Opposite effects of thyroid hormones on binding proteins for steroid hormones (sex hormone-binding globulin and corticosteroid-binding globulin) in humans

1995 ◽  
Vol 132 (5) ◽  
pp. 594-598 ◽  
Author(s):  
Sonia C Dumoulin ◽  
Bertrand P Perret ◽  
Antoine P Bennet ◽  
Philippe J Caron
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Hormones ◽  
Steroid Hormones ◽  
Sex Hormone ◽  
Sex Hormone Binding Globulin ◽  
Hormone Binding ◽  
Thyroid Status ◽  
Corticosteroid Binding Globulin ◽  
Hypothyroid Patients ◽  
Hyperthyroid Patients

Dumoulin SC, Perret BP, Bennet AP, Caron PJ. Opposite effects of thyroid hormones on binding proteins for steroid hormones (sex hormone-binding globulin and corticosteroid-binding globulin) in humans. Eur J Endocrinol 1995;132:594–8. ISSN 0804–4643 Sex hormone-binding globulin (SHBG) and corticosteroid-binding globulin (CBG) levels were evaluated in euthyroid (N = 111), hyper- (N = 58) and hypothyroid (N = 38) men, in pre- and postmenopausal women (study 1) and in hyper- (N = 24) and hypothyroid (N = 15) patients before and after treatment with carbimazole or levothyroxine therapy (study 2). The SHBG levels are increased in hyper- and decreased in hypothyroid patients, whereas CBG levels are increased in hypo- and decreased in hyperthyroid patients. The SHBG levels are higher in women than in men with similar thyroid status. Plasma SHBG levels are correlated positively whereas CBG levels are correlated negatively with free thyroid hormone concentrations in men as well as women. In hypothyroid patients, SHBG concentrations increased (p < 0.01) and CBG concentrations decreased (p < 0.01) during levothyroxine treatment. In hyperthyroid patients, SHBG concentrations decreased (p < 0.01) and CBG concentrations increased (p < 0.01) during antithyroid treatment. The SHBG and CBG concentrations in treated hypo- and hyperthyroid patients were not significantly different from those of euthyroid controls. Our data indicate that SHBG and CBG levels depend on thyroid status. Corticosteroid-binding globulin is an index of thyroid hormone action at the liver level whose changes are opposite to those of SHBG in hyper- and hypothyroidism. Philippe Caron, Service d'Endocrinologie et Maladies Métaboliques, CHU Rangueil, 1 Avenue J Poulhès, 31054 Toulouse Cedex, France

Thyroid hormone turnover in patients with small cell carcinoma of the lung

1988 ◽  
Vol 118 (3) ◽  
pp. 460-464 ◽  
Author(s):  
Jens Faber ◽  
Sven Poulsen ◽  
Per Iversen ◽  
Carsten Kirkegaard
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Hormones ◽  
Cell Carcinoma ◽  
Small Cell Carcinoma ◽  
Transit Time ◽  
Mean Transit Time ◽  
Small Cell ◽  
Sex Hormone ◽  
Sex Hormone Binding Globulin ◽  
Hormone Binding

Abstract. Patients with small cell carcinoma of the lung often present with symptoms suggestive of hyperthyroidism i.e. weight loss without anorexia. Consequently [125I]T4 and [131I]T3 turnover was studied using simultaneously iv bolus injection and noncompartmental analysis in 6 patients with untreated small cell carcinoma of the lung and 14 normal subjects of comparable ages. Both T4 and T3 production rates were enhanced, T4 production being in median 135 nmol · day−1 · 70 kg−1 (range 111–200) in patients with small cell carcinoma of the lung vs 98 nmol·day−1 ·70 kg−1 (range 69–134) in controls (P < 0.01), and T3 production being 46 nmol · day−1·70 kg−1 (range 33–65) vs 31 nmol ·day−1 ·70 kg−1 (range 24–45) (P < 0.01). The mean transit time was shortened for both T4 and T3, T4 mean transit time being 5.9 days (3.9–8.0 days) vs 8.3 days (6.1–11.2 days) in controls (P < 0.01), and T3 mean transit time being 0.74 days (0.36–0.98 days) vs 1.03 days (0.81–1.45 days) in controls (P < 0.01). Serum total and free T4 and T3 levels were unchanged. Basal serum TSH levels and the TSH response to iv TRH were also normal. Thyroid-stimulating immunoglobulins were only present in the serum in 1 of 6 patients. Thus, thyroid hormone production seemed under pituitary regulation. The peripheral effect of thyroid hormones was evaluated measuring serum sex hormone binding globulin levels, which were increased to in median 270% (77–310%) (P < 0.01) of that in controls, suggesting some degree of hyperthyroidism in liver tissue. One patient was re-investigated after complete remission, which resulted in normalization of T4 and T3 production and mean transit time, as well as serum sex hormone binding globulin levels. The data demonstrate that patients with untreated small cell carcinoma of the lung have enhanced turnover of thyroid hormones, a pattern quite different from that usually seen in non-thyroidal somatic illness.

