Olaniyi Kehinde Samuel, Sabinari Isaiah Woru, Olatunji Lawrence Aderemi
HOPE Cardiometabolic Research Team & Department of Physiology, College of Health Sciences, University of Ilorin, P.M.B. 1515, Ilorin, Nigeria.
Department of Physiology, College of Medicine and Health Sciences, Afe Babalola University, Ado-Ekiti, Nigeria.
Heliyon. 2020 Dec 28;6(12):e05863. doi: 10.1016/j.heliyon.2020.e05863. eCollection 2020 Dec.
Metabolic adaptation of pregnant mothers is crucial for placental development and fetal growth/survival. However, evidence exists that indiscriminate consumption of fructose-enriched drink (FED) during pregnancy disrupts maternal-fetal metabolic tolerance with attendant adverse fetal outcomes. Glutamine supplementation (GLN) has been shown to exert a modulatory effect in metabolic disorders. Nevertheless, the effects of GLN on FED-induced poor fetal outcome, and in particular the impacts on placental uric acid/lipid accumulation are unknown. The present study was conducted to test the hypothesis that oral GLN improves fetal outcome by attenuating placental lipid accumulation and uric acid synthesis in pregnant rats exposed to FED.
Pregnant Wistar rats (160-180 g) were randomly allotted to control, GLN, FED and FED + GLN groups (6 rats/group). The groups received vehicle by oral gavage, glutamine (1 g/kg) by oral gavage, fructose (10%; w/v) and fructose + glutamine, respectively, through gestation.
Data showed that FED during pregnancy caused placental inefficiency, reduced fetal growth, and caused insulin resistance with correspondent increase in fasting blood glucose and plasma insulin. FED also resulted in an increased placental triglyceride, total cholesterol and uric acid synthesis by activating adenosine deaminase and xanthine oxidase activities. Moreover, FED during pregnancy led to increased lipid peroxidation, lactate production with correspondent decreased adenosine and glucose-6-phosphate dehydrogenase-dependent antioxidant defense. These alterations were abrogated by GLN supplementation.
These findings implicate that high FED intake during pregnancy causes poor fetal outcome via defective placental uric acid/triglyceride-dependent mechanism. The findings also suggest that oral GLN improves fetal outcome by ameliorating placental defects through suppression of uric acid/triglyceride accumulation.
怀孕母亲的代谢适应对胎盘发育和胎儿生长/存活至关重要。然而，有证据表明，孕期无差别饮用富含果糖的饮料（FED）会破坏母婴代谢耐受性，并伴有不良胎儿结局。补充谷氨酰胺（GLN）已被证明在代谢紊乱中发挥调节作用。然而，GLN对FED诱导的不良胎儿结局的影响，特别是对胎盘尿酸/脂质积累的影响尚不清楚。本研究旨在验证以下假设：口服GLN可通过减轻暴露于FED的怀孕大鼠胎盘脂质积累和尿酸合成来改善胎儿结局。
将怀孕的Wistar大鼠（160 - 180克）随机分为对照组、GLN组、FED组和FED + GLN组（每组6只大鼠）。各组在整个妊娠期分别通过口服灌胃给予赋形剂、谷氨酰胺（1克/千克）、果糖（10%；w/v）和果糖 + 谷氨酰胺。
数据显示，孕期FED导致胎盘功能低下、胎儿生长受限，并引起胰岛素抵抗，同时空腹血糖和血浆胰岛素相应增加。FED还通过激活腺苷脱氨酶和黄嘌呤氧化酶活性导致胎盘甘油三酯、总胆固醇和尿酸合成增加。此外，孕期FED导致脂质过氧化增加、乳酸生成增加，同时腺苷和葡萄糖 - 6 - 磷酸脱氢酶依赖性抗氧化防御相应降低。补充GLN可消除这些改变。
这些发现表明，孕期高FED摄入量通过胎盘尿酸/甘油三酯依赖性机制导致不良胎儿结局。研究结果还表明，口服GLN可通过抑制尿酸/甘油三酯积累改善胎盘缺陷，从而改善胎儿结局。
