Search Results
You are looking at 1 - 2 of 2 items for
- Author: D Armanini x
- Refine by access: All content x
Search for other papers by R Vettor in
Google Scholar
PubMed
Search for other papers by C Macor in
Google Scholar
PubMed
Search for other papers by F Novo in
Google Scholar
PubMed
Search for other papers by C Gottardo in
Google Scholar
PubMed
Search for other papers by S Zovato in
Google Scholar
PubMed
Search for other papers by M Simoncini in
Google Scholar
PubMed
Search for other papers by G Federspil in
Google Scholar
PubMed
Search for other papers by D Armanini in
Google Scholar
PubMed
Abnormalities of the hypothalamus-pituitary-adrenal axis and hypersensitivity to corticosteroids have been suggested as major determinants of the development of visceral obesity. Since at the cellular level most effects of corticosteroids are mediated by specific receptors, we evaluated the number of type I and type II corticosteroid receptors in mononuclear leucocytes of 26 obese and 13 control subjects. We also studied the relationship between corticosteroid receptors, measured by radioreceptor assay, and abdominal visceral fat, evaluated by computed tomography scan, plasma and urine corticosteroid hormone concentrations and overall glucose metabolism, assessed by euglycaemic-hyperinsulinaemic clamp. We observed a decrease in type II receptors in the obese subjects (1746 +/- 160 vs 2829 +/- 201 per cell; P < 0.0001), with no change in type I receptors. Type II receptors decreased in relation to body mass index (r = -0.53; P < 0.005) and total glucose disposal (r = 0.51; P < 0.01). Abdominal visceral fat did not correlate with type II receptor number, but did correlate with total glucose disposal (r = -0.35; P < 0.05); the rate of glucose disposal was lower in obese subjects (3.3 +/- 0.3 vs 7.4 +/- 0.4 mg/kg per min; P < 0.001). Plasma and urine cortisol did not differ between the two groups. However, a direct correlation between type II receptor number and both plasma (r = 0.43; P < 0.02) and urine cortisol concentrations (r = 0.60; P < 0.05) was observed. In conclusion, the number of type II corticosteroid receptors in mononuclear leucocytes was found to be lower in obese subjects. This abnormality appears to be related to the degree of adiposity and to the main endocrine-metabolic features of the obesity syndrome, further supporting the hypothesis of involvement of hypothalamus-pituitary-adrenal axis hyperactivity in the pathophysiology of obesity.
Search for other papers by D Armanini in
Google Scholar
PubMed
Search for other papers by P Spinella in
Google Scholar
PubMed
Search for other papers by M Simoncini in
Google Scholar
PubMed
Search for other papers by A Basso in
Google Scholar
PubMed
Search for other papers by S Zovato in
Google Scholar
PubMed
Search for other papers by GB Pozzan in
Google Scholar
PubMed
Search for other papers by CB De Palo in
Google Scholar
PubMed
Search for other papers by G Bucciante in
Google Scholar
PubMed
Search for other papers by I Karbowiak in
Google Scholar
PubMed
We have studied 16 patients with anorexia nervosa (11 with a stabilised weight loss and 5 in the weight-losing phase), 11 healthy controls, and 10 patients with Cushing's syndrome, by measuring plasma cortisol (by enzyme-immunoassay), ACTH (by RIA), corticosteroid (Type I-mineralocorticoid and Type II-glucocorticoid) receptors in mononuclear leukocytes (by radio-receptor assay), and lymphocyte subpopulations (by cytofluorimetry). In anorexic patients with a stabilised weight loss and in Cushing's syndrome the mean value of both Type I and Type II corticosteroid receptors in mononuclear leukocytes was significantly lower than in controls. The correlation between Type II receptors and plasma cortisol was inverse in stabilised anorexia nervosa and in Cushing's syndrome, and direct in healthy controls. Anorexic patients in the weight-losing phase showed a significant increase in plasma cortisol levels and a normal number of Type II receptors. From these results we hypothesise that in anorexia nervosa there is a progression from an increase in plasma cortisol in the weight-losing phase, to a concomitant decrease in Type II receptors when the disease is stabilised.
