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

Scholz, Roland; Nohl, Hans

doi:10.1111/j.1432-1033.1976.tb10247.x

Cited by 62 publications

(20 citation statements)

References 48 publications

(23 reference statements)

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“…It is well established that O 2 uptake increases predictably in response to the energy demands for gluconeogenesis [18,191. In order to correlate changes in oxygen uptake with rates of glucose production under the conditions of this study, lactate was infused in a stepwise fashion from 0.1 -2.0 mM into a perfused liver from a fasted, phenobarbital-treated rat ( Fig.…”

Section: Correlation Between Glucose Production and Extra Oxygen Uptamentioning

confidence: 99%

Gluconeogenesis predominates in periportal regions of the liver lobule

et al. 1984

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1. Rates of gluconeogenesis from lactate were calculated in periportal and pericentral regions of the liver lobule in perfused rat livers from increases in O 2 uptake due to lactate. When lactate (0.1 -2.0 mM) was infused into livers from fasted rats perfused in either anterograde or the retrograde direction, a good correlation (r = 0.97) between rates of glucose production and extra O2 uptake by the liver was observed as expected.2. Rates of oxygen uptake were determined subsequently in periportal and pericentral regions of the liver lobule by placing miniature oxygen electrodes on the liver surface and measuring the local change in oxygen concentration when the flow was stopped. Basal rates of oxygen uptake of 142 & 11 and 60 f 4 pmol x g-' x h-' were calculated for periportal and pericentral regions, respectively. Infusion of 2 mM lactate increased oxygen uptake by 71 pmol x g-' x h-' in periportal regions and by 29 pmol x g-' x h -l in pericentral areas of the liver lobule. Since the stoichiometry between glucose production and extra oxygen uptake is well-established, rates of glucose production in periportal and pericentral regions of the liver lobule were calculated from local changes in rates of oxygen uptake for the first time.3. Maximal rates of glucose production from lactate (2 mM) were 60 f 7 and 25 f 4 pmol x g-' x h-l in periportal and pericentral zones of the liver lobule, respectively. The lactate concentrations required for halfmaximal glucose synthesis were similar (0.4-0.5 mM) in both regions of the liver lobule in the presence or absence of epinephrine (0.1 pM). In the presence of epinephrine, maximal rates of glucose production from lactate were 79 f 5 and 59 f 3 pmol x g-' x h-' in periportal and pericentral regions, respectively. Thus, gluconeogenesis from lactate predominantes in periportal areas of the liver lobule during perfusion in the anterograde direction ; however, the stimulation by added epinephrine was greatest in pericentral areas. Differences in local rates of glucose synthesis may be due to ATP availability, as a good correlation between basal rates of O2 uptake and rates of gluconeogenesis were observed in both regions of the liver lobule in the presence and absence of epinephrine.4. In marked contrast, when livers were perfused in the retrograde direction, glucose production was 28 f 5 pmol x g-' x h-' in periportal areas and 74 6 pmol x 8.' x h-' in pericentral regions. Epinephrine increased maximal rates of glucose production to 87 pmol x g-' x h-' and 58 pmol x g-' x h-' in pericentral and periportal regions, respectively. Thus, gluconeogenesis can be shifted rapidly from one region of the liver lobule to another in the hemoglobin-free perfused rat liver.Data has accumulated over the past decade showing that cells in various regions of the hepatic lobule contain different amounts and activities of key metabolic enzymes [I, 21. Using microdissection techniques, Guder and coworkers [3] demonstrated quantitative differences in mmy enzyme activities in tissues from periporta...

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Section: Correlation Between Glucose Production and Extra Oxygen Uptamentioning

confidence: 99%

Gluconeogenesis predominates in periportal regions of the liver lobule

et al. 1984

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“…This rate was about equal to the capacity of alcohol dehydrogenase, which was 474 +_ 32 pmol ethanol oxidized x (g dry weight)-' x h-' at 37 C ( Table 2). Limitation of ethanol oxidation by alcohol dehydrogenase activity was also reported previously for ethanol oxidation in the presence of pyruvate or fructose [4,28,32].…”

Section: Discussionmentioning

confidence: 96%

The Role of Hydrogen Translocating Shuttles during Ethanol Oxidation in Hepatocytes from Euthyroid and Hyperthyroid Rats

