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Early Life Nutrition and Cardiovascular Health and Development

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A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: closed (31 May 2021) | Viewed by 18973

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Special Issue Editors

Prof. Dr. David Ferguson

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Guest Editor

Department of Kinesiology, Michigan State University, East Lansing, MI, USA
Interests: early life growth restriction; exercise physiology; kinesiology; cardiovascular physiology; developmental origins of health and disease hypothesis; barker hypothesis; thrifty phenotype

Dr. Janna Morrison

E-Mail Website
Co-Guest Editor

Early Origins of Adult Health Research GroupSchool of Pharmacy and Medical Sciences, Sansom Institute for Health Research, University of South Australia, Adelaide, South Australia, Australia
Interests: fetus; early life nutrition; HypoxiA; intrauterine growth restriction; cardiovascular development; cardiovascular disease; maternal obesity; neonatal; programming; DOHaD
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Special Issue Information

Dear Colleagues,

Suboptimal nutrition (under and over nutrition) in early life can have lifelong consequences on cardiovascular development and health. The aim of this Special Issue aims to characterize mechanisms by which early life nutrition influences cardiovascular health and development. A secondary aim is to highlight interventions that may restore cardiac health following a period of suboptimal nutrition in early life. Lastly, investigations that address tissues (lungs, blood vessels, kidneys, skeletal muscle, nervous system) that support the cardiovascular system will be considered in order to provide an integrative physiology perspective.

Prof. David Ferguson
Guest Editor
Dr. Janna Morrison
Co-Guest Editor

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Keywords

early life nutrition
growth restriction
over nutrition
cardiovascular physiology
developmental biology

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Published Papers (6 papers)

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Research

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28 pages, 6432 KiB

Open AccessArticle

Maternal Undernutrition Modulates Neonatal Rat Cerebrovascular Structure, Function, and Vulnerability to Mild Hypoxic-Ischemic Injury via Corticosteroid-Dependent and -Independent Mechanisms

by Patsy Naomi Franco, Lara M. Durrant, Coleen Doan, Desirelys Carreon, Alejandra Beltran, Amandine Jullienne, Andre Obenaus and William J. Pearce

Int. J. Mol. Sci. 2021, 22(2), 680; https://doi.org/10.3390/ijms22020680 - 12 Jan 2021

Cited by 3 | Viewed by 2230

Abstract

The present study explored the hypothesis that an adverse intrauterine environment caused by maternal undernutrition (MUN) acted through corticosteroid-dependent and -independent mechanisms to program lasting functional changes in the neonatal cerebrovasculature and vulnerability to mild hypoxic-ischemic (HI) injury. From day 10 of gestation until term, MUN and MUN-metyrapone (MUN-MET) group rats consumed a diet restricted to 50% of calories consumed by a pair-fed control; and on gestational day 11 through term, MUN-MET groups received drinking water containing MET (0.5 mg/mL), a corticosteroid synthesis inhibitor. P9/P10 pups underwent unilateral carotid ligation followed 24 h later by 1.5 h exposure to 8% oxygen (HI treatment). An ELISA quantified MUN-, MET-, and HI-induced changes in circulating levels of corticosterone. In P11/P12 pups, MUN programming promoted contractile differentiation in cerebrovascular smooth muscle as determined by confocal microscopy, modulated calcium-dependent contractility as revealed by cerebral artery myography, enhanced vasogenic edema formation as indicated by T2 MRI, and worsened neurobehavior MUN unmasked HI-induced improvements in open-field locomotion and in edema resolution, alterations in calcium-dependent contractility and promotion of contractile differentiation. Overall, MUN imposed multiple interdependent effects on cerebrovascular smooth muscle differentiation, contractility, edema formation, flow-metabolism coupling and neurobehavior through pathways that both required, and were independent of, gestational corticosteroids. In light of growing global patterns of food insecurity, the present study emphasizes that infants born from undernourished mothers may experience greater risk for developing neonatal cerebral edema and sensorimotor impairments possibly through programmed changes in neonatal cerebrovascular function. Full article

(This article belongs to the Special Issue Early Life Nutrition and Cardiovascular Health and Development)

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17 pages, 3918 KiB

Open AccessArticle

Sex Differences in Placental Protein Expression and Efficiency in a Rat Model of Fetal Programming Induced by Maternal Undernutrition

by Sophida Phuthong, Cynthia Guadalupe Reyes-Hernández, Pilar Rodríguez-Rodríguez, David Ramiro-Cortijo, Marta Gil-Ortega, Raquel González-Blázquez, M. Carmen González, Angel Luis López de Pablo and Silvia M. Arribas

Int. J. Mol. Sci. 2021, 22(1), 237; https://doi.org/10.3390/ijms22010237 - 28 Dec 2020

