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On the mechanism of ethanol-induced fatty liver and its reversibility by adenosine.

作者信息

Hernández-Muñoz R, Santamaría A, García-Sáinz J A, Piña E, Chagoya de Sánchez V

出版信息

Arch Biochem Biophys. 1978 Sep;190(1):155-62. doi: 10.1016/0003-9861(78)90263-1.

DOI:10.1016/0003-9861(78)90263-1
PMID:213027
Abstract
摘要

相似文献

1
On the mechanism of ethanol-induced fatty liver and its reversibility by adenosine.
Arch Biochem Biophys. 1978 Sep;190(1):155-62. doi: 10.1016/0003-9861(78)90263-1.
2
Modification of metabolic effects of ethanol by fructose.
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3
Mechanism of the fatty liver induced by cycloheximide and its reversibility by adenosine.放线菌酮诱导脂肪肝的机制及其被腺苷逆转的情况。
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4
Esterification of cholesterol and hydrolysis of cholesteryl ester in alcohol induced fatty liver of rats.大鼠酒精性脂肪肝中胆固醇的酯化及胆固醇酯的水解
Lipids. 1974 May;9(5):353-7. doi: 10.1007/BF02533113.
5
Some new aspects on the acute alcohol-induced fatty liver.
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6
Prevention of the ethanol-induced fatty liver by chlorcyclizine-induced maintenance of hepatic lipid oxidation.通过氯环嗪诱导维持肝脏脂质氧化来预防乙醇诱导的脂肪肝。
Lab Invest. 1968 Jun;18(6):709-14.
7
Effects of adenosine on ethanol-induced modifications of liver metabolism. Role of hepatic redox state, purine and fatty acid metabolism.腺苷对乙醇诱导的肝脏代谢改变的影响。肝脏氧化还原状态、嘌呤和脂肪酸代谢的作用。
Biochem Pharmacol. 1980 Jun 15;29(12):1709-14. doi: 10.1016/0006-2952(80)90129-x.
8
Observations on the relationship of hepatic choline uptake to ethanolic fatty liver in the rat.大鼠肝脏胆碱摄取与乙醇性脂肪肝关系的观察
Can J Biochem. 1973 Jul;51(7):1010-3. doi: 10.1139/o73-131.
9
Chlorpromazine inhibition of ethanol metabolism without prevention of fatty liver.氯丙嗪对乙醇代谢的抑制作用与脂肪肝的预防无关。
Biochem Med. 1972 Feb;6(1):77-81. doi: 10.1016/0006-2944(72)90063-4.
10
The effect of (+)-catechin on the hepatic level of ATP and the lipid content of liver during experimental steatosis.(+)-儿茶素对实验性脂肪变性期间肝脏ATP水平及肝脏脂质含量的影响。
Biochem Pharmacol. 1972 Feb 15;21(4):594-600. doi: 10.1016/0006-2952(72)90338-3.

引用本文的文献

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An adenosine derivative prevents the alterations observed in metabolic syndrome in a rat model induced by a rich high-fat diet and sucrose supplementation.一种腺嘌呤衍生物可预防富含高脂肪和蔗糖饮食诱导的代谢综合征大鼠模型中观察到的代谢变化。
PLoS One. 2023 Oct 5;18(10):e0292448. doi: 10.1371/journal.pone.0292448. eCollection 2023.
2
Morphological and biochemical effects of weekend alcohol consumption in rats: Role of concentration and gender.周末饮酒对大鼠的形态学和生化影响:浓度和性别的作用。
World J Hepatol. 2018 Feb 27;10(2):297-307. doi: 10.4254/wjh.v10.i2.297.
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Recovery of the Cell Cycle Inhibition in CCl(4)-Induced Cirrhosis by the Adenosine Derivative IFC-305.
腺苷衍生物IFC-305对四氯化碳诱导的肝硬化细胞周期抑制的恢复作用
Int J Hepatol. 2012;2012:212530. doi: 10.1155/2012/212530. Epub 2012 Sep 27.
4
Effects of ethanol administration on hepatocellular ultrastructure of regenerating liver induced by partial hepatectomy.乙醇给药对部分肝切除诱导的再生肝肝细胞超微结构的影响。
Dig Dis Sci. 2001 Feb;46(2):360-9. doi: 10.1023/a:1005613201809.
5
Morphological and biochemical effects of a low ethanol dose on rat liver regeneration: role of route and timing of administration.低剂量乙醇对大鼠肝脏再生的形态学和生化影响:给药途径和时间的作用
Dig Dis Sci. 1999 Oct;44(10):1963-74. doi: 10.1023/a:1026601814082.
6
Dietary arachidonic acid reduces fatty liver, increases diet consumption and weight gain in ethanol-fed rats.膳食中的花生四烯酸可减轻乙醇喂养大鼠的脂肪肝,增加其饮食摄入量和体重。
Lipids. 1980 May;15(5):328-36. doi: 10.1007/BF02533548.
7
The prevention of alcoholic fatty liver using dietary supplements: dihydroxyacetone, pyruvate and riboflavin compared to arachidonic acid in pair-fed rats.使用膳食补充剂预防酒精性脂肪肝:在配对喂养的大鼠中,二羟基丙酮、丙酮酸和核黄素与花生四烯酸的比较
Lipids. 1981 Jan;16(1):43-51. doi: 10.1007/BF02534920.
8
Quantitative analysis of intermediary metabolism in rat hepatocytes incubated in the presence and absence of ethanol with a substrate mixture including ketoleucine.在有和没有乙醇存在的情况下,用包含酮亮氨酸的底物混合物培养大鼠肝细胞时,对中间代谢进行定量分析。
Biochem J. 1989 Feb 15;258(1):121-40. doi: 10.1042/bj2580121.
9
Acute effects of ethanol on the perfused rat liver. Studies on lipid and carbohydrate metabolism, substrate cycling and perfusate amino acids.乙醇对灌注大鼠肝脏的急性影响。脂质和碳水化合物代谢、底物循环及灌注液氨基酸的研究。
Biochem J. 1979 Oct 15;184(1):97-106. doi: 10.1042/bj1840097.