Search Results
Search for other papers by Yi Chen in
Google Scholar
PubMed
Search for other papers by Wen Zhang in
Google Scholar
PubMed
Search for other papers by Chi Chen in
Google Scholar
PubMed
Search for other papers by Yuying Wang in
Google Scholar
PubMed
Search for other papers by Ningjian Wang in
Google Scholar
PubMed
Search for other papers by Yingli Lu in
Google Scholar
PubMed
Objective
We aimed to evaluate whether thyroid hormones, autoimmune and thyroid homeostasis status were related to bone turnover in type 2 diabetes.
Methods
The data were obtained from a cross-sectional study, the METAL study. In this study, 4209 participants (2059 men and 2150 postmenopausal women) with type 2 diabetes were enrolled. Thyroid function, thyroid antibodies and three bone turnover markers (BTMs), including a large N-mid fragment of osteocalcin (N-MID osteocalcin), β-C-terminal cross-linked telopeptides of type I collagen (β-CTX) and procollagen type I N-terminal propeptide (P1NP), were measured. Thyroid homeostasis parameters, including the sum activity of step-up deiodinases (SPINA-GD), thyroid secretory capacity (SPINA-GT), Jostel’s TSH index (TSHI) and the thyrotroph thyroid hormone resistance index (TTSI), were calculated. The associations of thyroid parameters with BTMs were analyzed using linear regression.
Results
Free and total triiodothyronine were positively associated with N-MID osteocalcin and P1NP in both sexes and positively associated with β-CTX in postmenopausal women. Thyroid-stimulating hormone was negatively associated with β-CTX in postmenopausal women, and free thyroxine was negatively associated with N-MID osteocalcin and P1NP in men. SPINA-GD was positively associated with N-MID osteocalcin and P1NP in both sexes. There was a positive relationship of SPINA-GT with β-CTX, a negative relationship of TTSI with β-CTX, and a negative relationship of TSHI with β-CTX and P1NP in postmenopausal women.
Conclusions
Among men and postmenopausal women with type 2 diabetes, significant associations were observed between N-MID osteocalcin, β-CTX and P1NP with thyroid function and thyroid homeostasis. Further prospective studies are warranted to understand the causal relationship and underlying mechanism.
Search for other papers by Rui-yi Tang in
Google Scholar
PubMed
Search for other papers by Rong Chen in
Google Scholar
PubMed
Search for other papers by Miao Ma in
Google Scholar
PubMed
Search for other papers by Shou-qing Lin in
Google Scholar
PubMed
Search for other papers by Yi-wen Zhang in
Google Scholar
PubMed
Search for other papers by Ya-ping Wang in
Google Scholar
PubMed
Objective
To evaluate the clinical features of Chinese women with idiopathic hypogonadotropic hypogonadism (IHH).
Methods
We retrospectively reviewed the clinical characteristics, laboratory and imaging findings, therapeutic management and fertility outcomes of 138 women with IHH. All patients had been treated and followed up at an academic medical centre during 1990–2016.
Results
Among the 138 patients, 82 patients (59.4%) were diagnosed with normosmic IHH and 56 patients (40.6%) were diagnosed with Kallmann syndrome (KS). The patients with IHH experienced occasional menses (4.3%), spontaneous thelarche (45.7%) or spontaneous pubarche (50.7%). Women with thelarche had a higher percentage of pubarche (P < 0.001) and higher gonadotropin concentrations (P < 0.01). Olfactory bulb/sulci abnormalities were found during the magnetic resonance imaging (MRI) of all patients with KS. Most patients with IHH had osteopenia and low bone age. Among the 16 women who received gonadotropin-releasing hormone treatment, ovulation induction or assisted reproductive technology, the clinical pregnancy rate was 81.3% and the live birth rate was 68.8%.
Conclusions
The present study revealed that the phenotypic spectrum of women with IHH is broader than typical primary amenorrhoea with no secondary sexual development, including occasional menses, spontaneous thelarche or pubarche. MRI of the olfactory system can facilitate the diagnosis of KS. Pregnancy can be achieved after receiving appropriate treatment.
Search for other papers by Haojie Zhang in
Google Scholar
PubMed
Search for other papers by Yuke Cui in
Google Scholar
PubMed
Search for other papers by Ruihua Dong in
Google Scholar
PubMed
Search for other papers by Wen Zhang in
Google Scholar
PubMed
Search for other papers by Shihan Chen in
Google Scholar
PubMed
Search for other papers by Heng Wan in
Google Scholar
PubMed
Search for other papers by Chi Chen in
Google Scholar
PubMed
Search for other papers by Yi Chen in
Google Scholar
PubMed
Search for other papers by Yuying Wang in
Google Scholar
PubMed
Search for other papers by Chunfang Zhu in
Google Scholar
PubMed
Search for other papers by Bo Chen in
Google Scholar
PubMed
Search for other papers by Ningjian Wang in
Google Scholar
PubMed
Search for other papers by Yingli Lu in
Google Scholar
PubMed
Background
Bone is thought to be the reservoir of the human lead burden, and vitamin D is associated with bone turnover. We aimed to explore whether exposure to lower 25-hydroxy vitamin D (25(OH)D) levels was associated with higher blood lead levels (BLLs) by increasing the bone turnover rate in individuals with type 2 diabetes.
