Metabolic interactions of fructose and ethanol in perfused liver of normal and thyroxine-treated rats

Ylikahri, Reino; Hassinen, Ilmo E.; Kähönen, Matti T.

doi:10.1016/0026-0495(71)90004-7

Cited by 20 publications

(6 citation statements)

References 39 publications

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“…Livers were perfused with Krebs-Ringer bicarbonate solution as described earlier (58). After 20 minutes of perfusion 10 mM glucose or 10 mM fructose with or without 20 mM ethanol was added to the perfusion medium.…”

Section: Production or Elimination Of Metabolites In Liver Perfusiomentioning

confidence: 99%

“…Krebs et al used perfused livers, too, but found that ethanol markedly inhibited production of glucose from fructose (29). Our results confirm this (Table I) (58). Papenberg et al (46) also found that in perfused rat liver ethanol inhibited uptake of fructose and output of glucose.…”

Section: Fructose and Ethanol-induced Changes In Carbohydrate Metabolismmentioning

confidence: 99%

“…Because these studies throw some light on the metabolic effects of ethanol, we have a reasonable amount of data about the metabolic interactions of fructose and ethanol in man and laboratory animals. These interactions have been studied especially by 53,54), by Papenberg et al (46) and by Hassinen et al (18,20,57,58).…”

mentioning

confidence: 99%

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Modification of Metabolic Effects of Ethanol by Fructose

Ylikahri

Kähönen

Hassinen

1972

Journal of Internal Medicine

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Abstract. Present knowledge of the metabolic interactions between fructose and ethanol in man and laboratory animals is reviewed. The possible biochemical mechanisms of these interactions are considered. Some new data on the effects of fructose and ethanol on carbohydrate and lipid metabolism are included. Fructose increases the effects of ethanol on the hepatic lactate/pyruvate and a‐glycerophosphate/dihydroxyacetone phosphate ratios. Thus it augments the basic metabolic effect of ethanol, i.e. reduction of the hepatic redox state. The ethanol‐induced increase in hepatic a‐glycerophosphate concentration has been regarded as an important factor in the pathogenesis of the acute alcoholic fatty liver. But although fructose causes hypertriglyceridaemia and augments the effect of ethanol on hepatic a‐glycerophosphate concentration, it was found to diminish the ethanol‐induced accumulation of triglycerides in the liver. Glucose had a similar effect. The reason for this is uncertain, but the inhibition of peripheral lipolysis by fructose and glucose might be partly responsible. The most important effect of ethanol on carbohydrate metabolism is to inhibit hepatic gluconeogenesis by producing NADH in excess. Although the production of glucose from fructose is not directly dependent on the redox state of the liver, it is slightly inhibited by ethanol in vitro. However, in vivo fructose is effectively converted to glucose even during ethanol oxidation, and in ethanol‐induced hypoglycaemia it rapidly restores the blood glucose level.

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Section: Production or Elimination Of Metabolites In Liver Perfusiomentioning

confidence: 99%

Section: Fructose and Ethanol-induced Changes In Carbohydrate Metabolismmentioning

confidence: 99%

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Modification of Metabolic Effects of Ethanol by Fructose

Ylikahri

Kähönen

Hassinen

1972

Journal of Internal Medicine

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“…Hence, the availability of NADH does not seem to play an important role in the fructose effect. The biphasic effect of fructose has already been described by Ylikhari et al in perfused rat livers in 1971 (Ylikahri et al, 1971[ 54 ]). To our knowledge, there are not any more recent experiments giving insights into the immediate effect on OC after fructose-treatment of hepatocytes.…”

Section: Discussionmentioning

confidence: 73%

Continuous, non-invasive monitoring of oxygen consumption in a parallelized microfluidic in vitro system provides novel insight into the response to nutrients and drugs of primary human hepatocytes

Busche

Rabl

Fischer

et al. 2022

EXCLI Journal; 21:Doc144; ISSN 1611-2156

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Oxygen plays a fundamental role in cellular energy metabolism, differentiation and cell biology in general. Consequently, in vitro oxygen sensing can be used to assess cell vitality and detect specific mechanisms of toxicity. In 2D in vitro models currently used, the oxygen supply provided by diffusion is generally too low, especially for cells having a high oxygen demand. In organ-on-chip systems, a more physiologic oxygen supply can be generated by establishing unidirectional perfusion. We established oxygen sensors in an easy-to-use and parallelized organ-on-chip system. We demonstrated the applicability of this system by analyzing the influence of fructose (40 mM, 80 mM), ammonium chloride (100 mM) and Na-diclofenac (50 µM, 150 µM, 450 µM, 1500 µM) on primary human hepatocytes (PHH). Fructose treatment for two hours showed an immediate drop of oxygen consumption (OC) with subsequent increase to nearly initial levels. Treatment with 80 mM glucose, 20 mM lactate or 20 mM glycerol did not result in any changes in OC which demonstrates a specific effect of fructose. Application of ammonium chloride for two hours did not show any immediate effects on OC, but qualitatively changed the cellular response to FCCP treatment. Na-diclofenac treatment for 24 hours led to a decrease of the maximal respiration and reserve capacity. We also demonstrated the stability of our system by repeatedly treating cells with 40 mM fructose, which led to similar cell responses on the same day as well as on subsequent days. In conclusion, our system enables in depth analysis of cellular respiration after substrate treatment in an unidirectional perfused organ-on-chip system.

