Maternal n-3 polyunsaturated fatty acid deprivation during pregnancy and lactation affects neurogenesis and apoptosis in adult offspring: associated with DNA methylation of brain-derived neurotrophic factor transcripts

Fan, Chaonan; Fu, Huicong; Dong, Hua; Lu, Yuanyuan; Lu, Yanfei; Qi, Kemin

doi:10.1016/j.nutres.2016.06.005

Cited by 35 publications

(27 citation statements)

References 37 publications

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“…Therefore, the observed decreases in hippocampal function may have been a result of decreases in neurogenesis. Consistent with the findings of several previous reports, our findings further suggest that these decreases in neurogenesis may have been caused by reductions in BDNF expression (25, 34). The binding of BDNF to the TrkB receptor activates intracellular cascades that regulate neural development, proliferation, and survival, all of which are implicated in neurogenesis (29).…”

Section: Discussionsupporting

confidence: 93%

“…First, excess maternal fructose consumption may up-regulate the methylation of the BDNF promoter in the hippocampus. This notion is supported by the fact that increased methylation may be induced by maternal nutritional modulations (34). Second, decreases in the hippocampal function of offspring in the F group may have been caused by decreased activity of the demethylation process.…”

Section: Discussionmentioning

confidence: 94%

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Excess maternal fructose consumption impairs hippocampal function in offspring via epigenetic modification of BDNF promoter

Yamazaki¹,

Yamada²,

Munetsuna

et al. 2018

FASEB j.

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Recent increases in fructose consumption have raised concerns about the potential adverse intergenerational effects of excess fructose intake. In the present study, we investigated whether excess maternal fructose intake affects hippocampal function in offspring. Female Sprague-Dawley rats were divided into 3 experimental groups: one group received distilled water, one group received 20% fructose water, and one group received 20% glucose water in addition to standard chow during gestation and lactation. Hippocampal function of offspring was evaluated by using novel object recognition and fear conditioning tests. Impaired cognitive performance was observed in the offspring of fructose-fed dams at postnatal d 60, potentially a result of decreased hippocampal neurogenesis. Real-time PCR analysis demonstrated that offspring from fructose-fed dams exhibited decreased brain-derived neurotrophic factor ( BDNF) gene expression, whereas pyrosequencing assays revealed increased DNA methylation at the BDNF promoter. The potential association between BDNF transcription and levels of DNA methylation was confirmed on the basis of luciferase activity. Furthermore, longitudinal analysis revealed that increased methylation of the BDNF promoter region was maintained at least until rats reached maturity. These results indicate that epigenetic changes associated with BDNF may underlie hippocampal dysfunction that is induced by early-life exposure to excess maternal fructose consumption.-Yamazaki, M., Yamada, H., Munetsuna, E., Ishikawa, H., Mizuno, G., Mukuda, T., Mouri, A., Nabeshima, T., Saito, K., Suzuki, K., Hashimoto, S., Ohashi, K. Excess maternal fructose consumption impairs hippocampal function in offspring via epigenetic modification of BDNF promoter.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 94%

Excess maternal fructose consumption impairs hippocampal function in offspring via epigenetic modification of BDNF promoter

Yamazaki¹,

Yamada²,

Munetsuna

et al. 2018

FASEB j.

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“…Because ω‐3 and ω‐6 long‐chain polyunsaturated fatty acids (LCPUFAs) are critical for cognitive (12–19) and metabolic development (20–27), we focus here on α‐linolenic acid (ALA, C18:3 ω‐3) and linoleic acid (LA, C18:2 ω‐6), which are obtained solely from dietary sources and are mostly converted in the liver to docosahexaenoic acid (DHA, C22:6 ω‐3) and arachidonic acid (AA, C20:4 ω‐6) (28), respectively. Many studies have focused either on overall restriction (29–31) or supplementation (32, 33) with dietary ω‐3 LCPUFA; however, the ratio between dietary LA and ALA is a key determinant of ω‐3 LCPUFA status because LA and ALA compete for conversion to their respective LCPUFAs by the same enzymes. Therefore, the shift toward an increased intake of dietary LA in our modern society is considered a serious concern, because an increased ω‐6/ ω‐3 status (34–36) has been associated with both psychopathologies (14, 36–41) and obesity (42).…”

mentioning

confidence: 99%

Increasing availability of ω‐3 fatty acid in the early‐life diet prevents the early‐life stress‐induced cognitive impairments without affecting metabolic alterations