Concentrations of sex-hormone binding globulin and corticosteroid binding globulin in serum in relation to cardiovascular risk factors and to 12-year incidence of cardiovascular disease and overall mortality in postmenopausal women.

1986 ◽  
Vol 32 (1) ◽  
pp. 146-152 ◽  
Author(s):  
L Lapidus ◽  
G Lindstedt ◽  
P A Lundberg ◽  
C Bengtsson ◽  
T Gredmark
Keyword(s):  
Risk Factors ◽  
Cardiovascular Disease ◽  
Body Mass Index ◽  
Body Mass ◽  
Significant Risk ◽  
Sex Hormone ◽  
Sex Hormone Binding Globulin ◽  
Hormone Binding ◽  
Corticosteroid Binding Globulin ◽  
Overall Mortality

Abstract We determined sex-hormone binding globulin (SHBG) and corticosteroid binding globulin (CBG) by radioimmunoassay of serum samples from a group of 253 women, who were 54 or 60 years old when first studied in 1968-69. The SHBG concentration was highly significantly and inversely related to body mass, body mass index, waist-to-hip circumference ratio, and serum triglyceride concentration; CBG concentration was inversely related to body mass and body mass index. The concentration of neither protein was related to whether or not the subject smoked. Decrease in the concentration of SHBG, but not of CBG, was a significant risk factor for 12-year overall mortality. The plot of the 12-year incidence of myocardial infarction vs SHBG concentration was U-shaped. We recommend that SHBG be included when serum androgens or estrogens are being evaluated as risk factors for cardiovascular disease and death.

scholarly journals Thyroid hormones act indirectly to increase sex hormone-binding globulin production by liver via hepatocyte nuclear factor-4α

2009 ◽  
Vol 43 (1) ◽  
pp. 19-27 ◽  
Author(s):  
David M Selva ◽  
Geoffrey L Hammond
Keyword(s):  
Thyroid Hormones ◽  
Hepg2 Cells ◽  
Sex Hormone ◽  
Sex Hormone Binding Globulin ◽  
Mrna Levels ◽  
Nuclear Factor ◽  
Hepatocyte Nuclear Factor ◽  
Hormone Binding ◽  
Metabolic State ◽  
Hepatocyte Nuclear Factor 4Α

Thyroid hormones increase hepatic sex hormone-binding globulin (SHBG) production, which is also regulated by hepatocyte nuclear factor-4α (HNF-4α) in response to changes in the metabolic state of the liver. Since the human SHBG promoter lacks a typical thyroid hormone response element, and because thyroid hormones influence metabolic state, we set out to determine whether thyroid hormones mediate SHBG expression indirectly via changes in HNF-4α levels in HepG2 human hepatoblastoma cells, and in the livers of transgenic mice that express a 4.3 kb human SHBG transgene under the control of its own 0.8 kb promoter sequence. Thyroid hormones (triiodothyronine (T3) and thyroxine (T4)) increase SHBG accumulation in HepG2 cell culture medium over 5 days, and increase cellular SHBG mRNA levels. In addition, T4 treatment of HepG2 cells for 5 days increased HNF-4α mRNA and HNF-4α levels in concert with decreased cellular palmitate levels. Plasma SHBG levels were also increased in mice expressing a human SHBG transgene after 5 days treatment with T3 along with increased hepatic HNF-4α levels. In HepG2 cells, the human SHBG promoter failed to respond acutely (within 24 h) to T4 treatment, but a 4-day pre-treatment with T4 resulted in a robust response that was prevented by co-treatment with HNF-4α siRNA, or by blocking the β-oxidation of palmitate through co-treatment with the carnitine palmitoyltransferase I inhibitor, etomoxir. These data lead us to conclude that thyroid hormones increase SHBG production indirectly by increasing HNF-4α gene expression, and by reducing cellular palmitate levels that further contribute to increased HNF-4α levels in hepatocytes.

Sign in / Sign up

Export Citation Format

Share Document