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“…I n the perfused rat liver, the unstimulated ethanol oxidation rate is about twice that in the isolated rat-liver parenchymal cells (see above). Furthermore, no "fructose effect" and an increase in the cytosolic NADH/NAD+ ratio after administration of fructose to an ethanol-metabolizing perfused liver preparation is observed [22,23].…”

Section: Rate-limiting Steps In Ethanol Oxidation and The "Fructose Ementioning

confidence: 99%

Rate‐Limiting Factors in Ethanol Oxidation by Isolated Rat‐Liver Parenchymal Cells

Grunnet¹,

Quistorff²,

Thieden³

1973

European Journal of Biochemistry

126

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1. Isolated rat-liver parenchymal cells oxidized ethanol a t a rate of 1.4, 1.7, i.9 and 2.5 p.mol/ min per ml packed cells at 4, 20, 40 and 65 mM ethanol, respectively. Between 40 and 65 mM ethanol an abrupt 30°/, increase in the ethanol oxidation rate was observed.2. The activity of the NAD-dependent alcohol dehydrogenase in a homogenate of isolated cells corresponded to 1.25-5 U/ml packed cells, depending on the assay method used.3. Fructose or pyruvate enhanced the oxidation rate of ethanol by 1.4-2.0 pmol/min per ml packed cells independent of the ethanol concentration applied. No additive effect of the two compounds upon ethanol oxidation was observed.4. Pyrazole inhibited the NAD dependent alcohol dehydrogenase activity in a homogenate of isolated cells as well as the unstimulated and the fructose-stimulated ethanol oxidation with a Ki-value of 9-13 pM.by pyrazole concentrations, which inhibited the unstimulated ethanol oxidation only 30 Ole, indicating that the "fructose effect" is mediated via alcohol deh y drogenase .4mM pyrazole only slightly inhibited that part of the ethanol oxidation which was not catalyzed by alcohol dehydrogenase, whereas 18 mM pyrazole inhibited also this pathway significantly. 5. 50 pM pyrazole had no effect a t all upon the basal ethanol oxidation rate whereas the fructose-stimulated ethanol oxidation was 30°/, inhibited.6. The results concerning the effect of fructose and pyruvate upon ethanol oxidation are interpreted in terms of the mechanism for the reaction catalyzed by alcohol dehydrogenase. At low concentrations of ethanol and in the absence of fructose, the rate-limiting step in ethanol oxidation appears to be dissociation of the enzyme-NADH complex, whereas, in the presence of fructose, the maximal activity of ethanol dehydrogenase may be rate-limiting for the oxidation of ethanol.7. The results also suggest that enzyme systems other than alcohol dehydrogenase participate in ethanol oxidation a t high concentrations of ethanol.The "fructose effect" was inhibited 100Three different reaction mechanisms for oxidation of ethanol to acetaldehyde have been described in liver tissue. These are the pathway catalyzed by the NAD-dependent alcohol dehydrogenase [ 11, the pathway involving hydrogen peroxide and catalase [2 -51 and the microsomal ethanol-oxidizing system involving NADPH and cytochrome P-450 [6-81. The pathway catalyzed by alcohol dehydrogenase is localized to the cytoplasmic compartment of the cell, while the system dependent on cytochrome P-450 is microsome-bound. Eur. J. Bioohem. 40 (1973) The oxidation of ethanol catalyzed by alcohol dehydrogenase, which prevails a t low (below approx.

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Metabolic interactions of fructose and ethanol in perfused liver of normal and thyroxine-treated rats

Cited by 20 publications

References 39 publications

Modification of Metabolic Effects of Ethanol by Fructose

Modification of Metabolic Effects of Ethanol by Fructose

Continuous, non-invasive monitoring of oxygen consumption in a parallelized microfluidic in vitro system provides novel insight into the response to nutrients and drugs of primary human hepatocytes

Rate‐Limiting Factors in Ethanol Oxidation by Isolated Rat‐Liver Parenchymal Cells

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