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Titlebook: Metabolic Changes Induced by Alcohol; G. A. Martini,Ch. Bode Book 1971 Springer-Verlag Berlin · Heidelberg 1971 cancer.central nervous sys

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書目名稱Metabolic Changes Induced by Alcohol
編輯G. A. Martini,Ch. Bode
視頻videohttp://file.papertrans.cn/632/631224/631224.mp4
圖書封面Titlebook: Metabolic Changes Induced by Alcohol;  G. A. Martini,Ch. Bode Book 1971 Springer-Verlag Berlin · Heidelberg 1971 cancer.central nervous sys
描述In nearly all parts of the world, the consumption of alcohol is increasing, and the morbidity and mortality of diseases induced by alcohol are rising correspondingly. It has been stated that alcohol is consumed because it pro- duces intoxication. This effect is due to its toxicological influence on the central nervous system with the resulting functional disturbances. For many years, the concept that alcoholic liver disease was of nutritional origin and only indirectly related to alcohol consumption and metabolism was accepted. Opinion has changed gradually in recent years and tends now to regard alcohol itself through its combustion, as responsible for many metabolic disorders. Interest in this problem has increased during the past decade, and numerous papers bearing on this subject have appeared. It seems that the oxidation of alcohol in the liver interferes in many ways with the intermediary metabolism of lipids, carbohydrates and proteins, including enzymes and hormones, and exerts damaging influence on the liver, the musculature, the heart, the brain and the kidneys. The "Workshop Symposium" brought together a limited number of the scientists involved in the new development, b
出版日期Book 1971
關(guān)鍵詞cancer; central nervous system; diseases; heart; mortality; necrosis; nervous system; nutrition
版次1
doihttps://doi.org/10.1007/978-3-642-65131-1
isbn_softcover978-3-540-05296-8
isbn_ebook978-3-642-65131-1
copyrightSpringer-Verlag Berlin · Heidelberg 1971
The information of publication is updating

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The Influence of Ethanol on Metabolites and Coenzymes of the Energy-Producing Metabolism in Liver anA-SH and, thus blocks coenzyme-A dependent reactions. Fourthly, especially in the liver, which is mainly involved in the oxydation of alcohol, large amounts of acetate are provided and the NADH/NAD ratio is increased. Through the shifts of the redox state NADH consuming reactions are favoured and NAD dependent reactions are inhibited.
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On the Independence of the Ethanol-Induced Triglyceride Accumulation in the Liver from Metabolic Chain studies from other laboratories results have been obtained which led to the conclusion that increased mobilization of fatty acids from adipose tissue is of greater significance for the ethanol-induced triglyceride accumulation in the liver (5, 7, 10).
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Ethanol Metabolism of the Isolated Perfused Rat Liver. 1. Effect of Ethanol Oxidation on Substrate Lof 141 mg kg.h.. Children with glycogenosis type I (without liver glucose-6-phosphatase activity) oxidize ethanol about four times faster than do normal children (20), i.e., at a rate of 460 mg kg.h.. This is demonstrated in curve 3 (Figure 1).
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Experimental Hepatocellular Necrosis Induced by Ethanol after Partial Inhibition of Liver Alcohol De more than 160 g per day, on the average between 200 and 245 g per day (1). With respect to body weight this meant à consumption of about 130–150 mg/kg of body weight per hour. In man, the limited rate of ethanol oxidation is said to be 100 ± 30 mg/kg/h, with an individual range of 50–180 mg/kg/h (2).
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