Abstract

Docosahexaenoic acid (DHA), a crucial nervous system n-3 PUFA, may be obtained in the diet or synthesized in vivo from dietary alpha-linolenic acid (LNA). We addressed whether DHA synthesis is regulated by the availability of dietary DHA in artificially reared rat pups, during p8 to p28 development. Over 20 days, one group of rat pups was continuously fed deuterium-labeled LNA (d5-LNA) and no other n-3 PUFA (d5-LNA diet), and a second group of rat pups was fed a d5-LNA diet with unlabeled DHA (d5-LNA + DHA diet). The rat pups were then euthanized, and the total amount of deuterium-labeled docosahexaenoic acid (d5-DHA) (synthesized DHA) as well as other n-3 fatty acids present in various body tissues, was quantified. In the d5-LNA + DHA group, the presence of dietary DHA led to a marked decrease (3- to 5-fold) in the total amount of d5-DHA that accumulated in all tissues that we examined, except in adipose. Overall, DHA accretion from d5-DHA was generally diminished by availability of dietary preformed DHA, inasmuch as this was found to be the predominant source of tissue DHA. When preformed DHA was unavailable, d5-DHA and unlabeled DHA were preferentially accreted in some tissues along with a net loss of unlabeled DHA from other organs.

Highlights

  • Docosahexaenoic acid (DHA), a crucial nervous system n-3 PUFA, may be obtained in the diet or synthesized in vivo from dietary a-linolenic acid (LNA)

  • We recently reported a study in which rat pups were continuously fed all of their dietary LNA as deuterium-labeled LNA (d5-LNA), over a 20 day postgestational time period, to quantify the accumulation of newly biosynthesized deuterium-labeled docosahexaenoic acid (d5-DHA) in the developing brain and liver [10]

  • This study focused upon the issue of whether inclusion of preformed DHA in the diet decreases the net accretion of DHA derived from dietary LNA in growing rat pups

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Summary

Introduction

Docosahexaenoic acid (DHA), a crucial nervous system n-3 PUFA, may be obtained in the diet or synthesized in vivo from dietary a-linolenic acid (LNA). The adult rat liver does convert LNA to DHA, but at a rate sufficient to convert ,2% of the total LNA that enters the liver per unit time, with the majority (.70%) of the entering LNA being lost to b-oxidation; and similar results were obtained in both the presence and the absence of dietary DHA [40, 42]. In these studies, adult rat liver production of DHA is elevated 3-fold in the absence of dietary DHA and the rate of liver-to-plasma secretion of synthesized DHA exceeds the replacement rate for brain DHA losses by 10-fold, suggesting that LNA metabolism is able to approach the DHA demands of the adult brain [42, 43]

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