GLYCEROPHOSPHATEACYLTRANSFERASES AND THEIR FUNCTION IN METABOLISM OF FATTY-ACIDS

From different studies on the cellular localization, positional specificity and regulatory properties of acyl-CoA: glycerophosphate acyltransferase (EC 2.3.1.15) and acyl-CoA:1-acylglycerophosphate acyltransferase (EC 2.3.1.-) the following conclusions were drawn: The glycerophosphate acyltransferase was localized in the endoplasmatic reticulum (microsomes) and in the outer membrane of the mitochondria of the animal cell. Its reaction product was 1-acylglycerophosphate (1-lysophosphatidic acid). The mitochondrial enzyme showed a high perference for saturated fatty acids while the microsomal enzyme was less specific (alternatively the microsomes contained more than 1 glycerophosphate acyltransferase). The 1-acylglycerophosphate acyltransferase was localized in the endoplasmatic reticulum (microsomes) in the animal cell. Possibly a minor fraction of this enzyme was localized to the outer membrane of the mitochondria. This enzyme showed a strong preference for unsaturated fatty acids. Both the microsomal and the mitochondrial dihydroxyacetonephosphate acyltransferase showed similar fatty acid specificity as the corresponding glycerophosphate acyltransferases. Dihydroxyacetonephosphate and glycerophosphate were acylated by the same enzymes. The activity of the glycerophosphate acyltransferase(s) in the liver decreased in fasting or fat feeding and increased upon feeding of carbohydrate. The activity of carnitine palmityltransferase varied exactly oppositely. These enzymes did not show dietary variations in heart and adipose tissue. Under otherwise identical conditions, the rate of carnitine acylation in isolated mitochondria decreased more than the rate of glycerophosphate acylation when the concentration of palmityl-CoA was reduced. In isolated liver cells (which had lost most of their carnitine) addition of carnitine increased the rate of fatty acid oxidation and decreased the rate of triglyceride formation. Glycerol and fructose lowered the rate of fatty acid oxidation, probably by lowering the levels of acyl-CoA and acyl-carnitine in the cells. The relative activities of glycerophosphate acyltransferase and carnitine palmityltransferase probably influence the fate of fatty acids in the cell.