Effects of an n-3-deficient diet on brain, retina, and liver fatty acyl composition in artificially reared rats

Moriguchi, Takahiko; Lim, Seongyop; Greiner, Rebecca; Lefkowitz, William; Loewke, James; Hoshiba, Junji; Salem, Norman

doi:10.1194/jlr.m400087-jlr200

Cited by 59 publications

(34 citation statements)

References 16 publications

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“…After 250 mg of methyl docosatrienoate (22:3n-3) was added as an internal standard (19), the fatty acids esterified to phospholipids in ?100 mg (wet weight) of tissue were transmethylated, and the fatty aldehydes were converted to dimethylacetals (20). Fatty acids and aldehydes were identified by matching sample retention times with those of standards (Agilent Technology, Wilmington, DE), with modifications to improve separation for DHA (21).…”

Section: Sds-page and Western Blotsmentioning

confidence: 99%

F2-Dihomo-isoprostanes arise from free radical attack on adrenic acid

VanRollins

Woltjer

Yin

et al. 2008

Journal of Lipid Research

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Unlike F 4 -neuroprostanes (F 4 -NeuroPs), which are relatively selective in vivo markers of oxidative damage to neuronal membranes, there currently is no method to assess the extent of free radical damage to myelin with relative selectively. The polyunsaturated fatty acid adrenic acid (AdA) is susceptible to free radical attack and, at least in primates, is concentrated in myelin within white matter.

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Section: Sds-page and Western Blotsmentioning

confidence: 99%

F2-Dihomo-isoprostanes arise from free radical attack on adrenic acid

VanRollins

Woltjer

Yin

et al. 2008

Journal of Lipid Research

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“…Severe depletion of brain DHA, approaching 80%, can be achieved by subjecting rats to n-3 PUFA deprivation for two or more consecutive generations (4, 9, 10), or by artificially rearing newborn pups on a formula free of n-3 PUFA (12). In addition, singlegenerational n-3 PUFA deprivation in rodents, starting after weaning at 21 days, reduces brain DHA by about 40% (11,13).…”

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confidence: 99%

One generation of n-3 polyunsaturated fatty acid deprivation increases depression and aggression test scores in rats

DeMar

Bell

et al. 2006

Journal of Lipid Research

225

157

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Male rat pups at weaning (21 days of age) were subjected to a diet deficient or adequate in n-3 polyunsaturated fatty acids (n-3 PUFAs) for 15 weeks. Performance on tests of locomotor activity, depression, and aggression was measured in that order during the ensuing 3 weeks, after which brain lipid composition was determined. In the n-3 PUFA-deprived rats, compared with n-3 PUFA-adequate rats, docosahexaenoic acid (22:6n-3) in brain phospholipid was reduced by 36% and docosapentaenoic acid (22:5n-6) was elevated by 90%, whereas brain phospholipid concentrations were unchanged. N-3 PUFA-deprived rats had a significantly increased (P 5 0.03) score on the Porsolt forcedswim test for depression, and increased blocking time (P 5 0.03) and blocking number (P 5 0.04) scores (uncorrected for multiple comparisons) on the isolation-induced residentintruder test for aggression. Large effect sizes (d . 0.8) were found on the depression score and on the blocking time score of the aggression test. Scores on the open-field test for locomotor activity did not differ significantly between groups, and had only small to medium effect sizes. This single-generational n-3 PUFA-deprived rat model, which demonstrated significant changes in brain lipid composition and in test scores for depression and aggression, may be useful for elucidating the contribution of disturbed brain PUFA metabolism to human depression, aggression, and bipolar disorder.-DeMar, J. C., Jr., K. Ma, J. M. Bell, M. Igarashi, D. Greenstein, and S. I. Rapoport. One generation of n-3 polyunsaturated fatty acid deprivation increases depression and aggression test scores in rats.

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“…Lipid content of milk reflects the lipid profile of the mother's diet 9,11 . We found that retinal lipid composition in the pups reflected the pups' (and the mother's) dietary intake of lipids.…”

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Increased dietary intake of ω-3-polyunsaturated fatty acids reduces pathological retinal angiogenesis

Connor

SanGiovanni

Löfqvist

et al. 2007

Nat Med

Self Cite

634

572

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Many sight-threatening diseases have two critical phases, vessel loss followed by hypoxia-driven destructive neovascularization. These diseases include retinopathy of prematurity and diabetic retinopathy, leading causes of blindness in childhood and middle age affecting over 4 million people in the United States. We studied the influence of ω-3-and ω-6-polyunsaturated fatty acids (PUFAs) on vascular loss, vascular regrowth after injury, and hypoxia-induced pathological neovascularization in a mouse model of oxygen-induced retinopathy 1 . We show that increasing ω-3-PUFA tissue levels by dietary or genetic means decreased the avascular area of the retina by Reprints and permissions information is available online at http://npg.nature.com/reprintsandpermissionsCorrespondence should be addressed to L.E.H.S. (lois.smith@childrens.harvard.edu).. Supplementary information is available on the Nature Medicine website. COMPETING INTERESTS STATEMENTThe authors declare competing financial interests: details accompany the full-text HTML version of the paper at http:// www.nature.com/naturemedicine/. HHS Public AccessAuthor manuscript Nat Med. Author manuscript; available in PMC 2015 July 05. Published in final edited form as:Nat Med. 2007 July ; 13(7): 868-873. doi:10.1038/nm1591. Author Manuscript Author ManuscriptAuthor ManuscriptAuthor Manuscript increasing vessel regrowth after injury, thereby reducing the hypoxic stimulus for neovascularization. The bioactive ω-3-PUFA-derived mediators neuroprotectinD1, resolvinD1 and resolvinE1 also potently protected against neovascularization. The protective effect of ω-3-PUFAs and their bioactive metabolites was mediated, in part, through suppression of tumor necrosis factor-α. This inflammatory cytokine was found in a subset of microglia that was closely associated with retinal vessels. These findings indicate that increasing the sources of ω-3-PUFA or their bioactive products reduces pathological angiogenesis. Western diets are often deficient in ω-3-PUFA, and premature infants lack the important transfer from the mother to the infant of ω-3-PUFA that normally occurs in the third trimester of pregnancy 2 . Supplementing ω-3-PUFA intake may be of benefit in preventing retinopathy.Ocular neovascularization is the most common cause of blindness in all age groups: retinopathy of prematurity in children, diabetic retinopathy in working-age adults and agerelated macular degeneration in the elderly. In principle, destructive angiogenesis in the eye can be ameliorated by either direct inhibition of neovascularization or by controlling vessel loss in order to reduce the hypoxic stimulus that drives neovascularization. Retinopathy is modeled in the mouse eye with oxygen-induced vessel loss, which precipitates hypoxiainduced retinopathy, allowing for assessment of retinal vessel loss, vessel regrowth after injury and pathological angiogenesis 1 .The role of lipids in angiogenesis is just beginning to be defined 3,4 . The major polyunsaturated fatty acids (PUFA) found in the retina a...

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Effects of an n-3-deficient diet on brain, retina, and liver fatty acyl composition in artificially reared rats

Cited by 59 publications

References 16 publications

F2-Dihomo-isoprostanes arise from free radical attack on adrenic acid

F2-Dihomo-isoprostanes arise from free radical attack on adrenic acid

One generation of n-3 polyunsaturated fatty acid deprivation increases depression and aggression test scores in rats

Increased dietary intake of ω-3-polyunsaturated fatty acids reduces pathological retinal angiogenesis

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