Rat heart cannot synthesize docosahexaenoic acid from circulating α-linolenic acid because it lacks elongase-2

Abstract

The extent to which the heart can convert α-linolenic acid (α-LNA, 18:3n-3) to longer chain n-3 PUFAs is not known. Conversion rates can be measured in vivo using radiolabeled α-LNA and a kinetic fatty acid model. [1-14C]α-LNA was infused intravenously for 5 min in unanesthetized rats that had been fed an n-3 PUFA-adequate [4.6% α-LNA, no docosahexaenoic acid (DHA, 22:6n-3)] or n-3 PUFA-deficient diet (0.2% α-LNA, nor DHA) for 15 weeks after weaning. Arterial plasma was sampled, as was the heart after high-energy microwaving. Rates of conversion of α-LNA to longer chain n-3 PUFAs were low, and DHA was not synthesized at all in the heart. Most α-LNA within the heart had been β-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 Δ6 and Δ5, but elongase-2 mRNA could not be detected. In summary, the rat heart does not synthesize DHA from α-LNA, owing 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.

Keywords

• diet
• heart
• deprivation
• elongation
• synthesis
• n-3 polyunsaturated fatty acids