EFFECT OF ETHANOL AND FRUCTOSE ON LIVER-METABOLISM - A DYNAMIC (31)PHOSPHORUS MAGNETIC-RESONANCE SPECTROSCOPY STUDY IN NORMAL VOLUNTEERS

In vivo (31)Phosphorus magnetic resonance spectroscopy (P-31-MRS) perm its evaluation of dynamic changes of individual phosphorus-containing metabolites in the liver parenchyma, such as phosphomonoester (PME), a denosine triphosphate, and inorganic phosphate (P-i), Intravenous fruc tose load alters phosphorus metabolites and allows assessment of liver function by P-31-MRS, P-31-MRS data obtained in alcoholic liver disea se are however inconclusive. To study the hypothesis that fructose loa d can be used to investigate metabolic effects of ethanol ingestion, t he interaction of different metabolites-i.e., fructose and ethanol-wer e followed in vivo, Using a 1.5 Tesla magnetic resonance system, six h ealthy volunteers were examined in three sessions each: a session afte r administration of (a) fructose only (250 mg/kg) was compared with (b ) fructose load after ethanol ingestion (0.8g/kg), A control experimen t (c) was done after ethanol only, Spectra were acquired using one-dim ensional chemical shift imaging with a temporal resolution of 5 min, F ollowing a fructose load, the concomitant uptake of ethanol showed dra stic changes of individual metabolic steps of the hepatic metabolism ( averages a standard deviation), While the velocity of the net formatio n of PME (relative increase 0.46 +/- 0.11 without ethanol vs. 0.61 +/- 0.25 with ethanol) and the use of adenosine triphosphate (-0.13 +/- 0 .03 vs. -0.16 +/- 0.03) and P-i (-0.022 +/- 0.009 vs. -0.021 +/- 0.004 ) were not significantly affected by ethanol uptake, a significant (p < 0.01) reduction of PME degradation (31.3 +/- 9.4 vs. 61.9 +/- 16.9 r elative total area) and absence of an overshoot for P-i (10.5 +/- 4.9 vs. -7.1 +/- 5.3 relative area 13 min to 43 min) was observed after et hanol administration, Dynamic P-31-MRS allows the observation of indiv idual steps of hepatic metabolism in situ; fructose metabolism in the human liver is slowed down by concomitant ethanol ingestion after the phosphorylation step of fructose, This could be explained by inhibitio n of aldolase rather than ethanol-induced changes of the hepatic redox state, Fructose load can be used to study effects of alcohol ingestio n and might therefore be useful in patients with alcoholic liver disea se, (C) 1997 Elsevier Science Inc.