Triacylglycerol fluidity

This reaction is responsible for formation of most of the cholesteryl ester in plasma. The preferred substrate is phosphatidylcholine, which contains an unsaturated fatty acid residue on the 2-carbon of the glycerol moiety. HDL and LDL are the major sources of the phosphatidylcholine and cholesterol. Apo A-I, which is a part of HDL, is a powerful activator of LCAT. Apo C-I has also been implicated as an activator of this enzyme however, activation may depend on the nature of the phospholipid substrate. LCAT is synthesized in the liver. The plasma level of LCAT is higher in males than in females. The enzyme converts excess free cholesterol to cholesteryl ester with the simultaneous conversion of lecithin to lysolecithin. The products are subsequently removed from circulation. Thus, LCAT plays a significant role in the removal of cholesterol and lecithin from the circulation, similar to the role of lipoprotein lipase in the removal of triacylglycerol contained in chylomicrons and VLDL. Since LCAT regulates the levels of free cholesterol, cholesteryl esters, and phosphatidylcholine in plasma, it may play an important role in maintaining normal membrane structure and fluidity in peripheral tissue cells. 

Triacylglycerols Source of fatty acids Affect neutral lipid droplet fluidity in foam cells Liquid crystalline — liquid neutral transformation of foam cell droplets... 

However the activation of the A6 desaturation is shown later on. At 15 days it is very important. The apparent Km and Vm of the enz)mie are modified. This activation recovers the double bond index saturated acid ratio to 2.2 and is correlative to an increase of the triacylglycerol phosphatidyl choline ratio of the microsomes. Undoubtedly it is not correlative to the modification of the fatty acid composition of the membrane. Besides Ayala and Brenner have shown that the effect is not due to substrate deprivation (linoleate or a-linolenate) since rats fed on diets containing fish oil during 4 or 6 weeks have even lower A6 desaturation activity in liver microsomes than animals fed on sunflower seed oil compared to rats fed on EFA free diets (Table 2), Therefore the increase of the A6 desaturase activity in EFA deficiency is a physiological response of the cell to maintain the unsaturated/saturated acid ratio and fluidity of the membrane. 

Throughout these studies, mechanisms involved in the control of membrane fluidity have been shown to play a major role in the regulation of the degree of unsaturation exhibited by the major acyl lipid classes (see [7]). As both 15 and 30 C cultures possessed very active A9 desaturase systems, treatment of cultures with sterculate proved to be the only method by which the synthesis of unsaturated triacylglycerols could be significantly controlled. 

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