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Dan L, Laposata M.
Department of Pathology, Massachusetts General Hospital, Boston 02114, USA.
The possibility that fatty acid ethyl esters (FAEEs), esterification products of fatty acids and ethanol, are mediators of ethanol-induced organ damage was suggested by an autopsy study in which individuals who died while acutely intoxicated were found to have FAEEs predominantly in the organs damaged by ethanol abuse. We initially observed in human subjects after ethanol consumption that there is a marked preference for the synthesis of ethyl palmitate and ethyl oleate over other FAEEs. To investigate the basis for this relative fatty acid specificity for FAEE synthesis, we used an in vitro system of Hep G2 cells incubated with ethanol. The cells were capable of synthesizing FAEEs upon exposure to ethanol and they showed a preference for synthesis of ethyl palmitate and ethyl oleate, as was found in human plasma after ethanol ingestion. This finding allowed us to explore the metabolic preference for palmitate and oleate for FAEE synthesis at the biochemical level using intact cells. We demonstrated that the preferential selection of palmitate and oleate for FAEE synthesis was not likely to be the result of specificity for palmitate and oleate by FAEE synthase or preferential uptake of palmitate and oleate by Hep G2 cells. In studies to determine whether the preference for ethyl palmitate and ethyl oleate synthesis was a result of higher concentrations of palmitate and oleate in the extracellular medium, we observed that the synthesis of ethyl oleate, ethyl linoleate, and ethyl arachidonate, but not ethyl palmitate, is influenced by the extracellular concentration of its corresponding fatty acid. The results of our studies indicate that ethyl palmitate and ethyl oleate are the predominant ethyl esters synthesized, that there is no preferential uptake or enzyme affinity for their fatty acid precursors to explain the predominance, and that ethyl palmitate synthesis is uniquely unaffected by the concentration of palmitate in the extracellular medium.
PMID: 9113265 [PubMed - indexed for MEDLINE]
Department of Pathology, Massachusetts General Hospital, Boston 02114, USA.
The possibility that fatty acid ethyl esters (FAEEs), esterification products of fatty acids and ethanol, are mediators of ethanol-induced organ damage was suggested by an autopsy study in which individuals who died while acutely intoxicated were found to have FAEEs predominantly in the organs damaged by ethanol abuse. We initially observed in human subjects after ethanol consumption that there is a marked preference for the synthesis of ethyl palmitate and ethyl oleate over other FAEEs. To investigate the basis for this relative fatty acid specificity for FAEE synthesis, we used an in vitro system of Hep G2 cells incubated with ethanol. The cells were capable of synthesizing FAEEs upon exposure to ethanol and they showed a preference for synthesis of ethyl palmitate and ethyl oleate, as was found in human plasma after ethanol ingestion. This finding allowed us to explore the metabolic preference for palmitate and oleate for FAEE synthesis at the biochemical level using intact cells. We demonstrated that the preferential selection of palmitate and oleate for FAEE synthesis was not likely to be the result of specificity for palmitate and oleate by FAEE synthase or preferential uptake of palmitate and oleate by Hep G2 cells. In studies to determine whether the preference for ethyl palmitate and ethyl oleate synthesis was a result of higher concentrations of palmitate and oleate in the extracellular medium, we observed that the synthesis of ethyl oleate, ethyl linoleate, and ethyl arachidonate, but not ethyl palmitate, is influenced by the extracellular concentration of its corresponding fatty acid. The results of our studies indicate that ethyl palmitate and ethyl oleate are the predominant ethyl esters synthesized, that there is no preferential uptake or enzyme affinity for their fatty acid precursors to explain the predominance, and that ethyl palmitate synthesis is uniquely unaffected by the concentration of palmitate in the extracellular medium.
PMID: 9113265 [PubMed - indexed for MEDLINE]