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Updated: Jul 17, 2026
Using a Murine Model of Psychosocial Stress in Pregnancy as a Translationally Relevant Paradigm for Psychiatric Disorders in Mothers and Infants
Published on: June 13, 2021
Maternal stress alters endocrine function of the feto-placental unit in rats
Jérôme Mairesse1, Jean Lesage, Christophe Breton
1Perinatal Stress Unit, Bat SN4-1, Univ. of Lille 1, 59655 Villeneuve d'Ascq, France.
Insights
Prenatal stress in rats reduced fetal growth and altered placental function. This stress impacts fetal development and endocrine systems, potentially programming adult health issues.
Area of Science:
- Endocrinology
- Developmental Biology
- Reproductive Science
Background:
- Prenatal stress (PS) can significantly impact fetal development through altered maternal and fetal glucocorticoid exposure.
- Understanding the effects of gestational stress on the feto-placental unit is crucial for identifying developmental risks.
Purpose of the Study:
- To investigate the effects of chronic restraint stress during late gestation on the feto-placental unit in male rat fetuses at embryonic day 21.
- To assess the impact of prenatal stress on fetal growth, placental function, and endocrine parameters.
Main Methods:
- Rats were subjected to chronic restraint stress during late gestation.
- Fetal and placental tissues were analyzed for gene expression, enzyme activity, and organ weights.
- Plasma hormone and metabolite levels were measured in fetuses.
Main Results:
- Prenatal stress reduced dam body weight gain, food intake, and increased adrenal weight.
- Placental glucose transporter type 1 (GLUT1) expression decreased, while GLUT3 and GLUT4 increased.
- Placental 11beta-hydroxysteroid dehydrogenase type 2 expression and activity were significantly reduced.
- Prenatally stressed fetuses showed decreased body, adrenal, pancreas, and testis weights.
- Reduced pancreatic beta-cell mass, plasma glucose, growth hormone, and ACTH levels were observed in stressed fetuses.
Conclusions:
- Prenatal stress profoundly affects feto-placental physiology and fetal growth.
- Reduced placental glucocorticoid barrier function may contribute to altered fetal development.
- These findings suggest prenatal stress can program long-term developmental and pathophysiological changes.
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 type 1 (GLUT1) was decreased, whereas GLUT3 and GLUT4 were slightly increased. Moreover, placental expression and activity of the glucocorticoid "barrier" enzyme 11beta-hydroxysteroid dehydrogenase type 2 was strongly reduced. At E21, PS fetuses exhibited decreased body, adrenal pancreas, and testis weights. These alterations were associated with reduced pancreatic beta-cell mass, plasma levels of glucose, growth hormone, and ACTH, whereas corticosterone, insulin, IGF-1, and CBG levels were unaffected. These data emphasize the impact of PS on both fetal growth and endocrine function as well as on placental physiology, suggesting that PS could program processes implied in adult biology and pathophysiology.
