Endocrine Abstracts

Background: Chronically elevated brain glucocorticoid (GC) levels impair cognition. In rodents, raised GC levels prior to lipopolyaccharide (LPS) administration potentiate neuroinflammation although GC suppresses neuroinflammation if administered after LPS. 11β-hydroxysteroid dehydrogenase-1 (11β-HSD1) activity can increase intracellular GC levels, including in the brain, without alteration in circulating levels. 11β-HSD1 deficiency/inhibition protects against a...

11β-Hydroxysteroid dehydrogenase type 1 (11β-HSD1) regenerates glucocorticoids in intact cells, converting inert cortisone into active cortisol. We have previously shown attenuated atherosclerosis development, reduced plasma monocyte chemoattractant protein-1 (MCP-1) and reduced macrophage/T cell infiltration within atherosclerotic lesions in 11β-HSD1−/−×ApoE−/− double knock-out (DKO) mice fed western diet (WD)....

High plasma levels of glucocorticoids cause metabolic disease (central obesity, hypertension, diabetes) and increase risk of cardiovascular disease. 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) regenerates glucocorticoids in intact cells, converting inert cortisone (11-dehydrocorticosterone in rodents) into active cortisol (corticosterone in rodents). Recent work has shown the pathological importance of elevated adipose tissue 11β-HSD1 expression in develo...

Chronically elevated glucocorticoid (GC) level impairs cognition. In rodents, elevated plasma GC levels, prior to an inflammatory challenge, potentiates neuroinflammation that is abolished by GR but not MR antagonism. 11β-hydroxysteroid dehydrogenase type-1 (11β-HSD1) increases intracellular GC levels by regenerating active GCs from inert forms. Inhibition/deficiency of 11β-HSD1 is protective against age-related cognitive decline presumably by lifelong reduced b...