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

Lin, Chengcheng; Shao, Baiqi; Zhou, YuLei; Niu, Xiaoting; Lin, Yuanshao

doi:10.1530/jme-15-0226

Cited by 10 publications

(10 citation statements)

References 48 publications

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“…Using the same model and markers, the present study explores whether the co-existence of maternal HFD, known to induce an amplified response to acute stress, could act as an aggravating factor in PA. Data obtained have shown an intensified hippocampal neuroinflammation and injury in the HF-PA group when compared to the PA group, supporting a cumulative effect of maternal HFD on the extent of PA-induced hippocampal damage. Our findings are in accordance with Lin et al [15], who reported that HFD during pregnancy might worsen the post-ischemic outcome. This finding can be correlated with the long-lasting presence of low-levels of proinflammatory mediators induced by the maternal diet, which can be transmitted in utero to the fetus [16].…”

Section: Discussionsupporting

confidence: 94%

Maternal High-Fat Diet Modifies the Immature Hippocampus Vulnerability to Perinatal Asphyxia in Rats

Isac¹,

Panaitescu²,

Ieșanu

et al. 2018

Neonatology

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Background: High-fat diet (HFD) is a detrimental habit with harmful systemic consequences, including low-grade, long-lasting inflammation. During pregnancy, HFD can induce developmental changes. Moreover, HFD-related maternal obesity might enhance the risk of peripartum complications including hypoxic-ischemic encephalopathy secondary to perinatal asphyxia (PA). Objectives: Following our previous results showing that PA increases neuroinflammation and neuronal injury in the immature hippocampus and modifies hippocampal epigenetic programming, we further aimed to establish the impact of maternal HFD on offspring hippocampus response to PA. Methods: We assessed hippocampal tumor necrosis factor alpha (TNFα), interleukin 1 beta (IL-1b) and S-100B protein (S-100B), 24–48 h after PA exposure in postnatal day 6 Wistar rats, whose mothers received either the standard diet or HFD. The expression of small non-coding microRNA species miR124, miR132, miR134, miR146, and miR15a, as epigenetic markers for the maternal dietary influence on immature hippocampus response after PA, was determined 24 h after asphyxia exposure. Metabolic activity was measured using resazurin test in hippocampal cell suspension obtained 24 h after PA. Results: Our results indicate that maternal HFD additionally increases hippocampal TNFα, IL-1b, and S-100B after PA. Also, PA associated with maternal HFD induces miR124 upregulation and miR132 downregulation relative to PA only. Metabolic activity was increased in hippocampal cells from pups whose mothers received HFD. Conclusion: HFD increases the PA-induced neuroinflammation and neuronal injury, and epigenetically influences homeostatic synaptic plasticity and neuronal tolerance to asphyxia, processes associated with a higher hippocampal cellular metabolism.

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Section: Discussionsupporting

confidence: 94%

Maternal High-Fat Diet Modifies the Immature Hippocampus Vulnerability to Perinatal Asphyxia in Rats

Isac¹,

Panaitescu²,

Ieșanu

et al. 2018

Neonatology

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“…[2][3][4] Consistently, maternal HFD intake also renders the brain more susceptible to the consequences of ischemic injury in adult offspring. 5 The present study expands the result by demonstrating that maternal HFD consumption would substantially influence adult offspring cerebrovascular health, providing an important mechanism for maternal HFD-induced aggravated stroke outcome. Moreover, because of the cerebral circulation remodeling, maternal HFD exposure would also give rise to an offspring phenotype predisposed to the development of stroke and other cerebrovascular diseases in adulthood.…”

Section: Discussionsupporting

confidence: 74%

“…Baseline cerebrovascular ET-1 levels were also measured in the MCA homogenate, using the immunoassay kits. Subset of rats were applied with temporary middle cerebral artery occlusion (MCAO), 5 and post-stroke plasma ET-1 levels were determined 2 h later. In brief, a silicon-coated 5-0 nylon monofilament (tip diameter: 0.31 AE 0.02 mm) was introduced into the external carotid artery and advanced up the internal carotid artery to the Circle of Willis (18-19 mm from the carotid bifurcation), where it blocked the origin of the MCA to decrease blood flow for 1.5 h. Cerebral blood flow reduction of at least 80% of baseline was confirmed as ischemic attack by Laser Doppler Flowmetry (Moor Instruments, UK).…”

Section: Metabolic Parameters and Et-1 Measurementmentioning

confidence: 99%

“…Our previous study demonstrated that maternal high-fat diet (HFD) consumption renders the brain more susceptible to the consequences of ischemic injury, supported by the evidence showing that adult rat offspring of HFD-fed dams during pregnancy and lactation develops aggravated infarct volume and function deficits following stroke. 5 Although the study showed that the programing of the central neurotrophin and neuroendocrine system may contribute to aggravated stroke outcomes in maternal HFD offspring, 5 the mechanisms by which maternal HFD compromises adult ischemia occurrence and outcomes remain to be fully elucidated.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Maternal high-fat diet programs cerebrovascular remodeling in adult rat offspring