et al. 2019

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Exposure to early‐life stress (ES) is associated with cognitive and metabolic deficits in adulthood. The role of early nutrition in programming these long‐term effects is largely unknown. We focused on essential ω‐3 and ω‐6 long‐chain polyunsaturated fatty acids (LCPUFA) and investigated whether ES affects central and peripheral FA profiles, as well as if and how an early diet with increased availability of ω‐3 LCPUFA (via lowering ω‐6/ω‐3 ratio) protects against ES‐induced impairments. ES exposure [limited nesting and bedding paradigm from postnatal day (P)2 to P9] altered central and peripheral FA profiles in mice. An early diet with low ω‐6/ω‐3 ratio from P2 to P42 notably prevented the ES‐induced cognitive impairments, and the alterations in hippocampal newborn cell survival and in CD68+ microglia, without affecting the ES‐induced metabolic alterations. Other markers for hippocampal plasticity, apoptosis, and maternal care were unaffected by ES or diet. Our findings highlight the importance of early dietary lipid quality for later cognition in ES‐exposed populations.—Yam, K.‐Y., Schipper, L., Reemst, K., Ruigrok, S. R., Abbink, M. R., Hoeijmakers, L., Naninck, E. F. G., Zarekiani, P., Oosting, A., Van der Beek, E. M., Lucassen, P. J., Korosi, A. Increasing availability of ω‐3 fatty acid in the early‐life diet prevents the early‐life stress‐induced cognitive impairments without affecting metabolic alterations. FASEB J. 33, 5729–5740 (2019). http://www.fasebj.org

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“…Because v-3 and v-6 long-chain polyunsaturated fatty acids (LCPUFAs) are critical for cognitive (12)(13)(14)(15)(16)(17)(18)(19) and metabolic development (20)(21)(22)(23)(24)(25)(26)(27), we focus here on a-linolenic acid (ALA, C18:3 v-3) and linoleic acid (LA, C18:2 v-6), which are obtained solely from dietary sources and are mostly converted in the liver to docosahexaenoic acid (DHA, C22:6 v-3) and arachidonic acid (AA, C20:4 v-6) (28), respectively. Many studies have focused either on overall restriction (29)(30)(31) or supplementation (32,33) with dietary v-3 LCPUFA; however, the ratio between dietary LA and ALA is a key determinant of v-3 LCPUFA status because LA and ALA compete for conversion to their respective LCPUFAs by the same enzymes. Therefore, the shift toward an increased intake of dietary LA in our modern society is considered a serious concern, because an increased v-6/v-3 status (34-36) has been associated with both psychopathologies (14,(36)(37)(38)(39)(40)(41) and obesity (42).…”

mentioning

confidence: 99%

Hospital transfer after a breast cancer diagnosis: A population-based study in the Netherlands of the extent, predictive characteristics and its impact on time to treatment

Heeg

Schreuder²,

Spronk

et al. 2019

European Journal of Surgical Oncology

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Exposure to early-life stress (ES) is associated with cognitive and metabolic deficits in adulthood. The role of early nutrition in programming these long-term effects is largely unknown. We focused on essential v-3 and v-6 long-chain polyunsaturated fatty acids (LCPUFA) and investigated whether ES affects central and peripheral FA profiles, as well as if and how an early diet with increased availability of v-3 LCPUFA (via lowering v-6/v-3 ratio) protects against ES-induced impairments. ES exposure [limited nesting and bedding paradigm from postnatal day (P)2 to P9] altered central and peripheral FA profiles in mice. An early diet with low v-6/v-3 ratio from P2 to P42 notably prevented the ES-induced cognitive impairments, and the alterations in hippocampal newborn cell survival and in CD68 + microglia, without affecting the ES-induced metabolic alterations. Other markers for hippocampal plasticity, apoptosis, and maternal care were unaffected by ES or diet. Our findings highlight the importance of early dietary lipid quality for later cognition in ES-exposed populations. Increasing availability of v-3 fatty acid in the early-life diet prevents the early-life stress-induced cognitive impairments without affecting metabolic alterations. FASEB J. 33, 5729-5740 (2019). www.fasebj.org

show abstract

Maternal n-3 polyunsaturated fatty acid deprivation during pregnancy and lactation affects neurogenesis and apoptosis in adult offspring: associated with DNA methylation of brain-derived neurotrophic factor transcripts

Cited by 35 publications

References 37 publications

Excess maternal fructose consumption impairs hippocampal function in offspring via epigenetic modification of BDNF promoter

Excess maternal fructose consumption impairs hippocampal function in offspring via epigenetic modification of BDNF promoter

Increasing availability of ω‐3 fatty acid in the early‐life diet prevents the early‐life stress‐induced cognitive impairments without affecting metabolic alterations

Hospital transfer after a breast cancer diagnosis: A population-based study in the Netherlands of the extent, predictive characteristics and its impact on time to treatment

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