OBJECTIVE: Glucocorticoids were found to inhibit adiponectin gene expression and secretion both in vitro and in animal models. We evaluated first the acute effect of i.v. glucocorticoids on adiponectin in normal subjects and secondly plasma adiponectin levels in a series of patients with Cushing's syndrome compared with controls. DESIGN AND METHODS: Hydrocortisone (25 mg) was administered i.v. to five healthy volunteers, with blood samples taken at -15, 0, 30, 60, 120 and 180 min. Twenty-one patients with Cushing's syndrome were divided in two groups: one with 11 obese and the other with 10 non-obese Cushing's patients. Each group was compared with controls that were matched for sex, age, body mass index, waist circumference, glucose, insulin, lipid levels and blood pressure. RESULTS: In normal subjects, hydrocortisone produced a decrease in adiponectin at 30 and 60 min, compared with placebo (P<0.05). Adiponectin was lower in non-obese Cushing's patients than in non-obese controls (P<0.004). In contrast, there was no difference in adiponectin levels in obese Cushing's patients and in obese controls. Adiponectin was inversely correlated (P<0.05) with homeostasis model assessment index in both obese and non-obese Cushing's patients; in non-obese Cushing's patients only, adiponectin was inversely correlated with urinary cortisol (P<0.05). CONCLUSIONS: Glucocorticoids inhibit adiponectin in man, as shown by both exogenous administration to healthy subjects and endogenous cortisol hyperproduction. Similar levels of adiponectin in obese Cushing's patients and their obese controls indicate that obesity per se may act as a predominant factor in masking the relationship between adiponectin and cortisol.
OBJECTIVE: Glucocorticoids were found to inhibit adiponectin gene expression and secretion both in vitro and in animal models. We evaluated first the acute effect of i.v. glucocorticoids on adiponectin in normal subjects and secondly plasma adiponectin levels in a series of patients with Cushing's syndrome compared with controls. DESIGN AND METHODS: Hydrocortisone (25 mg) was administered i.v. to five healthy volunteers, with blood samples taken at -15, 0, 30, 60, 120 and 180 min. Twenty-one patients with Cushing's syndrome were divided in two groups: one with 11 obese and the other with 10 non-obese Cushing'spatients. Each group was compared with controls that were matched for sex, age, body mass index, waist circumference, glucose, insulin, lipid levels and blood pressure. RESULTS: In normal subjects, hydrocortisone produced a decrease in adiponectin at 30 and 60 min, compared with placebo (P<0.05). Adiponectin was lower in non-obese Cushing'spatients than in non-obese controls (P<0.004). In contrast, there was no difference in adiponectin levels in obese Cushing'spatients and in obese controls. Adiponectin was inversely correlated (P<0.05) with homeostasis model assessment index in both obese and non-obese Cushing'spatients; in non-obese Cushing'spatients only, adiponectin was inversely correlated with urinary cortisol (P<0.05). CONCLUSIONS: Glucocorticoids inhibit adiponectin in man, as shown by both exogenous administration to healthy subjects and endogenous cortisol hyperproduction. Similar levels of adiponectin in obese Cushing'spatients and their obese controls indicate that obesity per se may act as a predominant factor in masking the relationship between adiponectin and cortisol.
Authors: Jing Liu; Ming Guo; Di Zhang; Shao-Ying Cheng; Meilian Liu; Jun Ding; Philipp E Scherer; Feng Liu; Xin-Yun Lu Journal: Proc Natl Acad Sci U S A Date: 2012-07-09 Impact factor: 11.205
Authors: T R Castañeda; R Nogueiras; T D Müller; R Krishna; E Grant; A Jones; N Ottaway; G Ananthakrishnan; P T Pfluger; N Chaudhary; M B Solomon; S C Woods; J P Herman; M H Tschöp Journal: Diabetologia Date: 2010-12-22 Impact factor: 10.122