Lin

Zhou

et al. 2017

J Cereb Blood Flow Metab

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Maternal environmental factors such as diet have consequences on later health of the offspring. We found that maternal high-fat diet (HFD) exposure renders adult offspring brain more susceptible to ischemic injury. The present study was further to investigate whether HFD consumption during rat pregnancy and lactation influences the cerebral vasculature in adult male offspring. Besides the endothelial damage observed in the transmission electron microscopy, the MCAs of offspring from fat-fed dams fed with control diet (HFD/C) also displayed increased wall thickness and media/lumen ratio, suggesting that cerebrovascular hypertrophy or hyperplasia occurs. Moreover, smaller lumen diameter and elevated myogenic tone of the MCAs over a range of intralumenal pressures indicate inward cerebrovascular remodeling in HFD/C rats, with a concomitant increase in vessel stiffness. More importantly, both wire and pressure myography demonstrated that maternal HFD intake also enhanced the MCAs contractility to ET-1, accompanied by increases in ET types A receptor (ETR) but not B (ETR) density in the arteries. Furthermore, ETR antagonism but not ETR antagonism restored maternal HFD-induced cerebrovascular dysfunction in adult offspring. Taken together, maternal diet can substantially influence adult offspring cerebrovascular health, through remodeling of both structure and function, at least partially in an ET-1 manner.

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“…As discussed above, whether this is due to post-natal adaptations during brain maturation or insensitivity of the current methods to detect small or selective changes in BBB permeability remains unknown. Endothelial denudation and thickening of the middle cerebral artery has been reported in 6-month old rat offspring of obese mothers (Lin et al, 2018) and neonatal and adult HF/C offspring display larger infarct volumes and poorer functional deficits after stroke compared to C/C rats (Lin et al, 2016; Teo et al, 2017). We have previously reported that vessel morphology and thickness and GFAP expression were altered in the hippocampus of 5-month old HF/C male mice compared to C/C offspring (Hawkes et al, 2015).…”

Section: Discussionmentioning

confidence: 99%

Pre- and Post-natal High Fat Feeding Differentially Affects the Structure and Integrity of the Neurovascular Unit of 16-Month Old Male and Female Mice

et al. 2019

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Compelling experimental and clinical evidence supports a role for maternal obesity in offspring health. Adult children of obese mothers are at greater risk of obesity, diabetes, coronary heart disease and stroke. These offspring may also be at greater risk of age-related neurodegenerative diseases for which mid-life obesity is a risk factor. Rodent diet-induced obesity models have shown that high fat (HF) diet consumption damages the integrity of the blood–brain barrier (BBB) in the adult brain. However, there is currently little information about the effect of chronic HF feeding on the BBB of aged animals. Moreover, the long-term consequences of maternal obesity on the cerebrovasculature of aged offspring are not known. This study determined the impact of pre- and post-natal HF diet on the structure and integrity of cerebral blood vessels in aged male and female mice. Female C57Bl/6 mice were fed either a 10% fat control (C) or 45% HF diet before mating and during gestation and lactation. At weaning, male and female offspring were fed the C or HF diet until sacrifice at 16-months of age. Both dams and offspring fed the HF diet weighed significantly more than mice fed the C diet. Post-natal HF diet exposure increased hippocampal BBB leakiness in female offspring, in association with loss of astrocyte endfoot coverage of arteries. Markers of tight junctions, pericytes or smooth muscle cells were not altered by pre- or post-natal HF diet. Male offspring born to HF-fed mothers showed decreased parenchymal GFAP expression compared to offspring of mothers fed C diet, while microglial and macrophage markers were higher in the same female diet group. In addition, female offspring exposed to the HF diet for their entire lifespan showed more significant changes in vessel structure, BBB permeability and inflammation compared to male animals. These results suggest that the long-term impact of prenatal HF diet on the integrity of cerebral blood vessels differs between male and female offspring depending on the post-natal diet. This may have implications for the prevention and management of age- and obesity-related cerebrovascular diseases that differentially affect men and women.

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

Cited by 10 publications

References 48 publications

Maternal High-Fat Diet Modifies the Immature Hippocampus Vulnerability to Perinatal Asphyxia in Rats

Maternal High-Fat Diet Modifies the Immature Hippocampus Vulnerability to Perinatal Asphyxia in Rats

Maternal high-fat diet programs cerebrovascular remodeling in adult rat offspring

Pre- and Post-natal High Fat Feeding Differentially Affects the Structure and Integrity of the Neurovascular Unit of 16-Month Old Male and Female Mice

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