N Zhong 1 , B Xu 1 , R Cui 1 , M Xu 1 , J Su 1 , Z Zhang 1 , Y Liu 1 , L Li 1 , C Sheng 1 , H Sheng 1 , S Qu 1 Show Affiliations »
Abstract
PURPOSE: Animal studies suggested that there is an independent bone-osteocalcin-gonadal axis, except of the hypothalamic-pituitary-gonadal axis. Based on this hypothesis, the higher osteocalcin during the high bone turnover should be followed by higher testosterone formation. Yet such clinical evidence is limited. The patients with uncontrolled hyperthyroidism are proper model with high bone turnover. If this hypothesis is true, there should be high testosterone level in patients with uncontrolled hyperthyroidism. Therefore, Graves' disease patients were recruited to study the correlation between osteocalcin and testosterone. MATERIALS AND METHODS: 50 male hyperthyroidism patients with Graves' disease and 50 health persons matched by age and gender were enrolled in our cross-section study. Serum markers for thyroid hormone, sex hormone and bone metabolic markers including free triiodothyronine (FT3), free thyroxine (FT4), thyroid-stimulating hormone (TSH), testosterone, luteinizing hormone (LH), follicle-stimulating hormone (FSH) and osteocalcin (OC), C-terminal telopeptide fragments of type I collagen (CTX) were examined. The demographic parameters such as duration of disease were also collected. All data was analyzed by SPSS 20.0. RESULTS: High testosterone and osteocalcin level was observed in the hyperthyroidism patients (T 36.35±10.72 nmol/l and OC 46.79±26.83 ng/ml). In simple Pearson correlation, testosterone was positively associated with OC (r=0.486, P<0.001), and this positive relation still existed after adjusted for age, BMI, smoking, drinking, duration of disease, FT3, FT4, LH, FSH, CTX in multi-linear regression analysis (See Model 1-4). CONCLUSION: In male hyperthyroidism patients, osteocalcin was positively correlated with serum testosterone, which indirectly supports the hypothesis that serum osteocalcin participates in the regulation of sex hormone. © Georg Thieme Verlag KG Stuttgart · New York.
PURPOSE: Animal studies suggested that there is an independent bone-osteocalcin -gonadal axis, except of the hypothalamic-pituitary-gonadal axis . Based on this hypothesis, the higher osteocalcin during the high bone turnover should be followed by higher testosterone formation. Yet such clinical evidence is limited. The patients with uncontrolled hyperthyroidism are proper model with high bone turnover. If this hypothesis is true, there should be high testosterone level in patients with uncontrolled hyperthyroidism . Therefore, Graves' disease patients were recruited to study the correlation between osteocalcin and testosterone . MATERIALS AND METHODS: 50 male hyperthyroidism patients with Graves' disease and 50 health persons matched by age and gender were enrolled in our cross-section study. Serum markers for thyroid hormone, sex hormone and bone metabolic markers including free triiodothyronine (FT3), free thyroxine (FT4), thyroid-stimulating hormone (TSH), testosterone , luteinizing hormone (LH), follicle-stimulating hormone (FSH) and osteocalcin (OC ), C-terminal telopeptide fragments of type I collagen (CTX ) were examined. The demographic parameters such as duration of disease were also collected. All data was analyzed by SPSS 20.0. RESULTS: High testosterone and osteocalcin level was observed in the hyperthyroidism patients (T 36.35±10.72 nmol/l and OC 46.79±26.83 ng/ml). In simple Pearson correlation, testosterone was positively associated with OC (r=0.486, P<0.001), and this positive relation still existed after adjusted for age, BMI, smoking, drinking, duration of disease, FT3, FT4, LH, FSH, CTX in multi-linear regression analysis (See Model 1-4). CONCLUSION: In male hyperthyroidism patients , osteocalcin was positively correlated with serum testosterone , which indirectly supports the hypothesis that serum osteocalcin participates in the regulation of sex hormone. © Georg Thieme Verlag KG Stuttgart · New York.
Entities: Chemical
Disease
Gene
Species
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Year: 2016
PMID： 27219888 DOI： 10.1055/s-0042-107944
Source DB: PubMed Journal: Exp Clin Endocrinol Diabetes ISSN： 0947-7349 Impact factor: 2.949