Browsing by Author "Usman, Taofeek Oluwamayowa"

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    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
    (Elsevier, 2018-08-29) Usman, Taofeek Oluwamayowa; Areola, Emmanuel Damilare; Badmus, Olufunto; Kim, InKyeom; Olatunji, Lawrence Aderemi
    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. 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. 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, liver function marker enzymes, malondialdehyde, uric acid, 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. 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 and replenishment of hepatic oxidative capacity through suppression of ADA/XO pathway. Hence, utility of SCFA should be encouraged for prevention of glucose dysmetabolism and poor fetal outcome.
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    Treatment with acetate during late pregnancy protects dams against testosterone-induced renal dysfunction
    (Elsevier, 2021-01-05) Olatunji, Lawrence Aderemi; Areola, Emmanuel Damilare; Usman, Taofeek Oluwamayowa; Badmus, Olufunto; Olaniyi, Kehinde Samuel
    Cardiometabolic diseases are complicated by renal damage. Gestational hyperandrogenism causes gestational metabolic dysfunction that is associated with fetal and maternal tissue derangements as well as post-partum maternal androgen excess. Acetate (Ace) conferred hepatoprotection in pregnant rats exposed to excess testos terone (Tes). The effect of excess androgenic exposure on maternal kidney during and after pregnancy is not clear. Therefore, this study investigated the effect of late gestational and post-gestational testosterone exposure on renal functions and plausible renoprotective role of gestational Ace treatment in dams. Thirty pregnant Wistar rats were grouped (n ¼ 10/group) and treated (sc) with olive oil, testosterone propionate (0.5 mg/kg) with or without acetate (200 mg/kg sodium acetate; p.o) between gestational days 14 and 19. Data were obtained from half of the animals on gestational day 20. Data were also obtained from the other half (dams) after treatment of animals which received Tes with or without prior gestational acetate treatment with post-gestational Tes (sc; 0.5 mg/kg) for the last 6 days of an 8-week postpartum period. Biochemical and statistical analyses were performed with appropriate methods and SPSS statistical software respectively. Late gestational excess Tes led to low placental weight (p ¼ 0.0001, F ¼ 205.7), poor fetal outcomes, creatinine (p ¼ 0.0001, F ¼ 385.4), urea (p ¼ 0.0001, F ¼ 300.9) and renal uric acid (UA) (p ¼ 0.0001, F ¼ 123.2), gamma-glutamyl transferase (GGT) (p ¼ 0.004, F ¼ 26.9), malondialdehyde (p ¼ 0.0001, F ¼ 45.96), and lactate dehydrogenase (LDH) (p ¼ 0.0002, F ¼ 150.7). Postpartum Tes exposure also caused elevated plasma testosterone (p ¼ 0001, F ¼ 22.15), creatinine (p ¼ 0.0002, F ¼ 15.2), urea (p ¼ 0.01, F ¼ 13.8) and renal UA (p ¼ 0.0001, 226.8), adenosine deaminase (p ¼ 0001, F ¼ 544.7), GGT (p ¼ 0.0002, F ¼ 401.4) and LDH (p ¼ 0.01, F ¼ 23.7). However, gestational acetate treatment ameliorated the renal effects of gestational and post-gestational Tes exposure. Taken together, gestational acetate would pre-programme dams against renal dysfunction caused by Tes exposure.