Abstract
In the liver, the ability of ethanol to stimulate glycerolipid biosynthesis has been attributed mainly to its oxidation by alcohol dehydrogenase and to the subsequent enhanced production of glycerol 3-phosphate via the dihydroxyacetone phosphate pathway. To explore alternative pathways, rat reticulocytes, which are devoid of alcohol deshydrogenase, have been exposed to ethanol and their glycerolipid metabolism has been investigated using glycerol as a lipid precursor. The results indicate that short-term (< 30 min) cell exposure to ethanol (50–500 mM) stimulated the incorporation of [ 14C]glycerol into glycerol 3-phosphate, and thereby enhanced glycerolipid biosynthesis. The involvment of glycerol kinase in the stimulatory effect was confirmed by the stimulation by ethanol of glycerol kinase activity directly assayed in reticulocyte lysates. This ethanol effect may be important under physiological or pathophysiological conditions associated with increased glycerol to glucose ratio in blood.
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