Hensgens

Nieuwenhuis

Meer

et al. 1980

European Journal of Biochemistry

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A quantitative study of the contribution of the malate-aspartate and glycerol-3-phosphate cycles to the translocation of reducing equivalents from cytosol to mitochondria during ethanol oxidation has been made in hepatocytes from euthyroid and hyperthyroid rats.1. In hepatocytes from euthyroid rats both cycles have an almost equal capacity and their relative contribution to total hydrogen transport to the mitochondria depends on the conditions chosen.2. In hepatocytes from hyperthyroid rats maximal rates of ethanol oxidation were significantly lower than in hepatocytes from euthyroid rats, even though the capacity of the glycerol-3-phosphate cycle was increased. This was due to a decreased activity of alcohol dehydrogenase.Three factors can control the rate of hepatic ethanol oxidation : firstly, the activity of alcohol dehydrogenase; secondly, the translocation of reducing equivalents from cytosol to mitochondria; and thirdly, the oxidation of mitochondrial reducing equivalents by oxygen. Depending on the experimental conditions each of these factors can be rate-limiting for ethanol oxidation [l -61. Of the various possible shuttle systems involved in the transport of reducing equivalents from cytosol to mitochondria the malate-aspartate and the glycerol-3-phosphate cycles are presumably quantitatively the most important ones (see [7,8] for reviews). There is, however, no general agreement about the relative importance of these two shuttles during ethanol oxidation. According to Berry and coworkers [5,9] the malate-aspartate cycle plays only a minor role in ethanol oxidation. However, in other reports the contrary is stated [1-3,lO-131. In this paper we describe a quantitative study of the contribution of the malate-aspartate and glycerol-3-phosphate cycles to the translocation of reducing

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“…During ethanol catabolism NAD is reduced to NADH, and the supply of NAD might limit ethanol oxidation. It has been proposed that during fructose metabolism NADH is transformed into NAD, and thus fructose increases ethanol oxidation (Scholz and Nohl, 1976;Thieden et al, 1972;Tygstrup et al, 1965). However, this idea is not fully accepted yet (Mascord et al, 1991).…”

Section: Discussionmentioning

confidence: 98%

Sugars are complementary resources to ethanol in foods consumed by Egyptian fruit bats

Sánchez

Kotler

Korine

et al. 2008

Journal of Experimental Biology

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SUMMARYFood resources are complementary for a forager if their contribution to fitness is higher when consumed together than when consumed independently, e.g. ingesting one may reduce the toxic effects of another. The concentration of potentially toxic ethanol, [EtOH], in fleshy fruit increases during ripening and affects food choices by Egyptian fruit bats, becoming deterrent at high concentrations (у1%). However, ethanol toxicity is apparently reduced when ingested along with some sugars; more with fructose than with sucrose or glucose. We predicted (1) that ingested ethanol is eliminated faster by bats eating fructose than by bats eating sucrose or glucose, (2) that the marginal value of fructose-containing food (food+fructose) increases with increasing [EtOH] more than the marginal value of sucrose-or glucose-containing food (food+sucrose, food+glucose), and (3) that by increasing [EtOH] the marginal value of food+sucose is incremented more than that of food+glucose. Ethanol in bat breath declined faster after they ate fructose than after eating sucrose or glucose. When food [EtOH] increased, the marginal value of food+fructose increased relative to food+glucose. However, the marginal value of food+sucrose increased with increasing [EtOH] more than food+fructose or food+glucose. Although fructose enhanced the rate at which ethanol declined in Egyptian fruit bat breath more than the other sugars, the bats treated both fructose and sucrose as complementary to ethanol. This suggests that in the wild, the amount of ethanol-containing fruit consumed or rejected by Egyptian fruit bats may be related to the fruit's own sugar content and composition, and/or the near-by availability of other sucrose-and fructose-containing fruits.

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

Cited by 62 publications

References 48 publications

Gluconeogenesis predominates in periportal regions of the liver lobule

Gluconeogenesis predominates in periportal regions of the liver lobule

The Role of Hydrogen Translocating Shuttles during Ethanol Oxidation in Hepatocytes from Euthyroid and Hyperthyroid Rats

Sugars are complementary resources to ethanol in foods consumed by Egyptian fruit bats

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