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l-glutamine supplementation exerts cardio-renal protection in estrogen-progestin oral contraceptive-treated female rats.
Environmental Toxicology and Pharmacology ( IF 4.2 ) Pub Date : 2019-11-22 , DOI: 10.1016/j.etap.2019.103305
Kehinde Samuel Olaniyi 1 , Isaiah Woru Sabinari 2 , Lawrence Aderemi Olatunji 2
Affiliation  

Glycogen and lipid disruptions represent a spectrum of metabolic disorders that are crucial risk factors for cardiovascular disease in estrogen-progestin oral contraceptive (COC) users. l-glutamine (GLN) has been shown to exert a modulatory effect in metabolic disorders-related syndromes. We therefore hypothesized that GLN supplementation would protect against myocardial and renal glycogen-lipid mishandling in COC-treated animals by modulation of Glucose-6-phosphate dehydrogenase (G6PD) and xanthine oxidase (XO) activities. Adult female Wistar rats were randomly allotted into control, GLN, COC and COC + GLN groups (six rats per group). The groups received vehicle (distilled water, p.o.), GLN (1 g/kg), COC containing 1.0 μg ethinylestradiol plus 5.0 μg levonorgestrel and COC plus GLN respectively, daily for 8 weeks. Data showed that treatment with COC led to metabolically-induced obesity with correspondent increased visceral and epicardial fat mass. It also led to increased plasma, myocardial and renal triglyceride, free fatty acid, malondialdehyde (MDA), XO activity, uric acid content and decreased glutathione content and G6PD activity. In addition, COC increased myocardial but not renal glycogen content, and increased myocardial and renal glycogen synthase activity, increased plasma and renal lactate production and plasma aspartate transaminase/alanine aminotransferase (AST/ALT) ratio. However, these alterations were attenuated when supplemented with GLN except plasma AST/ALT ratio. Collectively, the present results indicate that estrogen-progestin oral contraceptive causes metabolically-induced obesity that is accompanied by differential myocardial and renal metabolic disturbances. The findings also suggest that irrespective of varying metabolic phenotypes, GLN exerts protection against cardio-renal dysmetabolism by modulation of XO and G6PD activities.



中文翻译:

l-谷氨酰胺补充剂在雌激素-孕激素口服避孕药治疗的雌性大鼠中发挥心脏肾脏保护作用。

糖原和脂质破坏代表了一系列代谢紊乱,这些代谢紊乱是雌激素-孕激素口服避孕药(COC)用户中心血管疾病的关键危险因素。1-谷氨酰胺(GLN)已显示出在代谢紊乱相关综合征中发挥调节作用。因此,我们假设补充GLN可以通过调节6磷酸葡萄糖脱氢酶(G6PD)和黄嘌呤氧化酶(XO)的活性来防止COC处理动物的心肌和肾脏糖原-脂质处理不当。将成年雌性Wistar大鼠随机分为对照组,GLN,COC和COC + GLN组(每组六只大鼠)。组接受载体(蒸馏水,),GLN(1 g / kg),分别含1.0μg乙炔雌二醇加5.0μg左炔诺孕酮的COC和COC加GLN,每天进行8周。数据显示,COC治疗可导致代谢性肥胖,同时内脏和心外膜脂肪量相应增加。它还导致血浆,心肌和肾甘油三酸酯,游离脂肪酸,丙二醛(MDA),XO活性,尿酸含量增加,谷胱甘肽含量和G6PD活性降低。另外,COC增加了心肌的糖原含量,但没有增加肾脏的糖原合酶的活性,增加了心肌和肾脏糖原合酶的活性,增加了血浆和肾脏乳酸的产生,并提高了血浆天冬氨酸转氨酶/丙氨酸氨基转移酶(AST / ALT)的比例。然而,除血浆AST / ALT比外,补充GLN后这些改变会减弱。总的来说,目前的结果表明,雌激素-孕激素口服避孕药会引起代谢性肥胖,并伴有不同的心肌和肾脏代谢紊乱。这些发现还表明,不管代谢表型如何变化,GLN都可以通过调节XO和G6PD的活性来发挥保护作用,防止心肾代谢不良。

更新日期:2019-11-22
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