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Lipid remodeling in mouse liver and plasma resulting from Δ6 fatty acid desaturase inhibition
Author(s) -
Duffin Kevin L.,
Obukowicz Mark G.,
Salsgiver William J.,
Welsch Dean J.,
Shieh Caroline,
Raz Amiram,
Needleman Philip
Publication year - 2001
Publication title -
lipids
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.601
H-Index - 120
eISSN - 1558-9307
pISSN - 0024-4201
DOI - 10.1007/s11745-001-0833-2
Subject(s) - arachidonic acid , docosahexaenoic acid , phosphatidylethanolamine , linoleic acid , palmitic acid , biochemistry , phospholipid , fatty acid , phosphatidylinositol , polyunsaturated fatty acid , chemistry , stearic acid , phosphatidylcholine , phosphatidylserine , lipidology , palmitoleic acid , biology , enzyme , signal transduction , organic chemistry , membrane
Electrospray/tandem mass spectrometry was used to quantify lipid remodeling in mouse liver and plasma during inhibition of polyunsaturated fatty acid synthesis by the Δ6 fatty acid desaturase inhibitor, SC‐26196. SC‐26196 caused increases in linoleic acid and corresponding decreases in arachidonic acid and docosahexaenoic acid in select molecular species of phosphatidylcholine, phosphatidylethanolamine, and cholesterol esters but not in phosphatidylserine, phosphatidylinositol, or triglycerides. For linoleic acid‐, arachidonic acid‐, and docosahexaenoic acid‐containing phospholipid species, this difference was, in part, determined by the fatty acid at the sn ‐1 position, namely, palmitic or stearic acid. An understanding of phospholipid remodeling mediated by Δ6 desaturase inhibition should aid in clarifying the contribution of arachidonic acid derived via de novo synthesis or obtained directly in the diet during inflammatory responses.