Showing papers on "Acyl-CoA published in 1973"
TL;DR: It is suggested that prolonged inhibition of adenine nucleotide translocation by long-chain acyl CoA esters may exert a deleterious effect on myocardial metabolism.
54 citations
TL;DR: Analysis of regions of intestine showed that this delay in transport was most marked in the midportion of the small intestine, and essential fatty acid deficiency appears to affect the synthesis or release of chylomicron lipid from the intestine.
46 citations
TL;DR: The mycobacterial polysaccharides MMP and MGLP markedly stimulate fatty acid synthesis catalyzed by a multienzyme complex from Mycobacterium phlei, and associate with the CoA derivatives of C(18), C(20), and C(22) acids to yield complexes containing maximally 1 mol of fatty acyl-CoA per mol of poly Saccharide.
Abstract: The mycobacterial polysaccharides MMP and MGLP, which contain numerous O-methyl-sugar residues, markedly stimulate fatty acid synthesis catalyzed by a multienzyme complex from Mycobacterium phlei [Ilton, M. et al. (1971) Proc. Nat. Acad. Sci. USA 68, 87-91]. When aqueous solutions containing MMP or MGLP and palmitoyl-CoA were chromatographed on Sephadex G-75 under conditions that widely separate the individual components, polysaccharide and fatty acyl-CoA were eluted in a single peak, indicating formation of a molecular complex. Similarly, the mycobacterial polysaccharides associate with the CoA derivatives of C18, C20, and C22 acids to yield complexes containing maximally 1 mol of fatty acyl-CoA per mol of polysaccharide. The formation of these novel complexes may result from hydrophobic interactions between the paraffin chains of the acyl-CoA derivatives and O-methyl-sugar residues of the polysaccharides.
29 citations
TL;DR: It is concluded that the rate of activation is a function of long-chain fatty acid solubility and the shape of the in vitro activation curve with respect to fatty acid concentration appears to be determined by fatty acid melting point as well as by the presence and position of double bonds.
7 citations
TL;DR: The results suggest that the acyl CoA synthetase may possess regulatory as well as enzymatic activity and suggest that strain D-2 may synthesize an altered fad regulatory protein.
6 citations
TL;DR: Differences in fatty acid composition between pyridoxine-deficient and supplemented rats can not be ascribed to lower liver transacylase activity in the deficient animals.
Abstract: In rats deficient in pyridoxine and essential fatty acids, liver phospholipids contained less arachidonic acid and more oleic and eicosatrienoic acids than those from animals only deficient in essential fatty acids. This pattern persisted after the animals were supplemented with linoleate for 6 days. Liver oleyl and arachidonyl CoA-lysophospholipid acyltransferase activities were significantly higher in pyridoxine-deficient animals. Supplementation with linoleate for 6 days resulted in a marked increase in arachidonyl CoA-acyltransferase activity in pyridoxine-deficient rats but a relatively small increase in the supplemented animals. Differences in fatty acid composition between pyridoxine-deficient and supplemented rats can not be ascribed to lower liver transacylase activity in the deficient animals.
5 citations
TL;DR: It can be excluded that the latter enzymes are involved in the production of the changes in the fatty acid composition of liver phospholipids occurring in choline-deficient rats, which result most likely from alterations in the biosynthesis of liver lecithins and cephalins.
Abstract: Feeding a choline-deficient diet to rats has no effect on the activity of fatty acyl CoA-lysophospholipid acyltransferases, even though liver microsomes are severely depleted of lecithins Thus lecithins appear to have no functional role in the activity of these transferases It can be excluded that the latter enzymes are involved in the production of the changes in the fatty acid composition of liver phospholipids occurring in choline-deficient rats These changes result most likely from alterations in the biosynthesis of liver lecithins and cephalins
3 citations