11β-HSD1 is the major regulator of the tissue-specific effects of circulating glucocorticoid excess.

[cushing syndrome]

The adverse metabolic effects of prescribed and endogenous glucocorticoid (GC ) excess , Cushing syndrome , create a significant health burden . We found that tissue regeneration of GCs by 11 β-hydroxysteroid dehydrogenase type 1 (11 β-HSD 1 ), rather than circulating delivery , is critical to developing the phenotype of GC excess ; 11 β-HSD 1 KO mice with circulating GC excess are protected from the glucose intolerance , hyperinsulinemia , hepatic steatosis , adiposity , hypertension , myopathy , and dermal atrophy of Cushing syndrome . Whereas liver -specific 11 β-HSD 1 KO mice developed a full Cushingoid phenotype , adipose-specific 11 β-HSD 1 KO mice were protected from hepatic steatosis and circulating fatty acid excess . These data challenge our current view of GC action , demonstrating 11 β-HSD 1 , particularly in adipose tissue , is key to the development of the adverse metabolic profile associated with circulating GC excess , offering 11 β-HSD 1 inhibition as a previously unidentified approach to treat Cushing syndrome .

Diseases
Validation

Diseases presenting "hypertension" symptom

achondroplasia

acute rheumatic fever

adrenal incidentaloma

aniridia

aromatase deficiency

cadasil

child syndrome

cohen syndrome

congenital adrenal hyperplasia

congenital diaphragmatic hernia

cushing syndrome

cystinuria

erdheim-chester disease

erythropoietic protoporphyria

esophageal adenocarcinoma

fabry disease

familial hypocalciuric hypercalcemia

gm1 gangliosidosis

heparin-induced thrombocytopenia

hereditary cerebral hemorrhage with amyloidosis

holt-oram syndrome

homocystinuria without methylmalonic aciduria

hydrocephalus with stenosis of the aqueduct of sylvius

inclusion body myositis

kallmann syndrome

kindler syndrome

lamellar ichthyosis

lymphangioleiomyomatosis

pendred syndrome

primary effusion lymphoma

scrub typhus

severe combined immunodeficiency

sneddon syndrome

typhoid

von hippel-lindau disease

well-differentiated liposarcoma

werner syndrome

x-linked adrenoleukodystrophy

zellweger syndrome

This symptom has already been validated