2015
DOI: 10.1016/j.ajog.2015.07.020
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Role of catecholamines in maternal-fetal stress transfer in sheep

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Cited by 39 publications
(30 citation statements)
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“…Although a high concentration of circulating glucocorticoids in the fetus is expected if chronic maternal stress is present, negative feedback mechanisms can prevent sustained high fetal concentrations of glucocorticoids. In this context, some authors have suggested that high levels of fetal catecholamines are the main effectors of the relationship between maternal stress and restricted fetal growth . Catecholamines are proposed as primary mediators that maintain glucose levels in the fetus, resulting in decreased insulin, increased glucagon, and altered fetal phenotype.…”
Section: Discussionmentioning
confidence: 99%
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“…Although a high concentration of circulating glucocorticoids in the fetus is expected if chronic maternal stress is present, negative feedback mechanisms can prevent sustained high fetal concentrations of glucocorticoids. In this context, some authors have suggested that high levels of fetal catecholamines are the main effectors of the relationship between maternal stress and restricted fetal growth . Catecholamines are proposed as primary mediators that maintain glucose levels in the fetus, resulting in decreased insulin, increased glucagon, and altered fetal phenotype.…”
Section: Discussionmentioning
confidence: 99%
“…Catecholamines are proposed as primary mediators that maintain glucose levels in the fetus, resulting in decreased insulin, increased glucagon, and altered fetal phenotype. These changes lead to a favoring of neural cells and tissues, with greater anaerobic metabolism in peripheral and skeletal tissues, and consequently restricted growth and increased lactate …”
Section: Discussionmentioning
confidence: 99%
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“…Experimental animal studies and natural experiments in humans suggest that prenatal exposure to maternal anxiety can elicit modulation of “ developmental programming ” in the offspring (Bock, Wainstock, Braun, & Segal, ; Daskalakis, Bagot, Parker, Vinkers, & de Kloet, ; de Kloet, Joels, & Holsboer, ; Laplante, Brunet, Schmitz, Ciampi, & King, ). Although potentially underlying mechanisms are not fully understood, it has frequently been proposed that maternal anxiety leads to increased production of maternal stress hormones (e.g., cortisol, noradrenaline) and down‐regulation of the placental 11β‐HSD2 enzyme that metabolizes maternal cortisol into inactive cortisone (O'Donnell et al., ; Rakers et al., ). This may result in increased levels of cortisol in the fetal circulation, which together with other processes such as inflammation (Christian, ) and neuro‐inflammation (Hanamsagar & Bilbo, ; Labouesse, Langhans, & Meyer, ) may elicit long‐term changes in structure and function of the developing brain via epigenetic pathways (Bock et al., ; Monk, Spicer, & Champagne, ; Van den Bergh, ).…”
Section: Introductionmentioning
confidence: 99%