Sodium acetate and androgen receptor blockade improve gestational androgen excess-induced deteriorated glucose homeostasis and antioxidant defenses in rats roles of adenosine deaminase and xanthine oxidase activities

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dc.contributor.authorAreola, Emmanuel
dc.contributor.authorBadmus, Olufunto
dc.contributor.authorUsman, Taofeek
dc.contributor.authorOlatunji, Lawrence Aderemi
dc.date.accessioned2025-05-12T09:58:37Z
dc.date.available2025-05-12T09:58:37Z
dc.date.issued2018-10
dc.description.abstractObjectives: Nutritional challenges and androgen excess have been implicated in the development of gestational diabetes and poor fetal outcome, but the mechanisms are not well delineated. The effects of short chain fatty acid (SCFA) on glucose dysmetabolism and poor fetal outcome induced by gestational androgen excess is also not known. We tested the hypothesis that blockade of androgen receptor (AR) and suppression of late gestational androgen excess prevents glucose dysmetabolism and poor fetal outcome through suppression of adenosine deaminase (ADA)/xanthine oxidase (XO) pathway. Methods: Twenty-four pregnant Wistar rats were treated (sc) with olive oil, testosterone propionate (0.5 mg/kg) singly or in combination with SCFA (sodium acetate; 200 mg/kg; po) or AR blocker (flutamide; 7.5 mg/kg; po) between gestational days 14 and 19. Results: The results showed that late gestational androgen excess led to glucose deregulation, poor fetal outcome, increased plasma and hepatic free fatty acid and lactate dehydrogenase (LDH), liver function marker enzymes, malondialdehyde (MDA), uric acid (UA), ADA and XO activities. Conversely, gestational androgen excess resulted in reduced body weight gain, visceral adiposity, plasma and hepatic anti-oxidant defenses (glutathione peroxidase, reduced glutathione/glutathione disulphide ratio, glucose-6-phosphate dehydrogenase, adenosine and nitric oxide). However, all these effects were ameliorated by either sodium acetate or flutamide treatment. Conclusion: The study demonstrates that suppression of testosterone by SCFA or AR blockade protects against glucose deregulation and poor fetal outcome by improvement of anti-oxidant defenses through suppression of ADA/XO pathway. Hence, utility of SCFA should be encouraged for prevention of glucose dysmetabolism and poor fetal outcome.
dc.description.sponsorshipInternational Society for Hypertension
dc.identifier.citationAreola E.D., Badmus O.O., Usman T.O., Olatunji L.A. (2018). Sodium acetate and androgen receptor blockade improve gestational androgen excess-induced deteriorated glucose homeostasis and antioxidant defenses in rats: roles of roles of adenosine deaminase and xanthine oxidase activities Journal of Hypertension 36:e33 proceedings of the 27th Scientific Meeting of the International Society of Hypertension Beijing, China. http://journals.lww.com/jhypertension/pages/default.aspx
dc.identifier.uri10.1097/01.hjh.0000548119.08608.3c
dc.identifier.urihttps://uilspace.unilorin.edu.ng/handle/123456789/16688
dc.language.isoen
dc.publisherWolters Kluwer Health
dc.relation.ispartofseries36; e33
dc.titleSodium acetate and androgen receptor blockade improve gestational androgen excess-induced deteriorated glucose homeostasis and antioxidant defenses in rats roles of adenosine deaminase and xanthine oxidase activities
dc.typeOther

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