Effects of the interaction of diabetes and iron supplementation on hepatic and pancreatic tissues, oxidative stress markers, and liver peroxisome proliferatoractivated receptorα expression.
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2011
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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.
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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.