Submitted on February 20, 2008
Revised on May 1, 2008
Accepted on May 1, 2008
Rat heart cannot synthesize docosahexaenoic acid from circulating 
-linolenic acid because it lacks elongase-2
Miki Igarashi, Kaizong Ma, Lisa Chang, Jane M. Bell, and Stanley I. Rapoport
BPMS/NIA/NIH, Bethesda, MD 20892
Corresponding Author: mikii{at}mail.nih.gov
Background: The extent to which the heart can convert a-linolenic acid (a-LNA, 18:3n-3) to longer chain n-3 polyunsaturated fatty acids is not known. Hypothesis: Conversion rates can be measured in vivo using radiolabeled a-LNA and a kinetic fatty acid model. Methods: [1-14C]a-LNA was infused intravenously for 5 min in unanesthetized rats that had been fed an n-3 PUFA “adequate” (4.6% a-LNA, no docosahexaenoic acid (DHA, 22:6n-3)) or “deficient” diet (0.2% a-LNA or DHA) for 15 weeks after weaning. Arterial plasma was sampled, as was brain after high energy microwaving. Results: Rates of conversion of a-LNA to longer chain n-3 PUFAs were low, and DHA was not synthesized at all in the heart. Most a-LNA within the heart had been ß-oxidized. In deprived compared with adequate rats, DHA concentrations in plasma and heart were both reduced by > 90%, whereas heart and plasma levels of docosapentaenoic acid (DPAn-6, 22:5n-6) were elevated. Dietary deprivation did not affect cardiac mRNA levels of elongase 5 or desaturases 6 and 5, but elongase 2 mRNA could not be detected. Conclusions: The rat heart does not synthesize DHA from a-LNA due to the absence of elongase 2, but must obtain its DHA entirely from plasma. Dietary n-3 PUFA deprivation markedly reduces heart DHA and increases heart DPAn-6, which may make the heart vulnerable to different insults.
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