PMID- 23729563 OWN - NLM STAT- MEDLINE DCOM- 20150615 LR - 20140918 IS - 2191-0286 (Electronic) IS - 0792-6855 (Linking) VI - 25 IP - 1 DP - 2014 Feb TI - Testosterone promotes glucose intolerance, lipid disorder and oxidative stress in type 1 diabetic rats. PG - 13-20 LID - 10.1515/jbcpp-2012-0072 [doi] AB - 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. FAU - Morakinyo, Ayodele Olufemi AU - Morakinyo AO FAU - Adekunbi, Daniel Abiodun AU - Adekunbi DA FAU - Dada, Kayode Akanni AU - Dada KA FAU - Adegoke, Olufeyi Adefunke AU - Adegoke OA LA - eng PT - Journal Article PL - Germany TA - J Basic Clin Physiol Pharmacol JT - Journal of basic and clinical physiology and pharmacology JID - 9101750 RN - 0 (Blood Glucose) RN - 0 (Insulin) RN - 0 (Lipids) RN - 3XMK78S47O (Testosterone) RN - 4Y8F71G49Q (Malondialdehyde) RN - EC 1.11.1.6 (Catalase) RN - EC 1.15.1.1 (Superoxide Dismutase) RN - GAN16C9B8O (Glutathione) SB - IM MH - Animals MH - Blood Glucose/metabolism MH - Catalase/blood MH - Diabetes Mellitus, Experimental/complications/*metabolism MH - Glucose Intolerance/blood/complications/*metabolism MH - Glucose Tolerance Test MH - Glutathione/blood MH - Insulin/blood MH - Lipids/*blood MH - Male MH - Malondialdehyde/blood MH - Orchiectomy MH - *Oxidative Stress MH - Rats MH - Superoxide Dismutase/blood MH - Testosterone/blood/deficiency/*metabolism EDAT- 2013/06/05 06:00 MHDA- 2015/06/16 06:00 CRDT- 2013/06/05 06:00 PHST- 2013/11/24 00:00 [received] PHST- 2013/04/02 00:00 [accepted] PHST- 2013/06/05 06:00 [entrez] PHST- 2013/06/05 06:00 [pubmed] PHST- 2015/06/16 06:00 [medline] AID - /j/jbcpp.ahead-of-print/jbcpp-2012-0072/jbcpp-2012-0072.xml [pii] AID - 10.1515/jbcpp-2012-0072 [doi] PST - ppublish SO - J Basic Clin Physiol Pharmacol. 2014 Feb;25(1):13-20. doi: 10.1515/jbcpp-2012-0072.