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The effects of chronic ethanol consumption on the intact rat liver studied by in vivo 31 P NMR spectroscopy
Author(s) -
Brauer Manfred,
Ling Mingfu
Publication year - 1991
Publication title -
magnetic resonance in medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.696
H-Index - 225
eISSN - 1522-2594
pISSN - 0740-3194
DOI - 10.1002/mrm.1910200111
Subject(s) - in vivo , glycerol , phosphomonoesters , chemistry , nuclear magnetic resonance spectroscopy , ethanol , glycolysis , biochemistry , nad+ kinase , gluconeogenesis , adenosine triphosphate , intracellular ph , metabolism , medicine , intracellular , phosphate , biology , enzyme , stereochemistry , inorganic phosphate , microbiology and biotechnology
In vivo 31 P nuclear magnetic resonance (NMR) spectroscopy provides unique opportunities to study the biochemistry of an organ within the intact animal in a totally noninvasive way. We have used in vivo and in vitro 31 P NMR spectroscopy to study steady state changes in the major phosphorus‐containing metabolites of the rat liver in control and chronically ethanol‐treated rats. Chronic (4 month) ethanol treatment caused a statistically significant increase in the inorganic phosphate and phosphodiester resonances of rat liver in in vivo 31 P NMR spectra relative to pair‐fed control rats. Phosphomonoester and adenosine 5'‐triphosphate resonances, as well as intracellular pH, were not appreciably altered. The effects of chronic ethanol treatment were particularly apparent in the response of the liver to a metabolic challenge of glycerol. Glycerol is phosphorylated almost exclusively in the liver and metabolized predominately via glycolysis and gluconeogenesis. Our in vivo 31 P NMR results after administration of glycerol showed a significant increase in the phosphomonoester resonance in the liver of chromic ethanol‐treated rats but not for their pair fed controls. In vitro 31 P NMR studies of perchloric acid extracts of liver showed that the increase was due to an accumulation of sn‐glycerol 3‐phosphate. This effect is due to the NAD + ‐dependent glycerol 3‐phosphate dehydrogenase step being inhibited in the chronic ethanol‐treated rats. This glycerol test may be useful in assessing the ability of the liver to rapidly regenerate NAD + in situ and may be a more sensitive indicator of redox imbalance than steady state ratios of redox pairs (e. g., lactate /pyruvate). © 1991 Academic Press, Inc.