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Int J Physiol Pathophysiol Pharmacol 2012;4(3):156-166

Original Article
Effects of estrogen on hyperglycemia and liver dysfunction in diabetic male rats

Marwa A Ahmed, Khaled M A Hassanein

Department of Physiology Faculty of Medicine, Assiut University, Assiut 71526, Egypt; Department of Pathology and Clinical Pathology,
Faculty of Veterinary Medicine, Assiut University, Assiut 71526, Egypt

Received July 7, 2012; accepted August 28, 2012; Epub September 20, 2012; Published September 30, 2012

Abstract: Objective: To study the possible beneficial effect of estrogen (17β-estradiol E2) on hyperglycemia, oxidative stress and liver
dysfunctions in STZ-induced diabetic rats. A total of 40 albino male rats were randomly divided into four groups: a control group (I), a
diabetic group (II), a group given 17β estradiol (E2) for 15 days (III), and a diabetic group given E2 for 30 days (IV). Diabetes was
induced in the rats by 65 mg/kg streptozosin (STZ) via an intraperitoneal (i.p.) injection. E2 was given in a dose of 500ug/kg/day by oral
gavage. Results: E2 administration significantly lowered plasma glucose levels, increased plasma insulin levels, and improved
glucose tolerance of groups III and IV. In addition, E2 enhanced glutathione peroxidase (GPX) and reduced lipid peroxidation in the
hepatic tissues (as compared to diabetic rats). E2 caused significant decrease of plasmatic phosphatase alkaline (PAL), lactate
dehydrogenase (LDH), aspartate and lactate transaminases (AST and ALT) activities of group III and IV compared to group II. Moreover,
E2 restored the histological structure of the liver and pancreas of treated groups and increased the insulin receptors expression in the
liver of groups III and IV compared to diabetic rats. Notably, these beneficial effects of E2 on diabetic rats were more prominent in group
IV compared to those of group III. Conclusion: E2 has a beneficial effect on hyperglycemia, oxidative stress and ameliorates the liver
dysfunction in diabetic rats and these effects may be mediated through stimulating β-cell proliferation in pancreas and increased the
insulin receptor expression in the liver tissues. (IJPPP1207003).

Keywords: 17 β estradiol, diabetes, insulin, glucose tolerance, liver-male rat


Address all correspondence to:
Dr. Marwa A Ahmed
Associate Professor of Physiology
Faculty of Medicine, Assiut University
Assiut 71526, Egypt.
Tel: +20882286584
E-mail: m_az_ahmed@yahoo.com