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Related Concept Videos

Cushing Syndrome II: Pathophysiology01:19

Cushing Syndrome II: Pathophysiology

Cortisol production is normally governed by the hypothalamic–pituitary–adrenal (HPA) axis, which maintains hormonal balance through tightly regulated feedback mechanisms. Disruption of this regulatory system is central to the development of Cushing syndrome, whether the excess cortisol originates from external medications or internal pathology. Persistent cortisol elevation alters metabolism, immune function, and endocrine signaling, producing the characteristic clinical features of the...
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Drugs for Treatment of Crohn's Disease in IBD Using Glucocorticoids

Glucocorticoids, a class of anti-inflammatory drugs, are pivotal in treating moderate to severe Crohn's disease by inducing remission. They exhibit their anti-inflammatory action by inhibiting the production of inflammatory cytokines such as tumor necrosis factor (TNF)-α, interleukin (IL)-1, and chemokines like IL-8. In addition, they reduce the expression of inflammatory cell adhesion molecules and inhibit gene transcription of nitric oxide synthase, phospholipase A2, cyclooxygenase-2 (COX-2),...
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Hormones of the Adrenal Glands

Adrenal hormones play a pivotal role in maintaining the body's electrolyte balance and orchestrating responses to stress, showcasing the intricate functions of the adrenal cortex and medulla.
The adrenal cortex, a powerhouse of hormone synthesis, generates over two dozen corticosteroid hormones. The zona glomerulosa produces mineralocorticoids, exemplified by aldosterone, influencing the electrolyte composition of body fluids. The synthesis of glucocorticoids such as cortisol and corticosterone...
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Inhaled corticosteroids (ICS) are anti-inflammatory drugs used primarily in treating persistent asthma and providing long-term maintenance. They target the bronchial mucosa, the lining of the airways, to control inflammation, a critical factor in asthma progression and exacerbation.
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Cushing Syndrome I: Introduction

Cushing syndrome refers to the collection of clinical manifestations that arise when tissues are exposed to excessive amounts of cortisol or cortisol-like medications over an extended period. Cortisol, a glucocorticoid produced by the adrenal cortex, regulates metabolism, immune responses, and the body’s adaptation to stress. When its concentration remains chronically elevated, these physiological pathways become dysregulated, resulting in the characteristic features of the syndrome.Exogenous...
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Hormones Regulating Blood Glucose

Insulin is released by beta cells of the pancreas when blood glucose levels are high. It facilitates glucose absorption and utilization in insulin-dependent cells with insulin receptors on their plasma membranes. Insulin promotes glucose uptake by increasing the number of glucose transport proteins in the cell membrane, allowing glucose to enter the cell. As a result, glucose utilization and ATP production are enhanced.
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Biochemical Reconstitution of Steroid Receptor•Hsp90 Protein Complexes and Reactivation of Ligand Binding
11:07

Biochemical Reconstitution of Steroid Receptor•Hsp90 Protein Complexes and Reactivation of Ligand Binding

Published on: September 21, 2011

Programming effects of glucocorticoids.

Rebecca M Reynolds1

  • 1Endocrinology Unit, University/BHF Centre for Cardiovascular Science, Queen's Medical Research Institute, Edinburgh, UK. r.reynolds@ed.ac.uk

Clinical Obstetrics and Gynecology
|June 1, 2013
PubMed
Summary
This summary is machine-generated.

Fetal glucocorticoid overexposure, linked to low birthweight, can cause long-term health issues. Protecting fetuses from excess steroids is crucial for healthy development and preventing future diseases.

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Primary Culture of Rat Adrenocortical Cells and Assays of Steroidogenic Functions
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Biochemical Reconstitution of Steroid Receptor•Hsp90 Protein Complexes and Reactivation of Ligand Binding
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04:33

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Published on: March 12, 2019

Area of Science:

  • Endocrinology
  • Developmental Biology
  • Perinatal Medicine

Background:

  • Fetal glucocorticoid overexposure is a potential mechanism linking low birthweight to adult diseases.
  • The placenta protects the fetus via 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2).
  • Antenatal glucocorticoid use and high maternal levels associate with lower birthweight.

Purpose of the Study:

  • To review the consequences of fetal glucocorticoid overexposure.
  • To highlight the role of placental 11β-HSD2 in fetal protection.
  • To discuss strategies for optimizing antenatal glucocorticoid use and identifying at-risk infants.

Main Methods:

  • Literature review of studies on fetal glucocorticoid exposure, birthweight, and long-term health outcomes.
  • Analysis of the protective role of placental 11β-HSD2.
  • Discussion of clinical implications for preterm labor management and infant health surveillance.

Main Results:

  • Fetal glucocorticoid overexposure is associated with low birthweight and adverse long-term health consequences.
  • Consequences include hypothalamic-pituitary-adrenal axis dysregulation, metabolic and cardiovascular disorders, and neurodevelopmental issues.
  • Placental 11β-HSD2 is a critical regulator of fetal exposure to maternal glucocorticoids.

Conclusions:

  • Limiting antenatal glucocorticoid exposure is essential for preventing adverse offspring outcomes.
  • Identifying pregnancies at risk for preterm labor and infants susceptible to future disease is critical.
  • Further research is needed to refine strategies for glucocorticoid use during pregnancy and postnatal monitoring.