Studies on modification of alcoholic liver disease by dietary carbohydrate and fat

膳食碳水化合物和脂肪改善酒精性肝病的研究

• 批准号: 63480179
• 负责人: MURAYAMA Ninzo
• 金额: $ 2.62万
• 依托单位: Shinshu University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for General Scientific Research (B)
• 财政年份: 1988
• 资助国家: 日本
• 起止时间: 1988 至 1989
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-63480179/
• 关键词: Ethanol; Hepatotoxicity; Lipid peroxidation; Carbohydrate; GAMMA-glutamyl transpeptidase; Triglyceride; Transaminase; Glutathione; 蛋白質; 脂肪; コレステロ-ル; アルコール性肝障害; チトクロームPー450; 赤血球溶血反応

The effects of dietary carbohydrate (CHO) level on lipid peroxidation caused by ethanol were investigated in rat liver. Ethanol treatment enhanced microsomal ethanol oxidation, which was potentiated by lowered CHO intake. Ethanol administration markedly increased lipid peroxidation and triglyceride content in the liver of rats fed with low-CHO diet, and slightly in rats fed with high-CHO diet: lipid peroxidation and triglyceride accumulation caused by ethanol were potentiated by low-CHO diet. Liver glutathione content was decreased not by ethanol intake but by lowered CHO intake. These results suggest that lowered-CHO intake involves in the development of ethanol-induced hepatic damage in rats.In order to investigate the effect of CHO intake on ethanol induced hepatic damage, liver function, frequencies of various food and alcohol intakes were surveyed in 2165 healthy men aged from 18 to 85 living in Nagano Prefecture. Serum gamma-glutamyl transpeptidase (gamma-GTP), glutamic-oxaloacetic transaminase(GOT), glutamate pyruvic transaminase(GPT) activities, ratio of GOT to GPT, triglyceride and HDL-cholesterole increased with increasing ethanol consumption. In contrast, the ratio of HDL to LDL de creased with increasing ethanol consumption. The intake of CHO clearly decreased with increasing ethanol consumption, but the intake of fat and protein not found to increase or decrease evidently following ethanol consumption. With ethanol intakeadjusted analysis, lowered- CHO intake may potentiate ethanolinduced increase in serum -GTP activity. We deduced that CHO intake contributes to l-induced hepatic damage.

本文研究了膳食碳水化合物（CHO）水平对乙醇引起的大鼠肝脏脂质过氧化反应的影响。乙醇处理增强了微粒体乙醇氧化，这是通过降低CHO摄入增强。乙醇管理显着增加脂质过氧化和甘油三酯含量在大鼠的肝脏喂养低CHO饮食，并略有高CHO饮食喂养的大鼠：脂质过氧化和甘油三酯的积累引起的乙醇增强低CHO饮食。肝脏谷胱甘肽含量下降，而不是乙醇的摄入量，但降低CHO摄入量。为了探讨CHO摄入量对酒精性肝损伤的影响，对长野县2165名18 ~ 85岁健康男性的肝功能、各种食物摄入频率和酒精摄入频率进行了调查。血清γ-谷氨酰转肽酶（γ-GTP）、谷草转氨酶（GOT）、谷丙转氨酶（GPT）活性、GOT/GPT比值、甘油三酯和高密度脂蛋白胆固醇均随饮酒量的增加而升高。与此相反，HDL与LDL的比值随着乙醇消耗量的增加而降低。随着乙醇摄入量的增加，CHO摄入量明显减少，但脂肪和蛋白质摄入量没有明显增加或减少。通过调整乙醇摄入量的分析，降低- CHO摄入量可增强乙醇诱导的血清-GTP活性的升高.我们推断，CHO摄入有助于l-诱导的肝损伤。

项目成果

中島民江,太田節子,村山忍三,釘本完: "アルコ-ル飲用者の栄養摂取状況について" 日本衛生学雑誌(準備中).

Tamie Nakajima、Setsuko Ota、Shinzo Murayama、Kan Kugimoto：“饮酒者的营养状况”日本卫生杂志（准备中）。

T. Nakajima, S. Ohta, N. Murayama, M. Kuginoto: "Nutritional condition in men and women of drinking habit." Jpn J Hyg.

T. Nakajima、S. Ohta、N. Murayama、M. Kuginoto：“男性和女性饮酒习惯的营养状况”。

中島民江,井勝久喜,王瑞生,沖野知範他: "肝過酸化脂質に対するアルコ-ルと糖質の相互作用" アルコ-ル代謝と肝. 8. 62-67 (1989)

Tamie Nakajima、Hisaki Ikatsu、Ruisheng Wang、Tomonori Okino 等：“酒精和碳水化合物对肝脂质过氧化的相互作用”《酒精代谢与肝脏》8. 62-67 (1989)。

T.Nakajima,S.Ohota,N.Murayama,A.Sato.: "Dietary carbohydrate as a modifying factor for the development of alcoholic liver disease" J.Nutr.

T.Nakajima、S.Ohota、N.Murayama、A.Sato.：“膳食碳水化合物作为酒精性肝病发展的调节因素”J.Nutr。

T.Nakajima,E.Elovaara and H.Vanio: "Monoclonal antibody-derected detection of lowered carbohydrate diet- and ethanol-induced eytochrome P450 isozymes" J.Nutr.(in preparation).

T.Nakajima、E.Elovaara 和 H.Vanio：“单克隆抗体直接检测低碳水化合物饮食和乙醇诱导的细胞色素 P450 同工酶”J.Nutr.（准备中）。