Cited by 20 | Viewed by 3099

Abstract

Fetal undernutrition programs cardiometabolic diseases, with higher susceptibility in males. The mechanisms implicated are not fully understood and may be related to sex differences in placental adaptation. To evaluate this hypothesis, we investigated placental oxidative balance, vascularization, glucocorticoid barrier, and fetal growth in rats exposed to 50% global nutrient restriction from gestation day 11 (MUN, n = 8) and controls (n = 8). At gestation day 20 (G20), we analyzed maternal, placental, and fetal weights; oxidative damage, antioxidants, corticosterone, and PlGF (placental growth factor, spectrophotometry); and VEGF (vascular endothelial growth factor), 11β-HSD2, p22^phox, XO, SOD1, SOD2, SOD3, catalase, and UCP2 expression (Western blot). Compared with controls, MUN dams exhibited lower weight and plasma proteins and higher corticosterone and catalase without oxidative damage. Control male fetuses were larger than female fetuses. MUN males had higher plasma corticosterone and were smaller than control males, but had similar weight than MUN females. MUN male placenta showed higher XO and lower 11β-HSD2, VEGF, SOD2, catalase, UCP2, and feto-placental ratio than controls. MUN females had similar feto-placental ratio and plasma corticosterone than controls. Female placenta expressed lower XO, 11β-HSD2, and SOD3; similar VEGF, SOD1, SOD2, and UCP2; and higher catalase than controls, being 11β-HSD2 and VEGF higher compared to MUN males. Male placenta has worse adaptation to undernutrition with lower efficiency, associated with oxidative disbalance and reduced vascularization and glucocorticoid barrier. Glucocorticoids and low nutrients may both contribute to programming in MUN males. Full article

(This article belongs to the Special Issue Early Life Nutrition and Cardiovascular Health and Development)

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22 pages, 6959 KiB

Open AccessArticle

Postnatal Growth Restriction in Mice Alters Cardiac Protein Composition and Leads to Functional Impairment in Adulthood

by Joseph R. Visker, Lawrence J. Dangott, Eric C. Leszczynski and David P. Ferguson

Int. J. Mol. Sci. 2020, 21(24), 9459; https://doi.org/10.3390/ijms21249459 - 12 Dec 2020

Cited by 5 | Viewed by 2571

Abstract

Postnatal growth restriction (PGR) increases the risk for cardiovascular disease (CVD) in adulthood, yet there is minimal mechanistic rationale for the observed pathology. The purpose of this study was to identify proteomic differences in hearts of growth-restricted and unrestricted mice, and propose mechanisms related to impairment in adulthood. Friend leukemia virus B (FVB) mouse dams were fed a control (CON: 20% protein), or low-protein (LP: 8% protein) isocaloric diet 2 weeks before mating. LP dams produce 20% less milk, inducing growth restriction. At birth (postnatal; PN1), pups born to dams fed the CON diet were switched to LP dams (PGR group) or a different CON dam. At PN21, a sub-cohort of CON (n = 3 males; n = 3 females) and PGR (n = 3 males; n = 3 females) were euthanized and their proteome analyzed by two-dimensional differential in-gel electrophoresis (2D DIGE) and mass spectroscopy. Western blotting and silver nitrate staining confirmed 2D DIGE results. Littermates (CON: n = 4 males and n = 4 females; PGR: n = 4 males and n = 4 females) were weaned to the CON diet. At PN77, echocardiography measured cardiac function. At PN80, hearts were removed for western blotting to determine if differences persisted into adulthood. 2D DIGE and western blot confirmation indicated PGR had reductions in p57^kip2, Titin (Ttn), and Collagen (Col). At PN77, PGR had impaired cardiac function as measured by echocardiography. At PN80, western blots of p57^kip2 showed protein abundance recovered from PN21. PN80 silver staining of large molecular weight proteins (Ttn and Col) was reduced in PGR. PGR reduces cell cycle activity at PN21, which is recovered in adulthood. However, collagen fiber networks are altered into adulthood. Full article

(This article belongs to the Special Issue Early Life Nutrition and Cardiovascular Health and Development)

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17 pages, 3146 KiB

Open AccessArticle

Transient Changes of Metabolism at the Pronuclear Stage in Mice Influences Skeletal Muscle Phenotype in Adulthood

by Christelle Bertrand-Gaday, Martine Letheule, Emilie Blanchet, Barbara Vernus, Laurence Pessemesse, Amélie Bonnet-Garnier, Anne Bonnieu and François Casas

Int. J. Mol. Sci. 2020, 21(19), 7203; https://doi.org/10.3390/ijms21197203 - 29 Sep 2020

