What is the Origin of Glucocorticoid Receptor Sensitivity?

The term is derived from molecular endocrinology, combining "glucocorticoid receptor," the specific protein that binds cortisol, with "sensitivity," denoting the degree of reaction to a stimulus. The concept became essential for understanding non-Addisonian and non-Cushingoid states of stress-related pathology where the issue lies not in hormone production but in cellular reception. It is a key metric in assessing the functional integrity of the stress response system.

What is the Mechanism of Glucocorticoid Receptor Sensitivity?

Sensitivity is governed by several factors, including the number of GRs expressed on the cell surface, the affinity of the receptor for cortisol, and the efficiency of the receptor's translocation into the nucleus to regulate gene transcription. Chronic, elevated stress exposure can lead to GR downregulation or post-receptor modifications, causing peripheral tissues to become resistant to cortisol's anti-inflammatory and metabolic effects. This resistance perpetuates HPA axis activation and systemic inflammation, a central feature of allostatic load.

Glucocorticoid Receptor Sensitivity

Meaning

Glucocorticoid receptor sensitivity refers to the degree of cellular responsiveness to the circulating glucocorticoid hormones, primarily cortisol, mediated by the nuclear glucocorticoid receptor (GR). This sensitivity is a critical determinant of how effectively cortisol can execute its functions, such as modulating inflammation, regulating glucose metabolism, and controlling the HPA axis negative feedback loop. Clinical states of chronic stress or inflammation can alter this sensitivity, leading to either tissue resistance or excessive response, independent of the total cortisol level.

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