Methods
A total of 4103 type 2 diabetic men and postmenopausal women in Shanghai, China, were enrolled in 2018. Their 25(OH)D, β-C-terminal telopeptide (β-CTX), N-MID osteocalcin and procollagen type 1 N-peptide (P1NP) levels were detected. Their BLLs were determined by atomic absorption spectrometry. Mediation analyses were performed to identify the possible role that bone turnover played in the underlying mechanisms.
Results
In both the men and postmenopausal women, all three bone turnover markers were inversely associated with 25(OH)D and positively associated with the BLL (all P < 0.01) after adjusting for age, current smoking habits, metabolic parameters, duration of diabetes, vitamin D intake, and use of anti-osteoporosis medication. In the mediation analyses, none of the direct associations between 25(OH)D and BLL was significant for the three bone turnover markers, but all three bone turnover markers were found to be significant mediators of the indirect associations between 25(OH)D and BLL.
Conclusion
The association between vitamin D and BLL was fully mediated by bone turnover markers in type 2 diabetic patients (mediation effect). This finding suggested that vitamin D may protect against blood lead exposure from the bone reservoir by decreasing bone turnover in individuals with type 2 diabetes.
Search for other papers by Xue-Lian Zhang in
Google Scholar
PubMed
Search for other papers by Xinyi Zhao in
Google Scholar
PubMed
Department of Biomedical Engineering, Faculty of Engineering, The Hong Kong Polytechnic University, Hong Kong, China
Search for other papers by Yong Wu in
Google Scholar
PubMed
Search for other papers by Wen-qing Huang in
Google Scholar
PubMed
Department of Biomedical Engineering, Faculty of Engineering, The Hong Kong Polytechnic University, Hong Kong, China
Search for other papers by Jun-jiang Chen in
Google Scholar
PubMed
Search for other papers by Peijie Hu in
Google Scholar
PubMed
Search for other papers by Wei Liu in
Google Scholar
PubMed
Search for other papers by Yi-Wen Chen in
Google Scholar
PubMed
Search for other papers by Jin Hao in
Google Scholar
PubMed
Search for other papers by Rong-Rong Xie in
Google Scholar
PubMed
Search for other papers by Hsiao Chang Chan in
Google Scholar
PubMed
Search for other papers by Ye Chun Ruan in
Google Scholar
PubMed
Search for other papers by Hui Chen in
Google Scholar
PubMed
Search for other papers by Jinghui Guo in
Google Scholar
PubMed
Objective
The beneficial effect of angiotensin(1–7) (Ang(1–7)), via the activation of its receptor, MAS-1, has been noted in diabetes treatment; however, how Ang(1–7) or MAS-1 affects insulin secretion remains elusive and whether the endogenous level of Ang(1–7) or MAS-1 is altered in diabetic individuals remains unexplored. We recently identified an important role of cystic fibrosis transmembrane conductance regulator (CFTR), a cAMP-activated Cl− channel, in the regulation of insulin secretion. Here, we tested the possible involvement of CFTR in mediating Ang(1–7)’s effect on insulin secretion and measured the level of Ang(1–7), MAS-1 as well as CFTR in the blood of individuals with or without type 2 diabetes.
Methods
Ang(1–7)/MAS-1/CFTR pathway was determined by specific inhibitors, gene manipulation, Western blotting as well as insulin ELISA in a pancreatic β-cell line, RINm5F. Human blood samples were collected from 333 individuals with (n = 197) and without (n = 136) type 2 diabetes. Ang(1–7), MAS-1 and CFTR levels in the human blood were determined by ELISA.
Results
In RINm5F cells, Ang(1–7) induced intracellular cAMP increase, cAMP-response element binding protein (CREB) activation, enhanced CFTR expression and potentiated glucose-stimulated insulin secretion, which were abolished by a selective CFTR inhibitor, RNAi-knockdown of CFTR, or inhibition of MAS-1. In human subjects, the blood levels of MAS-1 and CFTR, but not Ang(1–7), were significantly higher in individuals with type 2 diabetes as compared to those in non-diabetic healthy subjects. In addition, blood levels of MAS-1 and CFTR were in significant positive correlation in type-2 diabetic but not non-diabetic subjects.
Conclusion
These results suggested that MAS-1 and CFTR as key players in mediating Ang(1–7)-promoted insulin secretion in pancreatic β-cells; MAS-1 and CFTR are positively correlated and both upregulated in type 2 diabetes.
