Metabolism of 2-hexadecynoate and inhibition of fatty acid elongation.
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| Abstract |
Dietary methyl-2-hexadecynoate appeared to inhibit fatty acid elongation in intact animals (Wood, R., Lee, T., and Gershon, H. (1980) Lipids 15, 141-150). Data from the present in vitro studies indicate that the microsomal elongation system is inhibited preferentially to the mitochondrial system. A series of metabolic acyl-CoA thioester intermediates has been isolated, characterized, and identified from microsomal and mitochondrial incubations with the 2-hexadecynoic acid (16 identical to 1 delta 2). The data support the following conclusions: 1) 16 identical to 1 delta 2 is activated to the CoA ester; 2) 16 identical to 1 delta 2 is acted on by an isomerase to produce a 2,3-allene; 3) either 16 identical to 1 delta 2 or the allene, or both, are hydrated to yield a beta-keto-CoA thioester after rearrangement; 4) the beta-keto ester is reduced to the beta-hydroxyacyl-CoA; 5) dehydration of the beta-hydroxy ester gives rise to trans-delta 2-hexadecenoate which accumulates; and 6) accumulation of the latter results from the inhibition of enoyl-CoA reductase by the 2,3-allene. The occurrence of cis and trans delta 3-hexadecenoates indicates the allene is reduced, after which the delta 3 monoene isomer may be isomerized to the delta 2 monoene by the acetylene isomerase or a different enzyme. Indirect evidence suggests that the fatty acid elongation systems may also be inhibited at another site.
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| Authors | R Wood, T Lee |
| Journal | The Journal of biological chemistry (J Biol Chem) Vol. 256 Issue 23 Pg. 12379-86 (Dec 10 1981) ISSN: 0021-9258 [Print] United States |
| PMID | 7298663 (Publication Type: Journal Article, Research Support, U.S. Gov't, P.H.S.) |
| Chemical References |
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