Mechanisms of glucocorticoid-induced insulin resistance: focus on adipose tissue function and lipid metabolism.

[cushing syndrome]

Glucocorticoids (GCs ) are critical in the regulation of the stress response , inflammation and energy homeostasis . Excessive GC exposure results in whole-body insulin resistance , obesity , cardiovascular disease , and ultimately decreased survival , despite their potent anti-inflammatory effects . This apparent paradox may be explained by the complex actions of GCs on adipose tissue functionality . The wide prevalence of oral GC therapy makes their adverse systemic effects an important yet incompletely understood clinical problem . This article reviews the mechanisms by which supraphysiologic GC exposure promotes insulin resistance , focusing in particular on the effects on adipose tissue function and lipid metabolism .

Diseases
Validation

Diseases presenting "obesity" symptom

acute rheumatic fever

adrenal incidentaloma

aniridia

aromatase deficiency

carcinoma of the gallbladder

cohen syndrome

congenital adrenal hyperplasia

cushing syndrome

cystinuria

esophageal adenocarcinoma

esophageal carcinoma

esophageal squamous cell carcinoma

familial hypocalciuric hypercalcemia

familial mediterranean fever

heparin-induced thrombocytopenia

kabuki syndrome

monosomy 21

phenylketonuria

primary hyperoxaluria type 1

sneddon syndrome

werner syndrome

wolf-hirschhorn syndrome

x-linked adrenoleukodystrophy

This symptom has already been validated