Maternal obesity impairs hippocampal BDNF production and spatial learning performance in young mouse offspring

Tozuka, Yusuke; Kumon, Mami; Wada, Etsuko; Onodera, Masafumi; Mochizuki, Hideki; Wada, Keiji

doi:10.1016/j.neuint.2010.05.015

Cited by 221 publications

(224 citation statements)

References 79 publications

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“…Roth and his colleagues reported that exposure to early maltreatment can induce long-lasting changes in the methylation of the Bdnf gene in the prefrontal cortex and increases adult anxiety levels in mice (Roth et al 2009). More specifically, it has been demonstrated that maternal obesity impairs hippocampal BDNF production and spatial learning performance in young offspring (Tozuka et al 2010).…”

Section: Discussionmentioning

confidence: 99%

Maternal high-fat diet influences stroke outcome in adult rat offspring

Lin

Shao

Zhou

et al. 2015

Journal of Molecular Endocrinology

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Diet-induced epigenetic modifications in early life could contribute to later health problem. However, it remains to be established whether high-fat diet (HFD) consumption during pregnancy and the suckling period could predispose the offspring to stroke. The present study investigated the influence of maternal HFD on stroke outcome in adult offspring. Female Sprague-Dawley rats were fed a normal diet (5.3% fat) or a HFD (25.7% fat), just before pregnancy until the end of lactation. Male offspring were fed with the control diet or the HFD after weaning, to form four groups (control offspring fed with the control diet (C/C) or the HFD (C/HFD) and offspring of fat-fed dams fed with the control diet (HFD/C) or the HFD (HFD/HFD)). The offspring received middle cerebral artery occlusion on day 120 followed by behavioral tests (neurological deficit score, staircase-reaching test and beam-traversing test), and infarct volumes were also calculated. We found that the HFD/C rats displayed larger infarct volume and aggravated functional deficits (all P!0.05), compared with the C/C rats, indicating that maternal fat-rich diet renders the brain more susceptible to the consequences of ischemic injury. Moreover, maternal HFD offspring displayed elevated glucocorticoid concentrations following stroke, and increased glucocorticoid receptor expression. In addition, adrenalectomy reversed the effects of maternal HFD on stroke outcome when corticosterone was replaced at baseline, but not ischemic, concentrations. Furthermore, expression of brain-derived neurotrophic factor (BDNF) in the ipsilateral hippocampus was decreased in the HFD/C offspring (P!0.05), compared with the C/C offspring. Taken together, maternal diet can substantially influence adult cerebrovascular health, through the programming of central BDNF expression and the hypothalamic-pituitary-adrenal axis.

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Section: Discussionmentioning

confidence: 99%

Maternal high-fat diet influences stroke outcome in adult rat offspring

Lin

Shao

Zhou

et al. 2015

Journal of Molecular Endocrinology

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“…In animals, maternal consumption of a high-fat diet has been linked to a range of negative CNS outcomes, including increased anxiety-like behaviors, 31,32 decreased hippocampal dendritic arborization, 33 increased hypothalamic neurogenesis of orexigenic neurons (which can drive overeating and increase the obesity risk) 34 and alterations in the expression of serotonergic genes, dopaminergic genes, inflammation-related genes and neuropeptides related to food intake/metabolism. 31,32,34,35 Not all areas of the brain appear to be similarly sensitive to the effects of maternal consumption of a high-fat diet, as arcuate to paraventricular projections are not affected by maternal diet, 36 yet these projections are affected by maternal insulin status, 37 highlighting the complexity of the interactions between maternal environment (diet, obesity, diabetes) and the offspring outcome.…”

Section: Animal Modelsmentioning

confidence: 99%

High-fat diet alters the dopamine and opioid systems: effects across development

Reyes

2012

Int J Obes Supp

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Consumption of a high-fat diet has been linked to obesity, dyslipidemia and cardiovascular disease. Less well appreciated are adverse effects on the brain and behavior. Recent research has shown that consumption of a high-fat diet can alter gene expression within the brain, and the dopamine and opioid neurotransmitter systems appear to be vulnerable to dysregulation. This review will focus on recent reports in both humans and animal models that describe adverse effects of high-fat diet consumption on the central reward circuitry. In addition, the importance of different development windows will be discussed, with effects observed in both the prenatal/perinatal time period and with chronic high-fat diet consumption in adulthood.

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“…[6][7][8] It has been suggested that this adverse intrauterine environment may directly damage the developing fetal brain causing offspring cognitive, behavioral, and motor development delays. [9][10][11][12] Epidemiological research supporting an association between maternal prepregnancy body mass index (BMI) and children's neurodevelopment is beginning to emerge. Results from three studies suggest that prepregnancy obesity may be associated with lower general cognitive abilities in children; [13][14][15] however, these findings were not replicated in a study of children from two large cohorts.…”

Section: Introductionmentioning

confidence: 99%

Associations between maternal prepregnancy body mass index and child neurodevelopment at 2 years of age

et al. 2012

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OBJECTIVE: Both underweight and obese mothers have an increased risk for adverse offspring outcomes. Few studies have examined the association between prepregnancy body mass index (BMI) and children's neurodevelopment. SUBJECTS: We used data from the nationally representative Early Childhood Longitudinal Study-Birth Cohort (ECLS-B; n ¼ 6850). Children were classified according to their mother's prepregnancy BMI (kg m À 2 ) status: underweight (BMI o18.5), normal weight (BMI 18.5-24.9), overweight (BMI 25.0-29.9), obese class I (BMI 30.0-34.9), and obese class II and III (BMI X35.0). Children's ageadjusted mental development index (MDI) and psychomotor development index (PDI) T-scores (mean 50, s.d. 10) were obtained using a validated shortened version of the Bayley Scales of Infant Development-II at approximately 2 years of age. While adjusting for sociodemographics, we estimated the average MDI and PDI scores or the risk of delayed (o À 1 s.d. vs 41 s.d.) mental or motor development, relative to children of normal weight mothers. RESULTS: Compared with children of normal weight mothers, MDI scores were lower among children of mothers of all other prepregnancy BMI categories, with the greatest adjusted difference among children of class II and III obese mothers ( À 2.13 (95% CI À 3.32, À 0.93)). The adjusted risk of delayed mental development was increased among children of underweight (risk ratio (RR) 1.36 (95% CI 1.04, 1.78)) and class II and III obese (RR 1.38 (95% CI 1.03, 1.84)) mothers. Children's PDI scores or motor delay did not differ by maternal prepregnancy BMI. CONCLUSION: In this nationally representative sample of 2-year-old US children, low and very-high maternal prepregnancy BMI were associated with increased risk of delayed mental development but not motor development.

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Maternal obesity impairs hippocampal BDNF production and spatial learning performance in young mouse offspring

Cited by 221 publications

References 79 publications

Maternal high-fat diet influences stroke outcome in adult rat offspring

Maternal high-fat diet influences stroke outcome in adult rat offspring

High-fat diet alters the dopamine and opioid systems: effects across development

Associations between maternal prepregnancy body mass index and child neurodevelopment at 2 years of age

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