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The ability of a drug to produce structural deformations and functional abnormalities in the developing embryo or the fetus is called teratogenicity, and the drug producing this effect is known as a teratogen. Teratogenic effects include stillbirth, miscarriage, intrauterine growth restriction, and neurocognitive delay. A teratogen may affect the embryo at different stages of development, which is important in determining the type and extent of the damage. During blastocyst formation, the early...
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The gonads, namely the testes in males and the ovaries in females, are pivotal in producing gonadal hormones that orchestrate the intricate processes of sexual development and reproduction.
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The intricate hormonal interplay essential for male reproductive health begins with the release of gonadotropin-releasing hormone (GnRH) by the hypothalamus. This hormone prompts the pituitary gland to secrete follicle-stimulating hormone (FSH) and luteinizing hormone (LH). LH targets the Leydig cells in the testes, stimulating them to produce and release testosterone. In concert with testosterone, FSH acts on the Sertoli cells within the seminiferous tubules to facilitate the release of...
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Pathophysiology of Diabetes01:20

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Diabetes mellitus is a chronic metabolic disorder characterized by hyperglycemia. The four categories of diabetes are type 1 diabetes, type 2 diabetes, other specific types of diabetes, and gestational diabetes.
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Type 2 diabetes, characterized by insulin resistance, arises when the insulin receptors on cells lose responsiveness to insulin, diminishing the cell's capacity to take up glucose, resulting in elevated blood glucose levels. To receive a diagnosis of Type 2 diabetes, a series of blood glucose tests are necessary to assess whether the blood glucose falls within normal parameters. If the result is out of the normal range, a patient may be diagnosed as prediabetic or diabetic, depending on the...
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Hormonal Regulation01:33

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Related Experiment Video

Updated: Jul 10, 2025

Author Spotlight: Modeling an Aspect of Preeclampsia in Female Mice Using Hypoxic Human Placenta-Derived Small Extracellular Vesicles
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Elevated gestational testosterone impacts vascular and uteroplacental function.

Sathish Kumar1, Ruolin Song2, Jay S Mishra2

  • 1Department of Comparative Biosciences, School of Veterinary Medicine, University of Wisconsin, Madison, WI, 53706, USA; Department of Obstetrics and Gynecology, School of Medicine and Public Health, University of Wisconsin, Madison, WI, 53792, USA.

Placenta
|November 17, 2023
PubMed
Summary
This summary is machine-generated.

Elevated testosterone (T) in pregnancy may contribute to preeclampsia by affecting maternal cardiovascular and placental function via androgen receptors (AR). This review examines clinical and animal evidence supporting this role in hypertensive disorders of pregnancy.

Keywords:
AndrogensEndotheliumNutrient transportPlacentaPreeclampsiaTrophoblast

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Area of Science:

  • Reproductive biology
  • Maternal-fetal medicine
  • Endocrinology

Background:

  • Adequate maternal vascular adaptations are crucial for fetal development.
  • Failure in these adaptations increases the risk of antenatal complications like preeclampsia.
  • Androgens, particularly testosterone, are implicated in preeclampsia pathogenesis due to elevated levels and correlation with vascular dysfunction.

Purpose of the Study:

  • To critically evaluate the hypothesis that androgen receptor (AR)-mediated activity plays a significant role in preeclampsia.
  • To review clinical and preclinical evidence linking androgens to maternal cardiovascular and placental function in pregnancy.

Main Methods:

  • Review of clinical data from preeclamptic pregnancies, noting testosterone levels and AR expression.
  • Analysis of findings from animal studies that mimic elevated testosterone in pregnancy.
  • Synthesis of evidence connecting androgen activity to key features of preeclampsia.

Main Results:

  • Preeclamptic women exhibit elevated plasma testosterone (T) levels (2- to 3-fold) that correlate with vascular dysfunction.
  • Increased androgen receptor (AR) levels are observed in placental tissues of preeclamptic pregnancies.
  • Animal models with elevated T reproduce preeclampsia features: hypertension, endothelial dysfunction, impaired spiral artery remodeling, placental hypoxia, and fetal growth restriction.

Conclusions:

  • Androgen receptor-mediated activity is strongly suggested to play a significant role in the clinical presentation of preeclampsia.
  • Elevated testosterone and its effects on maternal vasculature and placental development are key factors to consider in preeclampsia research.
  • Further investigation into the AR pathway is warranted for understanding and potentially treating preeclampsia.