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一种新型口服低碳水化合物酒精液体饮食导致肝脏损伤:初步报告。

A new oral low-carbohydrate alcohol liquid diet producing liver lesions: a preliminary account.

作者信息

Lindros K O, Järveläinen H A

机构信息

National Public Health Institute, Alcohol Research Center, Helsinki, Finland.

出版信息

Alcohol Alcohol. 1998 Jul-Aug;33(4):347-53. doi: 10.1093/oxfordjournals.alcalc.a008403.

Abstract

Male Wistar rats were administered a modified, but nutritionally adequate, ethanol liquid diet with a low content of carbohydrate (5.5% of energy). The high daily intake of ethanol (mean 12.9 g/kg body wt) resulted in consistently sustained elevation of diurnal blood ethanol levels (mean 40.3 +/- 14.9mmol/l, corresponding to 180mg/dl). Marked micro- and macrovesicular panlobular steatosis, occasional inflammatory foci and a threefold elevation of serum alanine aminotransferase activity developed in 6 weeks. In livers from rats on regular 11% carbohydrate diet, lesions beyond periportally located steatosis were rare. These observations suggest that oral administration of a low-carbohydrate liquid ethanol diet may provide an affordable alternative to the technically demanding intragastric feeding model for experimental studies of alcoholic liver disease.

摘要

雄性Wistar大鼠被给予一种改良的、但营养充足的、碳水化合物含量低(占能量的5.5%)的乙醇液体饮食。每日高剂量的乙醇摄入(平均12.9克/千克体重)导致昼夜血液乙醇水平持续升高(平均40.3±14.9毫摩尔/升,相当于180毫克/分升)。6周后出现明显的微泡性和大泡性全小叶脂肪变性、偶发的炎症灶以及血清丙氨酸转氨酶活性升高三倍。在食用常规11%碳水化合物饮食的大鼠肝脏中,除了门静脉周围的脂肪变性外,很少有其他病变。这些观察结果表明,口服低碳水化合物液体乙醇饮食可能为酒精性肝病实验研究中技术要求较高的胃内喂养模型提供一种经济实惠的替代方法。

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