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Related Concept Videos

Feedback Loops01:01

Feedback Loops

In most cases, excessive hormone production is prevented by negative feedback—a loop that starts with a stimulus inducing the release of a particular substance, like a hormone, to maintain a certain level before triggering a signal that results in a decrease in further release of the hormone.
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...
Desensitization and Tachyphylaxis01:20

Desensitization and Tachyphylaxis

Tachyphylaxis is described as a rapid decrease in response to a drug after repeated or continuous administration of the same drug dose. It is a phenomenon where the body becomes less responsive to a particular substance or intervention over time, requiring higher doses or stronger interventions to achieve the same effect. It results from adaptive changes in the body's receptors, signaling pathways, or physiological processes that occur in response to prolonged exposure to a stimulus.
Several...
Glucagon-like Receptor Agonists01:24

Glucagon-like Receptor Agonists

Incretins include glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), which stimulate insulin secretion post-meals. In type 2 diabetes, GIP's efficacy is reduced, making GLP-1 a viable drug target. GIP originates from preproGIP.
GLP-1, when administered in high doses intravenously, triggers insulin secretion, inhibits glucagon release, slows gastric emptying, reduces food intake, and restores normal insulin secretion. However, its rapid inactivation by the...
Hypoglycemia and Glucagon01:15

Hypoglycemia and Glucagon

Without prolonged fasting, healthy individuals maintain blood glucose levels above 3.5 mM due to a well-adapted neuroendocrine counterregulatory system that effectively prevents acute hypoglycemia, a potentially life-threatening condition. The primary clinical scenarios for hypoglycemia encompass diabetes treatment, inappropriate production of endogenous insulin or insulin-like substances by tumors, and the use of glucose-lowering agents in non-diabetic individuals. Notably, hypoglycemia in the...
GPCR Desensitization01:12

GPCR Desensitization

G protein-coupled receptor (GPCR) signaling plays a crucial role in cell functioning. GPCR desensitization is an equally essential process. It allows cells to respond to changing environments and regain sensitivity to new stimuli while preventing unnecessary stimulation when no longer needed. Prolonged exposure to stimuli leads to GPCR desensitization. It involves blocking the receptors from binding and activating additional G proteins. This inhibits activation of downstream effectors, thereby...

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Related Experiment Video

Updated: Jul 6, 2026

Fecal Glucocorticoid Analysis: Non-invasive Adrenal Monitoring in Equids
08:02

Fecal Glucocorticoid Analysis: Non-invasive Adrenal Monitoring in Equids

Published on: April 25, 2016

Glucocorticoid feedback resistance.

E R De Kloet1, E Vreugdenhil, M S Oitzl

  • 1Division of Medical Pharmacology, Leiden/Amsterdam Center for Drug Research, Leiden University, , 2300 RA Leiden, Netherlands.

Trends in Endocrinology and Metabolism: TEM
|January 1, 1997
PubMed
Summary

Inherited glucocorticoid resistance enhances adrenal function without Cushing's syndrome symptoms. Acquired resistance, however, overexposes the body to glucocorticoids, increasing disease vulnerability.

Related Experiment Videos

Last Updated: Jul 6, 2026

Fecal Glucocorticoid Analysis: Non-invasive Adrenal Monitoring in Equids
08:02

Fecal Glucocorticoid Analysis: Non-invasive Adrenal Monitoring in Equids

Published on: April 25, 2016

Area of Science:

  • Endocrinology
  • Neuroendocrinology
  • Molecular Endocrinology

Background:

  • Glucocorticoid feedback resistance presents as either inherited or acquired.
  • These distinct forms have different implications for disease pathogenesis.
  • Understanding these differences is crucial for diagnosing and managing glucocorticoid-related disorders.

Purpose of the Study:

  • To differentiate the implications of inherited versus acquired glucocorticoid feedback resistance.
  • To elucidate the distinct mechanisms and clinical outcomes associated with each form of resistance.
  • To highlight the role of cell-specific resistance in disease vulnerability.

Main Methods:

  • Comparative analysis of inherited and acquired glucocorticoid resistance mechanisms.
  • Examination of adrenocortical function and hypercorticism in different resistance models.
  • Investigation of hypothalamic corticotropin-releasing hormone (CRH) neuron involvement in acquired resistance.

Main Results:

  • Inherited resistance, due to glucocorticoid receptor gene deficits, leads to compensated hypercorticism without Cushing's syndrome.
  • Acquired resistance at the CRH neuron level results in non-compensatory hypercorticism, overexposing tissues to glucocorticoids.
  • Cell-specific acquired resistance, influenced by early life events in predisposed individuals, increases disease vulnerability.

Conclusions:

  • Inherited and acquired glucocorticoid resistance have divergent pathophysiological consequences.
  • Acquired, cell-specific glucocorticoid resistance poses a significant risk for glucocorticoid-induced pathologies.
  • Further research into acquired resistance mechanisms is warranted for therapeutic development.