Metabolism of Ethanol and Fructose
in the Perfused Rat Liver

Papenberg, J.; Wartburg, J. P. von; Aebi, H.

doi:10.1159/000458360

Cited by 57 publications

(7 citation statements)

References 16 publications

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“…2. The data, therefore, disprove the notion that fructose has no effect on ethanol metabolism in rat liver [49]. The stimulation was dependent on the ethanol concentration; and glycerol (A-A).…”

Section: Stimulution Of Ethanol Oxidation By Fructosementioning

confidence: 48%

Mechanism of the Stimulatory Effect of Fructose on Ethanol Oxidation in Perfused Rat Liver

Scholz

Nohl

1976

Eur J Biochem

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The stimulatory effect of fructose on ethanol oxidation was studied in livers from fasted rats perfused with Krebs-Henseleit-bicarbonate buffer in a non-recirculating system. Two series of experiments were performed : (A) ethanol was infused with stepwise increasing concentrations (0.1 -20 mM) in the presence of 4 mM fructose; (B) fructose was infused with stepwise increasing concentrations (0.5 -10 mM) in the presence of 2 mM ethanol. From measured metabolic rates the following parameters were calculated : energy-rich phosphates consumed for fructose metabolism which were provided from oxidative phosphorylation (A -P) ; reducing equivalents derived from stimulated ethanol utilization which were disposed by mitochondrial oxidation ( A 2H). Under the various conditions studied a linear relationship between these parameters was observed. The ratio d -P/A2H was about 2.0. It is suggested that fructose stimulates ethanol oxidation indirectly by increasing the energy consumption of the liver due to the production of glucose from fructose. Consequently, the rate of oxidative phosphorylation is increased and, therefore, the capacity of the respiratory chain for oxidizing reducing equivalents derived from ethanol is enhanced. The data support the more general hypothesis that the rate of ethanol oxidation depend upon the rate of hepatic energy consumption in a given metabolic state.The rate-controlling factor in ethanol metabolism is still a subject of debate. Previously, it was suggested that the rate of ethanol oxidation is limited by the activity of hepatic alcohol dehydrogenase [l -41. However, this concept has been questioned, since it was observed that the rate of ethanol elimination varied with the metabolic state [5-71 and could be stimulated by various compounds, e.g. pyruvate [l, 6-91, fructose [8 -221, or dinitrophenol [23], and that peroxidatic processes play an important role in ethanol metabolism at high concentrations [24-261. The present concept of rate-control is the following.

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Section: Stimulution Of Ethanol Oxidation By Fructosementioning

confidence: 48%

Mechanism of the Stimulatory Effect of Fructose on Ethanol Oxidation in Perfused Rat Liver

Scholz

Nohl

1976

Eur J Biochem

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“…3). In addition to our general knowledge concerning ethanol oxidation in the liver by ADH and Acetaldehyd-dehydrogenase (17, 39), the limiting significance of NADH 2 reoxidation for ethanol degradation in the liver (21, 36)$ the increased NADH2/ NAD quotient of various redox systems, e. g. lactate-pyruvate, L-I-Glycerophosphate-dihydroxyacetonphosphate, are well known (2,11,12,28,41). L-Iglycerophosphate is the only FFA acceptor in the triglyceride synthesis.…”

Section: --mentioning

confidence: 99%

Alteration of plasma lipids and intermediates of lipid metabolism in healthy fasting volunteers by ethanol and fructose

Schneider

Tesdorfpf²,

Kaffarnik³

et al. 1976

Res. Exp. Med.

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After healthy persons, aged between 20 and 35 years, had consumed either ethanol or ethanol and fructose, triglycerides, free glycerol, FFA, phospholipids and total cholesterol were determined. After a basic dosage of 0.5 g ethanol/kg body weight, each person received a maeintenance dosage of 0.1 g ethanol/kg body weight and hour. Control experiments were carried out on persons receiving only fructose and on fasting persons who consumed no ethanol. After 8 hrs, triglycerides rose in the ethanol group by 107 %, in the ethanol-fructose group by 63 %. FFA exhibited in both ethanol and ethanol-fructose groups an initial decrease, with a secondary increase in the ethanol group. The initial decrease was greater in the ethanol-fructose group. A significant rise in free glycerol by 419 % was observed 30 min after the intake of combined ethanol/fructose. Free glycerol rose under ethanol alone by 144%. The ohospholipids exhibited a slight rise in the ethanol group; no significant changes occured in the cholesterol. The blood ethanol level was lower under ethanol-fructose than under ethanol alone. The addition of fructose diminishes the ethanol-induced hypertriglyceridemia. Our investigations give further proof that, under short-term ethanol load, the fatty acids necessary for the increased triglyceride synthesis in the liver, originate predominantly from a peripheral lipolysis, and that changes in liver metabolism depending on the oxidation of ethanol are not of less importance for the development of the acute ethanol-induced hyperlipidemia.

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“…The metabolism of ethanol can be catalyzed in vitro by various enzymes including alcohol dehydrogenase (ADH) [30,43], the microsomal ethanol-oxidizing sys tem (MEOS) [ The present study was undertaken to in vestigate the effect of testosterone, estradiol and castration on MEOS activity of livers derived from mature male rats. In addition, the data were compared with the microsomal content of cytochrome P-450 and the activi ties of microsomal NADPH-cytochrome c reductase as well as other hepatic alcoholmetabolizing enzymes.…”

Section: Introductionmentioning

confidence: 99%

Effect of Sex Hormones on the Activities of Hepatic Alcohol-Metabolizing Enzymes in Male Rats

Teschke¹,

Heymann²

1982

Enzyme

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In mature male rats both estradiol administration as well as castration had a striking suppressive effect on the hepatic activity of the microsomal ethanol-oxidizing system, whereas alcohol dehydrogenase activity was increased under these experimental conditions. The castration effects on the activities of the alcohol-metabolizing enzymes could be completely prevented by the administration of testosterone. Therefore, these results indicate the sex-dependent nature of the hepatic microsomal ethanol-oxidizing system and alcohol dehydrogenase.

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Metabolism of Ethanol and Fructose in the Perfused Rat Liver

Cited by 57 publications

References 16 publications

Mechanism of the Stimulatory Effect of Fructose on Ethanol Oxidation in Perfused Rat Liver

Mechanism of the Stimulatory Effect of Fructose on Ethanol Oxidation in Perfused Rat Liver

Alteration of plasma lipids and intermediates of lipid metabolism in healthy fasting volunteers by ethanol and fructose

Effect of Sex Hormones on the Activities of Hepatic Alcohol-Metabolizing Enzymes in Male Rats

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