/49/2/49_10-135/_article>. Acesso em: 20 de jul. 2017.