Endocrine Abstracts

Introduction: Glucocorticoid excess (GE) causes severe metabolic dysfunction within skeletal muscle (SM) which includes reduced muscle accrual and increased proteolysis. The NAD+ metabolome is crucial for SM health and metabolic function, however, whether this is disrupted by GE remains unknown.Methods: Male and female C57BL/6J mice (n=12) were treated with a vehicle control or corticosterone (100 mg/l) ad libitum via drinking water for 3 weeks ...

Introduction: Glucocorticoids are vital metabolic regulators. However, glucocorticoid excess (GE) causes severe metabolic dysfunction, ultimately leading to Cushing’s Syndrome. This dysfunction is often dependent on the presence of the enzyme 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1). Whether GE also alters metabolic rate, and whether this is also dependent on 11β-HSD1, remains unclear.Methods: Male and female wild-type (WT) ...

Introduction: The endoplasmic reticulum (ER) lumen enzyme 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) obtains NADPH from hexose-6-phosphate dehydrogenase to reduce cortisone to the active glucocorticoid cortisol. Cells depleted in NAD+ (parent molecule of NADPH) have impaired 11β -HSD1 activity, which can be rapidly rescued with supplementation of the NAD+ precursor nicotinamide riboside. This suggests the existence of an ER-specific pathway to NAD(P)(H)....