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An analysis of the effects of various compounds on alcohol and high-fat-diet-induced steatosis in rats and mice.

机译：分析各种化合物对大鼠和小鼠酒精和高脂饮食诱发的脂肪变性的作用。

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摘要

Excessive alcohol consumption is known to result in fatty liver, or steatosis. A high-fat, low-carbohydrate diet also results in fatty liver. Furthermore, fatty liver is known to precede cirrhosis in both animals and humans, and cirrhosis precedes primary hepatocellular carcinoma in humans. A series of studies was first undertaken to determine whether exercise and/or certain dietary manipulations could affect fatty liver. Long-Evans rats were given either a high-fat, low-carbohydrate or a high-carbohydrate, low-fat version of liquid diet with or without alcohol. Livers were analyzed for fat and measures of carbohydrate metabolism in liver and plasma were taken, as well as blood glucose alcohol concentrations. Next, added exercise (run wheel), caffeine, antioxidants such as Vitamin E, diphenyl-para-phenylene diamine (DPPD), and selenium were examined as were the dietary additives cranberry powder and soy protein. Finally, based on ambiguous results involving each agent separately, caffeine and DPPD were combined. Following the conclusion of rat studies, C57BL6 mice were given a modified version of the Leiber-deCarli liquid diet with alcohol. The calorie manipulation described above was repeated in mice to determine whether alcohol-induced fatty liver would be exacerbated in the presence of a high-fat diet. Subsequently, the dietary additives Vitamin E, DPPD and Trolox were added. Striatum was taken for HPLC, and livers were taken for liver fat analysis and malondialdehyde (MDA) assay (as a measure of oxidative stress) respectively. Finally, an experiment was undertaken to determine a time course for withdrawal seizures in mice.;In rats, differences in liver glycogen did not account for differences in liver fat. Exercise and caffeine both resulted in significant changes in weight gain, and while combined they appeared to reduce alcohol-induced fatty liver, the effect was not significant. Separately, no protective properties of either exercise or caffeine were observed. Vitamin E and selenium were found to exacerbate alcohol-induced fatty liver, while DPPD did not. Neither cranberry powder nor soy protein affected alcohol-induced fatty liver. DPPD combined with caffeine reduced alcohol-induced fatty liver significantly (p0.05). Adult mice were able to tolerate 4.5% ethanol in a high-fat liquid diet. The high-fat diet resulted in liver fat values significantly higher than high-carbohydrate when combined with alcohol. Vitamin E appeared to exacerbate fatty liver in mice, but differences were not significant. There were significant differences in oxidative stress; Vitamin E and Trolox reduced MDA significantly over diet plus alcohol alone. All animals experienced withdrawal seizures between 3 and 5 hours after removal of alcohol. There were significant differences in serotonin turnover (5HIAA/5HT) in animals fed a high-fat diet without alcohol vs. chow controls.
机译：已知过量饮酒会导致脂肪肝或脂肪变性。高脂肪，低碳水化合物饮食也会导致脂肪肝。此外，已知脂肪肝在动物和人中都在肝硬化之前，而肝硬化在人中原发性肝细胞癌之前。首先进行了一系列研究，以确定运动和/或某些饮食操作是否会影响脂肪肝。给予Long-Evans大鼠高脂，低碳水化合物或高碳水化合物，低脂的流质饮食，含或不含酒精。分析肝脏中的脂肪，并测量肝脏和血浆中碳水化合物的代谢以及血糖酒精浓度。接下来，检查了补充运动（转轮），咖啡因，抗氧化剂（如维生素E，二苯基对亚苯基二胺（DPPD））和硒，以及膳食添加剂酸果蔓粉和大豆蛋白。最后，根据分别涉及每种药物的不确定结果，将咖啡因和DPPD合并在一起。在完成大鼠研究后，为C57BL6小鼠提供了含酒精的Leiber-deCarli流质饮食的改良版。在小鼠中重复上述卡路里操作，以确定在高脂饮食的存在下酒精诱导的脂肪肝是否会恶化。随后，添加了饮食添加剂维生素E，DPPD和Trolox。纹状体用于HPLC，肝用于肝脂肪分析和丙二醛（MDA）测定（作为氧化应激的量度）。最后，进行了一项实验，确定了小鼠癫痫发作的时程。在大鼠中，肝糖原的差异不能解释肝脂肪的差异。运动和咖啡因都会导致体重增加发生显着变化，虽然两者合起来似乎可以减少酒精引起的脂肪肝，但效果并不显着。另外，没有观察到运动或咖啡因的保护作用。发现维生素E和硒会加剧酒精引起的脂肪肝，而DPPD则不会。酸果蔓粉和大豆蛋白都不会影响酒精引起的脂肪肝。 DPPD联合咖啡因可显着降低酒精诱导的脂肪肝（p <0.05）。成年小鼠能够耐受高脂流质饮食中的4.5％乙醇。当与酒精混合使用时，高脂饮食导致肝脏脂肪值明显高于高碳水化合物。维生素E似乎会加剧小鼠脂肪肝，但差异并不显着。氧化应激存在显着差异；维生素E和Trolox与单独饮食和酒精相比，可显着降低MDA。去除酒精后3至5小时内，所有动物均出现抽搐发作。与高脂饮食相比，高酒精饮食喂养动物的血清素转换（5HIAA / 5HT）存在显着差异。

著录项

  • 作者

    Nolan, Bonnie.;

  • 作者单位

    Rutgers The State University of New Jersey - New Brunswick.;

  • 授予单位 Rutgers The State University of New Jersey - New Brunswick.;
  • 学科 Biology Neuroscience.;Health Sciences Nutrition.;Health Sciences Toxicology.
  • 学位 Ph.D.
  • 年度 2009
  • 页码 78 p.
  • 总页数 78
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 神经科学;毒物学（毒理学）;预防医学、卫生学;
  • 关键词

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