The glycerophosphateacyltransferases and their function in the metabolism of fatty acids.

Abstract

1. From different studies on the cellular localization, postional 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 can be drawn: The glycerophosphate acyltransferase is localized in the endoplasmatic reticulum (microsomes) and in the outer membrane of the mitochondria of the animal cell. Its reaction product is 1-acylglycerophosphate (1-lysophosphatidic acid). The mitochondrial enzyme shows a high preference for saturated fatty acids while the microsomal enzyme is less specific (alternatively the microsomes contain more than one glycerophsophate acyltransferase). 2. The 1-acylglycerphosphate acyltransferase is localized in the endoplasmatic reticulum (microsomes) in the animal cell. Possibly a minor fraction of this enzyme is localized to the outer membrane of the mitochondria. This enzyme shows a strong preference for unsaturated fatty acids. 3. Both the microsomal and the mitochondrial dihydroxyacetonephosphate acyltransferase show similar fatty acid specificity as the corresponding glycerophosphate acyltransferases. It cannot be excluded that dihydroxy-acetonephosphate and glycerophosphate are acylated by the same enzymes. 4. The activity of the glycerophosphate acyltransferase(s) in the liver decreases in fasting or fat feeding and increases upon feeding of carbohydrate. The activity of carnitine palmityltransferase varies exacty opposit. These enzymes do not show dietary variations in heart and adipose tissue. 5. Under the otherwise identical conditions the rate of carnitine acylation in isolated mitochondria decreases more than the rate of glycerophosphate acylation when the concentration of palmityl-CoA is reduced. 6. In isolated liver cells (which has lost most of their carnitine) addition of carnitine increases the rate of fatty acid oxidation and decreases the rate of triglyceride formation. 7. Glycerol and fructose lower the rate of fatty acid oxidation, probably by lowering the levels of acyl-CoA and acyl-carnitine in the cells. 8. It is concluded that the relative activities of glycerophosphate acyltranse and carnitine palmityltransferase probably influence the fate of fatty acids in the cell.