Deficient maternal zinc intake—but not folate—is associated with lower fetal heart rate variability

Spann, Marisa; Smerling, Jennifer; Gustafsson, Hanna; Foss, Sophie; Altemus, Margaret; Monk, Catherine

doi:10.1016/j.earlhumdev.2015.01.007

Cited by 11 publications

(7 citation statements)

References 44 publications

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“…Additionally, MUN rats did not show an elevated HR, which was detected in the SHR model. The lack of HR alterations of MUN rats is in line with other studies using maternal low protein [ 35 , 86 ] or low micronutrients, such as zinc [ 87 ] or vitamin B12 [ 88 ] diets during pregnancy. In SHR, the tachycardia probably reflects an alteration in baroreceptor regulation, as previously reported [ 86 ], which may contribute to the higher blood pressure in this strain.…”

Section: Discussionsupporting

confidence: 88%

Elevated Vascular Sympathetic Neurotransmission and Remodelling Is a Common Feature in a Rat Model of Foetal Programming of Hypertension and SHR

et al. 2022

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Hypertension is of unknown aetiology, with sympathetic nervous system hyperactivation being one of the possible contributors. Hypertension may have a developmental origin, owing to the exposure to adverse factors during the intrauterine period. Our hypothesis is that sympathetic hyperinnervation may be implicated in hypertension of developmental origins, being this is a common feature with essential hypertension. Two-animal models were used: spontaneously hypertensive rats (SHR-model of essential hypertension) and offspring from dams exposed to undernutrition (MUN-model of developmental hypertension), with their respective controls. In adult males, we assessed systolic blood pressure (SBP), diastolic blood pressure (DBP), heart rate (HR), sympathetic nerve function (3H-tritium release), sympathetic innervation (immunohistochemistry) and vascular remodelling (histology). MUN showed higher SBP/DBP, but not HR, while SHR exhibited higher SBP/DBP/HR. Regarding the mesenteric arteries, MUN and SHR showed reduced lumen, increased media and adventitial thickness and increased wall/lumen and connective tissue compared to respective controls. Regarding sympathetic nerve activation, MUN and SHR showed higher tritium release compared to controls. Total tritium tissue/tyrosine hydroxylase detection was higher in SHR and MUN adventitia arteries compared to respective controls. In conclusion, sympathetic hyperinnervation may be one of the contributors to vascular remodelling and hypertension in rats exposed to undernutrition during intrauterine life, which is a common feature with spontaneous hypertension.

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Section: Discussionsupporting

confidence: 88%

Elevated Vascular Sympathetic Neurotransmission and Remodelling Is a Common Feature in a Rat Model of Foetal Programming of Hypertension and SHR

et al. 2022

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“…A second possible underlying process is increased uterine artery resistance and the limited blood flow to the fetus (e.g., O'Donnell et al, 2009). Inadequate prenatal care and less healthy habits associated with depression can also affect fetal neurobehavioral maturity (e.g., Monk, Georgieff, & Osterholm, 2013;Nordentoft et al, 1996;Spann et al, 2015). The limitations of this study include the self-reported prenatal depression.…”

Section: Discussionmentioning

confidence: 94%

Fetal heart rate variability mediates prenatal depression effects on neonatal neurobehavioral maturity

Figueiredo

Pinto

Pacheco

et al. 2017

Biological Psychology

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This study analyzed the mediating role of fetal heart rate variability (FHR) on prenatal depression and neonatal neurobehavioral maturity. A sample of 104 pregnant women was recruited and divided into two groups according to their Edinburgh Postnatal Depression Scale (EPDS) scores (depressed/non-depressed). FHR variability in response to speech stimuli was assessed at term (between 37 and 39 weeks gestation). The neonates were then assessed on the Neonatal Behavioral Assessment Scale (NBAS) during the first 5days after birth. The fetuses of non-depressed pregnant women showed higher HR variability than the fetuses of depressed pregnant women in response to speech stimuli, and later as neonates they performed more optimally on the NBAS (on autonomic stability and total scores). FHR variability mediated the relationship between the mother's prenatal depression and the neonatés NBAS performance. Prenatal depression effects on neonatal behavior may be partially explained by its adverse effects on fetal neurobehavioral maturity.

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“…Also maternal infections, diabetes, and toxicant exposures that stimulate an acute-phase response causes a decreased transport of zinc to the developing fetus (Nuttall et al, 2017 ), which can lead to increased risk of NTDs (Chua et al, 2006 ; Uriu-Adams and Keen, 2010 ). On the other hand, a marginally low dietary zinc intake during pregnancy is associated with decreased fetal heart rate variability, suggesting impaired regulation of the autonomic nervous system (Spann et al, 2015 ). Accordingly, prenatal zinc supplementation improves the regulation of the autonomic nervous system later in life (Caulfield et al, 2011 ).…”

Section: Discussionmentioning

confidence: 99%

Early Developmental Marginal Zinc Deficiency Affects Neurogenesis Decreasing Neuronal Number and Altering Neuronal Specification in the Adult Rat Brain

Adamo

Liu

Mathieu

et al. 2019

Front. Cell. Neurosci.

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During pregnancy, a decreased availability of zinc to the fetus can disrupt the development of the central nervous system leading to defects ranging from severe malformations to subtle neurological and cognitive effects. We previously found that marginal zinc deficiency down-regulates the extracellular signal-regulated kinase 1/2 (ERK1/2) signaling pathway and affects neural progenitor cell (NPC) proliferation. This study investigated if marginal zinc deficiency during gestation in rats could disrupt fetal neurogenesis and affect the number and specification of neurons in the adult offspring brain cortex. Rats were fed a marginal zinc deficient or adequate diet throughout gestation and until postnatal day (P) 2, and subsequently the zinc adequate diet until P56. Neurogenesis was evaluated in the offspring at embryonic day (E)14, E19, P2, and P56 measuring parameters of NPC proliferation and differentiation by Western blot and/or immunofluorescence. At E14 and E19, major signals (i.e., ERK1/2, Sox2, and Pax6) that stimulate NPC proliferation and self-renewal were markedly downregulated in the marginal zinc deficient fetal brain. These alterations were associated to a lower number of Ki67 positive cells in the ventricular (VZs) and subventricular zones (SVZs). Following the progression of NPCs into intermediate progenitor cells (IPCs) and into neurons, Pax6, Tbr2 and Tbr1 were affected in the corresponding areas of the brain at E19 and P2. The above signaling alterations led to a lower density of neurons and a selective decrease of glutamatergic neurons in the young adult brain cortex exposed to maternal marginal zinc deficiency from E14 to P2. Current results supports the concept that marginal zinc deficiency during fetal development can disrupt neurogenesis and alter cortical structure potentially leading to irreversible neurobehavioral impairments later in life.

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Deficient maternal zinc intake—but not folate—is associated with lower fetal heart rate variability

Cited by 11 publications

References 44 publications

Elevated Vascular Sympathetic Neurotransmission and Remodelling Is a Common Feature in a Rat Model of Foetal Programming of Hypertension and SHR

Elevated Vascular Sympathetic Neurotransmission and Remodelling Is a Common Feature in a Rat Model of Foetal Programming of Hypertension and SHR

Fetal heart rate variability mediates prenatal depression effects on neonatal neurobehavioral maturity

Early Developmental Marginal Zinc Deficiency Affects Neurogenesis Decreasing Neuronal Number and Altering Neuronal Specification in the Adult Rat Brain

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