Incorporation of dietary 5,11,14-icosatrienoate into various mouse phospholipid classes and tissues
1993
Berger, A. | Fenz, R. | German, J.B.
To investigate the basis of acyl specificity in the phosphatidylinositol (PI) lipid class, we fed mice fatty acids lacking the usual methylene interrupted double bonds. Mice were fed 10 wt% diets containing either 2.9 or 16% 5,11,14-icosatrienoate (5,11,14-20:3) as a component of seed oil mixtures, or control oil mixtures in which either 18:1n-9 or 18:3n-3 replaced the 5,11,14-20:3 content of the seed oils, for a 2-week period. 5,11,14-20:3 was found to be maximally incorporated into cardiac and hepatic PI (15-17 area%), and hepatic phosphatidylcholine (13%), but minimally incorporated into neutral lipids and those phospholipids that contain small amounts of 20:4n-6, such as hepatic sphingomyelin and cardiolipin. Within the PI class, there were important differences in the tissue distribution of 5,11,14-20:3: liver>heart>kidney = spleen>thymus = visceral fat. There was a clear selectivity for the incorporation of this fatty acid into PI as compared with other phospholipids. 5,11,14-20:3 was also extensively incorporated into hepatic phosphatidylinositol bisphosphate (PIP,), a precursor of second messengers. In hepatic PI, 5,11,14-20:3 replaced 20:4n-6, resulting in a 50% reduction in the level of 20:4n-6. By contrast, in phosphatidylcholine and phosphatidylethanolamine lipid classes, 5,11,14-20:3 replaced several polyenes, including 18:2n-6, 20:4n-6, and 20:5n-3. In comparison with dietary 18:3n-3, 5,11,14-20.3 was found to be more effective at decreasing hepatic PI 20:4n-6 levels. Because leukotrienes and prostaglandins cannot be formed from 5,11,14-20:3 due to the lack of an internal delta-8 double bond, and because 20:4n-6 was dramatically reduced in some PI pools, we expect that 5,11,14-20:3 may alter eicosanoid signaling.
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