Antibiotics protect against fructose-induced hepatic lipid accumulation in mice:: Role of endotoxin
Antibiotics protect against fructose-induced hepatic lipid accumulation in mice:: Role of endotoxin
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DOI：
10.1016/j.jhep.2008.01.035
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发表时间：
2008-06-01
影响因子：
25.7
通讯作者：
Bischoff, Stephan C.
中科院分区：
文献类型：
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作者：
Bergheim, Ina;Weber, Synia;Bischoff, Stephan C.
背景/目标：软饮料中精制碳水化合物的消耗被认为是非酒精性脂肪肝（NAFLD）发展的关键因素。本研究的目的是测试随意获取饮用水中消耗的不同糖对肝脏脂肪积累的影响。方法：在 8 周内，C57BL/J6 小鼠可以自由获取含有 30% 葡萄糖、果糖、蔗糖或用人工甜味剂 (AS) 增甜的水或白水的溶液。评估体重、热量摄入、肝脏脂肪变性和脂质过氧化。结果：暴露于葡萄糖的小鼠的总热量摄入和体重增加最高。相反，与所有其他组相比，食用果糖的小鼠的肝脏脂质积累明显更高。此外，果糖喂养小鼠的门静脉血内毒素水平、脂质过氧化以及TNFα表达均显着高于所有其他组。用抗生素（例如多粘菌素 B 和新霉素）同时治疗果糖喂养小鼠，可显着减少果糖喂养小鼠的肝脏脂质积累。结论：这些数据支持这样的假设：高果糖消耗不仅可能因过度喂养而导致肝损伤，而且还可能通过增加内毒素的肠道移位而直接促炎症。 (c) 2008 年欧洲肝脏研究协会。由 Elsevier B.V. 出版。保留所有权利。
Background/Aims: Consumption of refined carbohydrates in soft drinks has been postulated to be a key factor in the development of non-alcoholic fatty liver disease (NAFLD). The aim of the present study was to test the effects of ad libitum access to different sugars consumed in drinking water on hepatic fat accumulation.Methods: For 8 weeks, C57BL/J6 mice had free access to solutions containing 30%) glucose, fructose, sucrose, or water sweetened with artificial sweetener (AS) or plain water. Body weight, caloric intake, hepatic steatosis and lipid peroxidation were assessed.Results: Total caloric intake and weight gain were highest in mice exposed to glucose. In contrast, hepatic lipid accumulation was significantly higher in mice consuming fructose compared to all other groups. Moreover, endotoxin levels in portal blood and lipid peroxidation as well as TNF alpha expression were significantly higher in fructose fed mice than in all other groups. Concomitant treatment of fructose fed mice with antibiotics (e.g., polymyxin B and neomycin) markedly reduced hepatic lipid accumulation in fructose fed mice.Conclusions: These data support the hypothesis that high fructose consumption may not only lead to liver damage through overfeeding but also may be directly pro-inflammatory by increasing intestinal translocation of endotoxin. (c) 2008 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved.