Novel causes of generalized glucocorticoid resistance

E. Charmandari, Tomoshige Kino

Research output: Contribution to journalArticle

10 Citations (Scopus)

Abstract

Glucocorticoid resistance is a rare condition characterized by generalized, partial, target-tissue insensitivity to glucocorticoids. Compensatory elevations in circulating adrenocorticotropic hormone (ACTH) concentrations lead to increased secretion of cortisol and adrenal steroids with mineralocorticoid and/or androgenic activity, but no clinical evidence of hypercortisolism. The clinical spectrum of the condition is broad, ranging from asymptomatic to severe cases of hyperandrogenism, fatigue and/or mineralocorticoid excess. The molecular basis of glucocorticoid resistance has been ascribed to mutations in the human glucocorticoid receptor (hGR) gene, which impair glucocorticoid signal transduction, thereby altering tissue sensitivity to glucocorticoids. The study of functional defects of natural hGR mutants enhances our understanding of the molecular mechanisms of hGR action and highlights the importance of integrated cellular and molecular signaling mechanisms for maintaining homeostasis and preserving normal physiology.

Original languageEnglish
Pages (from-to)445-450
Number of pages6
JournalHormone and Metabolic Research
Volume39
Issue number6
DOIs
Publication statusPublished - Jun 2007
Externally publishedYes

Fingerprint

Glucocorticoid Receptors
Glucocorticoids
Mineralocorticoids
Hyperandrogenism
Cushing Syndrome
Adrenocorticotropic Hormone
Fatigue
Hydrocortisone
Signal Transduction
Tissue
Homeostasis
Signal transduction
Steroids
Physiology
Mutation
Genes
Glucocorticoid Receptor Deficiency
Fatigue of materials
Defects

Keywords

  • Glucocorticoid receptor (GR)
  • Glucocorticoid resistance
  • Human glucocorticoid receptor (hGR) gene
  • Mutations

ASJC Scopus subject areas

  • Biochemistry
  • Endocrinology

Cite this

Novel causes of generalized glucocorticoid resistance. / Charmandari, E.; Kino, Tomoshige.

In: Hormone and Metabolic Research, Vol. 39, No. 6, 06.2007, p. 445-450.

Research output: Contribution to journalArticle

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