Literature DB >> 23729563

Testosterone promotes glucose intolerance, lipid disorder and oxidative stress in type 1 diabetic rats.

Ayodele Olufemi Morakinyo, Daniel Abiodun Adekunbi, Kayode Akanni Dada, Olufeyi Adefunke Adegoke.   

Abstract

BACKGROUND: A bidirectional relationship has been established between testosterone deficiency (TD) and type 2 diabetes mellitus (T2DM). Low testosterone level has been reported to be a predisposing factor to T2DM, whereas recent clinical studies have shown a high prevalence of low testosterone in diabetic individuals. However, it is not known if any relationship exists between type 1 diabetes mellitus (T1DM) and testosterone level. This study was designed to investigate the effects of TD on T1DM. Twenty-four Sprague-Dawley rats were randomly divided into four groups designated as control, diabetic, orchiectomized and orchiectomized-diabetic.
METHODS: Diabetes was induced with an intravenous injection of alloxan, and orchiectomy was done under sterile conditions. Fasting blood glucose (FBG), insulin level, lipid and oxidative parameters were determined in all experimental rats.
RESULTS: The area under the curve during oral glucose tolerance test showed that the orchiectomized-diabetic group expressed an enhanced ability to metabolize glucose than the diabetic group. The malondialdehyde level in the diabetic group was significantly higher compared with that in the control and orchiectomized groups. Moreover, there was a significant decrease in glutathione (GSH) activity and an increase in superoxide dismutase activity in the diabetic group compared with control. Meanwhile, the activities of GSH and catalase were significantly reduced in the orchiectomized as well as the orchiectomized-diabetic group when compared with both control and diabetic groups.
CONCLUSIONS: These data indicate that TD attenuates glucose intolerance under diabetic conditions and is equally associated with a considerable reduction in oxidative stress, which implies that testosterone may be a pro-oxidant.

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Year:  2014        PMID: 23729563     DOI: 10.1515/jbcpp-2012-0072

Source DB:  PubMed          Journal:  J Basic Clin Physiol Pharmacol        ISSN: 0792-6855


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