Viewed by 2731

Abstract

Skeletal muscle has a remarkable plasticity, and its phenotype is strongly influenced by hormones, transcription factors, and physical activity. However, whether skeletal phenotype can be oriented or not during early embryonic stages has never been investigated. Here, we report that pyruvate as the only source of carbohydrate in the culture medium of mouse one cell stage embryo influenced the establishment of the muscular phenotype in adulthood. We found that pyruvate alone induced changes in the contractile phenotype of the skeletal muscle in a sexually dependent manner. For male mice, a switch to a more glycolytic phenotype was recorded, whereas, in females, the pyruvate induced a switch to a more oxidative phenotype. In addition, the influence of pyruvate on the contractile phenotypes was confirmed in two mouse models of muscle hypertrophy: the well-known myostatin deficient mouse (Mstn−/−) and a mouse carrying a specific deletion of p43, a mitochondrial triiodothyronine receptor. Finally, to understand the link between these adult phenotypes and the early embryonic period, we assessed the levels of two histone H3 post-translational modifications in presence of pyruvate alone just after the wave of chromatin reprogramming specific of the first cell cycle. We showed that H3K4 acetylation level was decreased in Mstn−/− 2-cell embryos, whereas no difference was found for H3K27 trimethylation level, whatever the genotype. These findings demonstrate for the first time that changes in the access of energy substrate during the very first embryonic stage can induce a precocious orientation of skeletal muscle phenotype in adulthood. Full article

(This article belongs to the Special Issue Early Life Nutrition and Cardiovascular Health and Development)

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Review

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14 pages, 753 KiB

Open AccessReview

Cardiovascular and Cerebrovascular Implications of Growth Restriction: Mechanisms and Potential Treatments

by Charmaine R. Rock, Tegan A. White, Beth R. Piscopo, Amy E. Sutherland, Suzanne L. Miller, Emily J. Camm and Beth J. Allison

Int. J. Mol. Sci. 2021, 22(14), 7555; https://doi.org/10.3390/ijms22147555 - 14 Jul 2021

Cited by 18 | Viewed by 5093

Abstract

Fetal growth restriction (FGR) is a common complication of pregnancy, resulting in a fetus that fails to reach its genetically determined growth potential. Whilst the fetal cardiovascular response to acute hypoxia is well established, the fetal defence to chronic hypoxia is not well understood due to experiment constraints. Growth restriction results primarily from reduced oxygen and nutrient supply to the developing fetus, resulting in chronic hypoxia. The fetus adapts to chronic hypoxia by redistributing cardiac output via brain sparing in an attempt to preserve function in the developing brain. This review highlights the impact of brain sparing on the developing fetal cardiovascular and cerebrovascular systems, as well as emerging long-term effects in offspring that were growth restricted at birth. Here, we explore the pathogenesis associated with brain sparing within the cerebrovascular system. An increased understanding of the mechanistic pathways will be critical to preventing neuropathological outcomes, including motor dysfunction such as cerebral palsy, or behaviour dysfunctions including autism and attention-deficit/hyperactivity disorder (ADHD). Full article

(This article belongs to the Special Issue Early Life Nutrition and Cardiovascular Health and Development)

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16 pages, 610 KiB

Open AccessReview

Programming of Cardiovascular Dysfunction by Postnatal Overfeeding in Rodents

by Marie Josse, Eve Rigal, Nathalie Rosenblatt-Velin, Luc Rochette, Marianne Zeller, Charles Guenancia and Catherine Vergely

Int. J. Mol. Sci. 2020, 21(24), 9427; https://doi.org/10.3390/ijms21249427 - 11 Dec 2020

Cited by 9 | Viewed by 2668

Abstract

Nutritional environment in the perinatal period has a great influence on health and diseases in adulthood. In rodents, litter size reduction reproduces the effects of postnatal overnutrition in infants and reveals that postnatal overfeeding (PNOF) not only permanently increases body weight but also affects the cardiovascular function in the short- and long-term. In addition to increased adiposity, the metabolic status of PNOF rodents is altered, with increased plasma insulin and leptin levels, associated with resistance to these hormones, changed profiles and levels of circulating lipids. PNOF animals present elevated arterial blood pressure with altered vascular responsiveness to vasoactive substances. The hearts of overfed rodents exhibit hypertrophy and elevated collagen content. PNOF also induces a disturbance of cardiac mitochondrial respiration and produces an imbalance between oxidants and antioxidants. A modification of the expression of crucial genes and epigenetic alterations is reported in hearts of PNOF animals. In vivo, a decreased ventricular contractile function is observed during adulthood in PNOF hearts. All these alterations ultimately lead to an increased sensitivity to cardiac pathologic challenges such as ischemia-reperfusion injury. Nevertheless, caloric restriction and physical exercise were shown to improve PNOF-induced cardiac dysfunction and metabolic abnormalities, drawing a path to the potential therapeutic correction of early nutritional programming. Full article

(This article belongs to the Special Issue Early Life Nutrition and Cardiovascular Health and Development)

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