Providing male rats deficient in iron and n-3 fatty acids with iron and alpha-linolenic acid alone affects brain serotonin and cognition differently from combined provision.

Jeannine Baumgartner,Cornelius M Smuts,Michael B Zimmermann

doi:10.1186/1476-511x-13-97

Jeannine Baumgartner, Cornelius M Smuts + Show 1 more

Open Access

https://doi.org/10.1186/1476-511x-13-97

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Journal: Lipids in Health and Disease	Publication Date: Jun 13, 2014
Citations: 65	License type: cc-by

Affiliation: North-West University, ETH Zurich

Abstract

BackgroundWe recently showed that a combined deficiency of iron (ID) and n-3 fatty acids (n-3 FAD) in rats disrupts brain monoamine metabolism and produces greater memory deficits than ID or n-3 FAD alone. Providing these double-deficient rats with either iron (Fe) or preformed docosahexaenoic acid (DHA)/eicosapentaenoic acid (EPA) alone affected brain monoamine pathways differently from combined repletion and even exacerbated cognitive deficits associated with double-deficiency. Iron is a co-factor of the enzymes responsible for the conversion of alpha-linolenic acid (ALA) to EPA and DHA, thus, the provision of ALA with Fe might be more effective in restoring brain EPA and DHA and improving cognition in double-deficient rats than ALA alone.MethodsIn this study we examined whether providing double-deficient rats with ALA and Fe, alone or in combination, can correct deficits in monoamine metabolism and cognition associated with double-deficiency. Using a 2 × 2 design, male rats with concurrent ID and n-3 FAD were fed an Fe + ALA, Fe + n-3 FAD, ID + ALA, or ID + n-3 FAD diet for 5 weeks (postnatal day 56–91). Biochemical measures, and spatial working and reference memory (using the Morris water maze) were compared to age-matched controls.ResultsIn the hippocampus, we found a significant Fe × ALA interaction on DHA: Compared to the group receiving ALA alone, DHA was significantly higher in the Fe + ALA group. In the brain, we found significant antagonistic Fe × ALA interactions on serotonin concentrations. Provision of ALA alone impaired working memory compared with age-matched controls, while in the reference memory task ALA provided with Fe significantly improved performance.ConclusionThese results indicate that providing either iron or ALA alone to double-deficient rats affects serotonin pathways and cognitive performance differently from combined provision. This may be partly explained by the enhancing effect of Fe on the conversion of ALA to EPA and DHA.

Highlights

We recently showed that a combined deficiency of iron (ID) and n-3 fatty acids (n-3 n-3 fatty acid deficiency (FAD)) in rats disrupts brain monoamine metabolism and produces greater memory deficits than iron (Fe) deficiency (ID) or n-3 FAD alone
We found that the repletion with either Fe or docosahexaenoic acid (DHA)/eicosapentaenoic acid (EPA) alone affected monoamine pathways differently from the combined repletion and, surprisingly, even exacerbated the working memory deficits associated with double deficiency [13]
ID + n-3 FAD rats repleted with an Fe + DHA/EPA, ID + DHA/EPA, Fe + n-3 FAD, or an ID + n-3 FAD diet for 5 weeks. (A) Mean distance moved per day to reach hidden platform located at same positions across 4 days, with 4 trials per day in the reference memory task; (B) Mean overall distance moved in the reference memory task

Summary

Introduction

We recently showed that a combined deficiency of iron (ID) and n-3 fatty acids (n-3 FAD) in rats disrupts brain monoamine metabolism and produces greater memory deficits than ID or n-3 FAD alone. Providing these double-deficient rats with either iron (Fe) or preformed docosahexaenoic acid (DHA)/eicosapentaenoic acid (EPA) alone affected brain monoamine pathways differently from combined repletion and even exacerbated cognitive deficits associated with double-deficiency. Iron is a co-factor of the enzymes responsible for the conversion of alpha-linolenic acid (ALA) to EPA and DHA, the provision of ALA with Fe might be more effective in restoring brain EPA and DHA and improving cognition in double-deficient rats than ALA alone. We found that the repletion with either Fe or DHA/EPA alone affected monoamine pathways differently from the combined repletion and, surprisingly, even exacerbated the working memory deficits associated with double deficiency [13]

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