Oleyl CoA

The activated glycerol can now react with first one and then a second molecule of palmityl-, stearyl-, or oleyl-CoA (12,13) ... 

Hence ricinoleic acid may be built either from oleyl CoA or from linoleyl CoA (Fig. 57). 

Again all these studies, and of course the more recent ones, pointed to a requirement for lipid as seen in the original microsomes. We examined the role of lipid over the years and succeeded in eliminating two postulated roles that lipid was required to provide the true substrate for the reaction—it does not. Stearyl CoA is the true substrate and oleyl CoA the product (Holloway Holloway, 1974). A second postulate, that lipid altered the redox behaviour of cytochrome, was also shown to be incorrect (Sullivan Holloway, 1973). Indeed, the fact that we saw no alteration in redox behaviour, spectral properties or ease of reduction by NADH-cytochrome reductase when detergent-isolated cytochrome was bound to phosphatidylcholine vesicle was the first direct proof that the catalytic portion of the molecule was remote from the lipid bilayer and was in an aqueous environment (Sullivan Holloway, 1973). 

Rat liver mlcrosomes have the capacity to convert stearoyl CoA to oleyl CoA by an enzymatic reaction requiring both oxygen and the Integrity of the NADH-llnked microsomal electron transport chain of which A9 desaturase Is the terminal component (Wilson et al., 1967). 

Since the specific radioactivity of ll- cl stearoyl CoA would be similar to the specific radioactivity of l- c oleyl CoA (Holloway and Holloway, 1974), the relative distribution of the l- C radioactivity in the stearic and oleic acid incorporated into lipids could account for the liver capacity to desaturated in vivo stearic acid. Nevertheless, the loss of oleic acid and its precursor, stearic acid, from the liver, excreted as lipoproteins... 

The increase in the A9 desaturase capacity of isolated diabetic hepatocytes promoted by glycerol could be explained by the Increase in the rate of fatty acid desaturation promoted by the enhancement of stearoyl CoA formation and/or by the removal of oleyl CoA by its esterification into lipids, since oleyl CoA is a competitive inhibitor of the desaturation reaction (Oshino et al., 1966). 

Nervonic acid, the homologous mono-unsaturated fatty acid of lignoceric acid, is synthesized by elongation of erucyl-CoA stea-ryl-CoA and oleyl-CoA are elongated with the same kinetics. This finding explains why myelin mono-unsaturated fatty acids are n-9 and elucidates the reduction of both mono-unsaturated and saturated very long chain fatty acids in the Quaking mutant (7). 

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