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高脂饮食组成的改变可能会通过扰乱抗氧化剂和自由基的平衡而产生活性氧。

Altered composition of high-lipid diet may generate reactive oxygen species by disturbing the balance of antioxidant and free radicals.

机构信息

Department of Physiology (UG and PG), Serampore College, 9 William Carey Road, Serampore, Hooghly-712201, West Bengal, India.

Department of Physiology (UG and PG), Serampore College, 9 William Carey Road, Serampore, Hooghly-712201, West Bengal, India, Phone: +91-9433509890.

出版信息

J Basic Clin Physiol Pharmacol. 2020 Mar 30;31(3):/j/jbcpp.2020.31.issue-3/jbcpp-2019-0141/jbcpp-2019-0141.xml. doi: 10.1515/jbcpp-2019-0141.

Abstract

Background In the present era, obesity is increasing rapidly, and high dietary intake of lipid could be a noteworthy risk factor for the occasion of obesity, as well as nonalcoholic fatty liver disease, which is the independent risk factor for type 2 diabetes and cardiovascular disease. For a long time, high-lipid diet (HLD) in "fast food" is turning into part of our everyday life. So, we were interested in fulfilling the paucity of studies by means of preliminary evaluation of these three alternative doses of HLD on a rat model and elucidating the possible mechanism of these effects and divulging the most alarming dose. Methods Thirty-two rats were taken, and of these, 24 were fed with HLD in three distinctive compositions of edible coconut oil and vanaspati ghee in a ratio of 2:3, 3:2 and 1:1 (n = 8), orally through gavage at a dose of 10 mL/kg body weight for a period of 28 days, whereas the other eight were selected to comprise the control group. Results After completion of the experiment, followed by analysis of data it was revealed that hyperlipidemia with increased liver and cardiac marker enzymes, are associated with hepatocellular injury and cardiac damage. The data also supported increased proinflammatory cytokines such as interleukin 6 (IL-6) and tumor necrosis factor α (TNF-α). As oxidative stress parameter increased in both liver and heart, there is also an increased in TNF-α due to an increased expression of inducible nitric oxide (NO) synthase, which led to a high production of NO. Moreover, HLD treatment explicitly weakens reasonability of hepatocytes and cardiomyocytes conceivably through G0/G1 or S stage capture or perhaps by means of enlistment of sub-G0/G1 DNA fragmentation and a sign of apoptosis. Conclusions Based on the outcomes, it tends to be inferred that consequences of the present examination uncovered HLD in combination of 2:3 applies most encouraging systemic damage by reactive oxygen species generation and hyperlipidemia and necroapoptosis of the liver and heart. Hence, outcome of this study may help to formulate health care strategy and warns about the food habit in universal population regarding the use of hydrogenated and saturated fats (vanaspati ghee) in diet.

摘要

背景

在当今时代,肥胖症迅速增加,而高脂饮食可能是肥胖症以及非酒精性脂肪肝(NAFLD)发生的一个值得关注的危险因素,NAFLD 是 2 型糖尿病和心血管疾病的独立危险因素。长期以来,“快餐”中的高脂饮食(HLD)已成为我们日常生活的一部分。因此,我们有兴趣通过初步评估 HLD 在大鼠模型中的三种替代剂量来填补这方面研究的空白,并阐明这些影响的可能机制,以及揭示最令人震惊的剂量。

方法

共纳入 32 只大鼠,其中 24 只大鼠以食用椰子油和人造黄油的不同比例(2:3、3:2 和 1:1)通过灌胃给予 10ml/kg 体重的 HLD,28 天后进行实验,其余 8 只大鼠作为对照组。

结果

实验完成后,对数据进行分析发现,高脂血症伴肝和心脏标志物酶升高与肝细胞损伤和心脏损伤有关。数据还支持促炎细胞因子(如白细胞介素 6(IL-6)和肿瘤坏死因子 α(TNF-α))增加。由于肝和心脏中的氧化应激参数增加,诱导型一氧化氮合酶(iNOS)的表达增加导致 TNF-α增加,从而导致 NO 大量产生。此外,HLD 治疗明显削弱了肝细胞和心肌细胞的合理性,可能通过 G0/G1 期或 S 期捕获,或者通过招募亚 G0/G1 DNA 片段和细胞凋亡的迹象。

结论

根据研究结果推断,本研究结果揭示了 HLD 与 2:3 的组合应用最能通过活性氧生成和肝、心脏的高脂血症和坏死凋亡引起全身性损伤。因此,本研究的结果可能有助于制定卫生保健策略,并就普遍人群饮食中使用氢化和饱和脂肪(人造黄油)的问题提出警告。

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