Olatunji Lawrence A, Areola Emmanuel D, Usman Taofeek O, Badmus Olufunto O, Olaniyi Kehinde S
HOPE Cardiometabolic Research Team and Department of Physiology, College of Health Sciences, University of Ilorin, Nigeria.
Cardiovascular Unit, Department of Physiology, College of Health Sciences, Osun State University, Osogbo, Nigeria.
Heliyon. 2021 Jan 7;7(1):e05920. doi: 10.1016/j.heliyon.2021.e05920. eCollection 2021 Jan.
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 testosterone . 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 = 10/group) and treated (sc) with olive oil, testosterone propionate (0.5 mg/kg) with or without acetate (200 mg/kg sodium acetate; ) 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 with or without prior gestational acetate treatment with post-gestational (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 led to low placental weight (p = 0.0001, F = 205.7), poor fetal outcomes, creatinine (p = 0.0001, F = 385.4), urea (p = 0.0001, F = 300.9) and renal uric acid (UA) (p = 0.0001, F = 123.2), gamma-glutamyl transferase (GGT) (p = 0.004, F = 26.9), malondialdehyde (p = 0.0001, F = 45.96), and lactate dehydrogenase (LDH) (p = 0.0002, F = 150.7). Postpartum exposure also caused elevated plasma testosterone (p = 0001, F = 22.15), creatinine (p = 0.0002, F = 15.2), urea (p = 0.01, F = 13.8) and renal UA (p = 0.0001, 226.8), adenosine deaminase (p = 0001, F = 544.7), GGT (p = 0.0002, F = 401.4) and LDH (p = 0.01, F = 23.7). However, gestational acetate treatment ameliorated the renal effects of gestational and post-gestational exposure. Taken together, gestational acetate would pre-programme dams against renal dysfunction caused by exposure.
心脏代谢疾病常伴有肾脏损害。妊娠期雄激素过多会导致妊娠代谢功能障碍，这与胎儿和母体组织紊乱以及产后母体雄激素过多有关。醋酸盐（Ace）对暴露于过量睾酮的妊娠大鼠具有肝脏保护作用。孕期及产后过量雄激素暴露对母体肾脏的影响尚不清楚。因此，本研究调查了妊娠晚期及产后睾酮暴露对肾功能的影响，以及妊娠期醋酸盐治疗对母鼠可能的肾脏保护作用。将30只妊娠Wistar大鼠分组（每组n = 10），并在妊娠第14至19天期间皮下注射橄榄油、丙酸睾酮（0.5 mg/kg），同时或不同时给予醋酸盐（200 mg/kg醋酸钠）。在妊娠第20天从一半动物获取数据。在产后8周的最后6天，对接受或未接受妊娠醋酸盐治疗的动物进行产后皮下注射丙酸睾酮（0.5 mg/kg）处理后，也从另一半动物（母鼠）获取数据。分别采用适当方法和SPSS统计软件进行生化和统计分析。妊娠晚期雄激素过多导致胎盘重量降低（p = 0.0001，F = 205.7）、胎儿结局不良、肌酐水平升高（p = 0.0001，F = 385.4）、尿素水平升高（p = 0.0001，F = 300.9）、肾脏尿酸（UA）水平升高（p = 0.0001，F = 123.2）、γ-谷氨酰转移酶（GGT）水平升高（p = 0.004，F = 26.9）、丙二醛水平升高（p = 0.0001，F = 45.96）以及乳酸脱氢酶（LDH）水平升高（p = 0.0002，F = 150.7）。产后雄激素暴露还导致血浆睾酮水平升高（p = 0.001，F = 22.15）、肌酐水平升高（p = 0.0002，F = 15.2）、尿素水平升高（p = 0.01，F = 13.8）、肾脏UA水平升高（p = 0.0001，F = 226.8）、腺苷脱氨酶水平升高（p = 0.001，F = 544.7）、GGT水平升高（p = 0.0002，F = 401.4）以及LDH水平升高（p = 0.01，F = 23.7）。然而，妊娠期醋酸盐治疗改善了妊娠晚期及产后雄激素暴露对肾脏的影响。综上所述，妊娠期醋酸盐可使母鼠预先抵御雄激素暴露引起的肾功能障碍。
