Adeyemi Toluwalope E, Ajonijebu Duyilemi C, Channa Mahendra L, Nadar Anand
Discipline of Human Physiology, School of Laboratory Medicine and Medical Sciences, College of Health Sciences, University of KwaZulu-Natal, Private Bag X54001, Durban, 4000, South Africa.
Department of Physiology, School of Biomolecular and Chemical Sciences, Nelson Mandela University, Port Elizabeth, South Africa.
Heliyon. 2021 Apr 28;7(4):e06847. doi: 10.1016/j.heliyon.2021.e06847. eCollection 2021 Apr.
Oxidative stress is usually associated with prolonged intake of high-fat diet (HFD). However, little is known about the impact of maternal HFD on endogenous modulation of antioxidant-defence-enzyme-network, its link to adverse fetal growth and overall effects of Quercetin-3-o-rutinoside (QR) supplementation. Sprague-Dawley rats were initially assigned to normal diet (ND) or HFD for 8 weeks and mated. Post-conception, rats were further divided into four groups, of which two groups had diets supplemented with QR while others continued with their respective diets until delivery. Measurements include food and water consumption, physical parameters (body weight, body mass index (BMI) and fur appearance), oral glucose tolerance, lipid profiles, and placental/liver oxidative changes. We observed that water consumption was significantly increased in dams fed HFD without marked differences in food intake, body weight, BMI and glucose tolerance. Surprisingly, offspring of HFD-fed dams had reduced body weight marked by delayed fur appearance compared to the ND offspring. In dams, there were alterations in lipid profile. Lipid peroxidation was increased in the placenta and liver of gestational day (GD) 19 HFD-fed dams and their postnatal day (PND) 21 male offspring. There was evidence of HFD-induced nitrosative stress in dams and PND28 female offspring. Adaptive defence indicate decreased placenta and liver superoxide dismutase (SOD) levels as well as differential changes in total antioxidant capacity (TAC) and catalase (CAT) activity in HFD treated dams and their progenies. Overall, the results indicate that intrauterine metabolic alterations associated with maternal high-fat consumption may induce oxidative challenge in the offspring accompanied by mild developmental consequences, while QR supplementation has little or no beneficial effects.
氧化应激通常与长期摄入高脂饮食（HFD）有关。然而，关于母体高脂饮食对抗氧化防御酶网络内源性调节的影响、其与胎儿生长不良的联系以及槲皮素-3-O-芸香糖苷（QR）补充的总体效果，人们了解甚少。将Sprague-Dawley大鼠最初分为正常饮食（ND）组或高脂饮食组，持续8周，然后进行交配。受孕后，大鼠进一步分为四组，其中两组的饮食补充了QR，而其他两组继续各自的饮食直至分娩。测量指标包括食物和水的消耗量、身体参数（体重、体重指数（BMI）和皮毛外观）、口服葡萄糖耐量、血脂谱以及胎盘/肝脏的氧化变化。我们观察到，喂食高脂饮食的母鼠水消耗量显著增加，而食物摄入量、体重、BMI和葡萄糖耐量没有明显差异。令人惊讶的是，与正常饮食组的后代相比，喂食高脂饮食的母鼠所产后代体重减轻，皮毛出现延迟。母鼠的血脂谱发生了改变。在妊娠第19天喂食高脂饮食的母鼠及其出生后第21天的雄性后代的胎盘和肝脏中，脂质过氧化增加。有证据表明，在母鼠和出生后第28天的雌性后代中存在高脂饮食诱导的亚硝化应激。适应性防御表明，在接受高脂饮食处理的母鼠及其后代中，胎盘和肝脏超氧化物歧化酶（SOD）水平降低，总抗氧化能力（TAC）和过氧化氢酶（CAT）活性也有不同变化。总体而言，结果表明，与母体高脂肪摄入相关的子宫内代谢改变可能会在后代中引发氧化应激，并伴有轻度发育后果，而补充QR几乎没有有益效果。
