2007
DOI: 10.1152/ajpendo.00574.2006
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Maternal stress alters endocrine function of the feto-placental unit in rats

Abstract: Prenatal stress (PS) can cause early and long-term developmental effects resulting in part from altered maternal and/or fetal glucocorticoid exposure. The aim of the present study was to assess the impact of chronic restraint stress during late gestation on feto-placental unit physiology and function in embryonic (E) day 21 male rat fetuses. Chronic stress decreased body weight gain and food intake of the dams and increased their adrenal weight. In the placenta of PS rats, the expression of glucose transporter… Show more

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Cited by 340 publications
(265 citation statements)
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“…Research into the interplay between the HPA axis and metabolism suggests that the relationship between these systems is established during the prenatal and early postnatal period (3,10,39,53), and maternal stress experienced by the fetus during gestation has proven developmental and metabolic effects (26,34,37,38). Persistent stress also influences bone function, with chronic elevations of cortisol leading to low bone mineral in humans (12).…”
Section: Discussionmentioning
confidence: 99%
“…Research into the interplay between the HPA axis and metabolism suggests that the relationship between these systems is established during the prenatal and early postnatal period (3,10,39,53), and maternal stress experienced by the fetus during gestation has proven developmental and metabolic effects (26,34,37,38). Persistent stress also influences bone function, with chronic elevations of cortisol leading to low bone mineral in humans (12).…”
Section: Discussionmentioning
confidence: 99%
“…In addition to the structural separation within the labyrinth zone that prevents direct contact between maternal and fetal blood supplies (depicted in Figure 1, inset), metabolizing enzymes localized within trophoblasts facilitate fetal protection from excess glucocorticoids and amines (Brown et al, 1996;Nguyen et al, 1999). These barrier enzymes can be sensitive to maternal stress, where, eg, reduced placental expression of the glucocorticoid-inactivating enzyme, 11β-hydroxysteroid dehydrogenase type-2 (11βHSD2), has been associated with maternal anxiety and depressed mood in humans, as well as with chronic maternal stress in rodents (Blakeley et al, 2013;Jensen Peña et al, 2012;Mairesse et al, 2007;O'Donnell et al, 2012;Pankevich et al, 2009;Ponder et al, 2011). The result is for a potential fetal glucocorticoid overexposure to impact ongoing developmental events including a restriction of fetal growth, premature maturation of proliferative neural precursors, and altered HPA axis development (Seckl and Holmes, 2007).…”
Section: Transplacental Barrier Permeabilitymentioning
confidence: 99%
“…In humans and in animal models, placental 11β-HSD2 expression is reduced in adverse situations, including poor maternal nutrition or maternal stress (13)(14)(15). Bypass of this protective enzyme, be it through synthetic glucocorticoids that are poor substrates (9,16), inhibition (by liquorice), or genetic ablation of Hsd11b2 that encodes 11β-HSD2 (10), reduces placental weight.…”
mentioning
confidence: 99%