Mechanisms of docosahexaenoic acid accretion in the fetal brain

Green, P.; Yavin, Ephraïm

doi:10.1002/(sici)1097-4547(19980415)52:2<129::aid-jnr1>3.0.co;2-c

Cited by 77 publications

(42 citation statements)

References 58 publications

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“…This is in contradiction with earlier findings that circulating DHA is preferentially taken up by the brain (Scott and Bazan, 1989). However, it is in line with the observation that after a single intraamniotic DHA-EE injection in fetal rats, a steeper increase of DHA was found in the fetal liver than in the brain (Green and Yavin, 1998).…”

Section: Discussioncontrasting

confidence: 58%

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Docosahexaenoic Acid Deficit Is Not a Major Pathogenic Factor in Peroxisome-Deficient Mice

Janssen

Baes

Gressèns

et al. 2000

Laboratory Investigation

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SUMMARY: Docosahexaenoic acid (DHA), a major component of membrane phospholipids in brain and retina, is profoundly reduced in patients with peroxisome biogenesis disorders (Zellweger syndrome). Supplementing newborn patients with DHA resulted in improved muscular tone and visual functions. The purpose of this study was to investigate (a) whether DHA levels were also reduced in newborn PEX5 knockout mice, the mouse model of Zellweger syndrome that we recently generated; (b) whether these levels could be normalized by supplying DHA; and (c) whether this results in longer survival. The DHA concentration in brain of newborn PEX5 Ϫ/Ϫ mice was reduced by 40% as compared with levels in normal littermates; in liver, no differences were noticed. The daily administration of 10 mg of DHA-ethyl ester (EE) to pregnant heterozygous mothers during the last 8 days of gestation resulted in a normalization of brain DHA levels in Zellweger pups. However, no clinical improvement was observed in these pups, and the neuronal migration defect was unaltered. These data suggest that the accretion of DHA in the brain at the end of embryonic development is not only supported by the maternal supply but also depends on synthesis in the fetal brain. Furthermore, the DHA deficit does not seem to be a major pathogenic factor in the newborn Zellweger mice. (Lab Invest 2000, 80:31-35).

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Section: Discussioncontrasting

confidence: 58%

“…Dietary deficiency of n-3 fatty acids is associated with disturbances in vision and other neurological abnormalities (Green and Yavin, 1998). A rapid accretion of DHA that starts during the last period of gestation and continues for a short time after birth has been documented in man and in rat (Martinez, 1992b;Green and Yavin, 1996).…”

mentioning

confidence: 99%

Docosahexaenoic Acid Deficit Is Not a Major Pathogenic Factor in Peroxisome-Deficient Mice

Janssen

Baes

Gressèns

et al. 2000

Laboratory Investigation

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“…Nevertheless, evidence shows that DHA can modulate the PS levels in vivo and in vitro. For example, intraamniotic injection of DHA during pregnancy can increase PS in a newborn rat brain (19). Similarly, DHA supplementation in cultured glia or neuronal cells has been shown to increase PS content (20,21).…”

mentioning

confidence: 99%

Docosahexaenoic acid: A positive modulator of Akt signaling in neuronal survival

Akbar

Calderón

Zhao

et al. 2005

Proc. Natl. Acad. Sci. U.S.A.

408

319

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Phosphatidylinositol 3-kinase [PI (3)K]/Akt signaling is a critical pathway in cell survival. Here, we demonstrate a mechanism where membrane alteration by the n-3 fatty acid status affects Akt signaling, impacting neuronal survival. Docosahexaenoic acid (DHA), an n-3 polyunsaturated fatty acid highly enriched in neuronal membranes, promotes neuronal survival by facilitating membrane translocation/activation of Akt through its capacity to increase phosphatidylserine (PS), the major acidic phospholipid in cell membranes. The activation of PI (3)K and phosphatidylsinositol triphosphate formation were not affected by DHA, indicating that membrane interaction of Akt is the event responsible for the DHA effect. Docosapentaenoic acid, which replaces DHA during n-3 fatty acid deficiency, was less effective in accumulating PS and translocating Akt and thus less effective in preventing apoptosis. Consistently, in vivo reduction of DHA by dietary depletion of n-3 fatty acids decreased hippocampal PS and increased neuronal susceptibility to apoptosis in cultures. This mechanism may contribute to neurological deficits associated with n-3 fatty acid deficiency and support protective effects of DHA in pathological models such as brain ischemia or Alzheimer's disease

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“…The n-3 family includes alinolenic acid (18:3), eicosapentaenoic acid (EPA,20:5) and docosahexaenoic acid (DHA,22:6). DHA is the major polyunsaturated fatty acid in the adult mammalian brain (Anderson et al, 1990;Green & Yavin, 1998;Innis, 2000) and is selectively concentrated at synaptic neuronal membranes (Innis, 2000). DHA and EPA are present in fatty fish (salmon, tuna, mackerel), although it can be obtained from n-3-enriched eggs (Lewis et al, 2000).…”

Section: Introductionmentioning

confidence: 99%

Dietary intake of n-3, n-6 fatty acids and fish: Relationship with hostility in young adults—the CARDIA study

et al. 2003

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Background: Hostility has been shown to predict both the development and manifestation of coronary disease. Examining the inter-relation of dietary intake of fish and of polyunsaturated (n-3 and n-6) essential fatty acids with hostility may provide additional insights into the cardioprotective effect of dietary fish and polyunsaturated fatty acids. Objective: To examine the association of dietary n-3, n-6 fatty acids and fish with level of hostility in a sample of 3581 urban white and black young adults. Design: Cross-sectional observational study as part of an ongoing cohort study. A dietary assessment in 1992-1993 and measurement of hostility and other covariates in 1990-1991 were used in the analysis. Results: The multivariate odds ratios of scoring in the upper quartile of hostility (adjusting for age, sex, race, field center, educational attainment, marital status, body mass index, smoking, alcohol consumption and physical activity) associated with one standard deviation increase in docosahexaenoic acid (DHA, 22:6) intake was 0.90 (95% CI ¼ 0.82-0.98; P ¼ 0.02). Consumption of any fish rich in n-3 fatty acids, compared to no consumption, was also independently associated with lower odds of high hostility (OR ¼ 0.82; 95% CI ¼ 0.69-0.97; P ¼ 0.02). Conclusions: These results suggest that high dietary intake of DHA and consumption of fish rich in n-3 fatty acids may be related to lower likelihood of high hostility in young adulthood. The association between dietary n-3 fatty acids and hostile personality merits further research.

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Mechanisms of docosahexaenoic acid accretion in the fetal brain

Cited by 77 publications

References 58 publications

Docosahexaenoic Acid Deficit Is Not a Major Pathogenic Factor in Peroxisome-Deficient Mice

Docosahexaenoic Acid Deficit Is Not a Major Pathogenic Factor in Peroxisome-Deficient Mice

Docosahexaenoic acid: A positive modulator of Akt signaling in neuronal survival

Dietary intake of n-3, n-6 fatty acids and fish: Relationship with hostility in young adults—the CARDIA study

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