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Diet and fatty acid metabolism interact in yet unknown ways to modulate membrane fatty acid composition and certain cellular functions. For example, dietary precursors or metabolic products of n-3 fatty acid metabolism differ in their ability to modify specific membrane components. In the present study, the effect of dietary 22:6n-3 or its metabolic precursor, 18:3n-3, on the selective accumulation of 22:6n-3 by heart was investigated. The mass and fatty acid compositions of individual phospholipids (PL) in heart and liver were quantified in mice fed either 22:6n-3 (from crocodile oil) or 18:3n-3 (from soybean oil) for 13 wk. This study was conducted to determine if the selective accumulation of 22:6n-3 in heart was due to the incorporation of 22:6n-3 into cardiolipin (CL), a PL most prevalent in heart and known to accumulate 22:6n-3. Although heart was significantly enriched with 22:6n-3 relative to liver, the accumulation of 22:6n-3 by CL in heart could not quantitatively account for this difference. CL from heart did accumulate 22:6n-3, but only in mice fed preformed 22:6n-3. Diets rich in non-22:6n-3 fatty acids result in a fatty acid composition of phosphatidylcholine (PC) in heart that is unusually enriched with 22:6n-3. In this study, the mass of PC in heart was positively correlated with the enrichment of 22:6n-3 into PC. The increased mass of PC was coincident with a decrease in the mass of phosphatidylethanolamine, suggesting that 22:6n-3 induced PC synthesis by increasing phosphatidylethanolamine-N-methyltransferase activity in the heart.
Watkins et al. (Thu,) studied this question.