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Weibin Zhou, Yanyun Gu, Hong Li, and Min Luo

Objective: To assess the cutoff values at different time points for impaired glucose regulation (IGR) and diabetes, the glucose curve and isolated 1-h hyperglycemia were monitored during an oral glucose tolerance test (OGTT).

Methods: Two thousand eight hundred and eighty-six subjects (1300 men and 1586 women) were recruited to have an OGTT. Plasma was collected at 0, 30, 60, 120, and 180 min to analyze glucose and insulin. The diagnosis of impaired fasting glucose, impaired glucose tolerance, and diabetes was based on World Health Organization and American Diabetes Association’s criteria. Those with fasting plasma glucose (FPG)<5.6 and 2-h plasma glucose (PG)<7.8, but 1-h PG≥7.8 and <11.1 mmol/l were defined as 1h-High7.8, and those with FPG<7.0 and 2-h PG<11.1, but 1-h PG≥11.1 mmol/l as 1h-High11.1. The cutoff values were calculated by receiver operating characteristic (ROC) curve. The correlation between β-cell function and the area under the curve of glucose (AUCg) and the shape index was analyzed with linear regression.

Results: The cutoff values for IGR were 5.6, 9.7, 10.1, 7.8 and 6.1 mmol/l for blood glucose at 0, 30, 60, 120 and 180 min, 24 for AUCg and 1.3 mmol/l for the shape index. The cutoff values for diabetes were 6.8, 11.2, 13, 11.1 and 7 mmol/l for 0, 30, 60, 120 and 180 min, 30.9 for AUCg and 2 mmol/l for the shape index. Both AUCg and the shape index were inversely related to β-cell function. The profiles of glucose and insulin in the subgroup with isolated 1-h hyperglycemia were very different from those seen in subjects with normal glucose tolerance or IGR.

Conclusions: The present study provides new information on measures other than the fasting and 2-h PG to evaluate glucose metabolism in vivo and stimulates further research aimed at assessing the value of the OGTT 1-h PG concentration prospectively.

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Xiaohui Luan, Yuxun Zhou, Wei Wang, Hong Yu, Pin Li, Xiaohong Gan, Dongzhi Wei, and Junhua Xiao

Objective: The kisspeptin/GPR54 pathway has been proven to be crucial in the process of puberty onset, yet the polymorphisms in the KISS1 gene and their relationships with central precocious puberty (CPP) have not been investigated. This study was performed to reveal the relationship between the gene and the disease.

Design and Methods: 272 Chinese Han girls diagnosed to be CPP patients were recruited as Case Group I, 43 unrelated African women as Case Group II, and 288 unrelated normal Chinese Han girls as Control Group. Polymorphism scans of the KISS1 gene were performed for the first time by bidirectional resequencing of the whole gene in a subset of the patients, and then by ligase detection reaction some of the polymorphisms identified were typed in the two groups and the respective haplotypes were constructed. The relationships of the typed polymorphisms and the haplotypes with CPP were evaluated by an association study between genotypes and phenotypes.

Results: By resequencing, eight polymorphisms were identified, five of which were typed forming 18 haplotypes. Although one novel nonsynonymous single nucleotide polymorphism substituting one amino acid in kisspeptin (P110T) was found to be statistically related to the disease (P = 0.025), no further supporting evidence has yet been found. The other polymorphisms and all the haplotypes were not found to be related.

Conclusion: The polymorphism scanning and typing of KISS1 uncovered several potentially meaningful polymorphisms, but the conclusion was not solid and further studies are necessary for function validation of these polymorphisms.

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Zhimin Miao, Yufang Gao, René J M Bindels, Wendong Yu, Yanhua Lang, Nan Chen, Hong Ren, Fang Sun, Yushan Li, Xianghua Wang, and Leping Shao


Primary aldosteronism (PA) is the most common form of secondary hypertension, while Gitelman's syndrome (GS) is the most common inherited renal tubular disease. However, coexistence of these two diseases has never been previously reported.

Aim and subjects

The aim of our study was to describe the association of GS and PA in two unrelated patients and compare their clinical presentation with a group of patients with GS.


Ten subjects suspected to have only GS were assigned to the control group. Saline infusion test was used to confirm the diagnosis of PA. GS was confirmed by sequencing of the causal genes (SLC12A3 and CLCNKB) and functional analyses in Xenopus laevis oocytes.


Confirmatory tests, gene analysis, and functional studies demonstrated the coexistence of GS and PA in both patients. In total, nine novel SLC12A3 gene variants, including seven missense mutations, one splice mutation, and one frameshift deletion, were found in 12 subjects. Four mutations (p.T60M, p.T304M, p.T465P, and p.N611T) harbored by the two patients with both PA and GS were revealed to be loss-of-function variants. Although both patients were normotensive, neither of them had normal nocturnal dip.


Two rare diseases GS and PA may occasionally coexist in one subject. In these patients, salt depletion and volume constriction might explain the absence of hypertension normally seen in PA patients. However, the protective mechanism against hypertension via down-regulation of renal sodium handling was probably not sufficient in those patients, since their normal circadian rhythm of blood pressure was disrupted.

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Guoyu Tong, Xiaomin Hua, Yingjie Zhong, Kui Zhang, Guangyu Gu, Wenhuan Feng, Hong Huang, Weimin Wang, Lirong Li, Yanjun Sun, Tianyan Zhang, and Yun Hu


Many studies have shown that low sex hormone-binding globulin (SHBG) is associated with insulin resistance, but only few studies have examined how serum SHBG is regulated by insulin in humans. This interventional study aimed to investigate the effect of insulin therapy (IT) on serum SHBG levels in newly diagnosed type 2 diabetic patients.


A total of 80 newly diagnosed type 2 diabetic subjects were enrolled and randomly grouped into a 2-week intensive IT with/without metformin. Serum SHBG, total testosterone, glucose, liver enzymes, lipids, insulin, and C-peptide levels were measured before and after IT.


Before IT, serum SHBG levels were negatively correlated with BMI, waist circumference (WC), alanine aminotransferase (ALT), gamma-glutamyl transpeptidase (γ-GT), triglyceride (TG), fasting insulin, and C-peptide, and homeostatic model assessment of insulin resistance (HOMA-IR), and positively with HDL-C (all P for trend <0.05), after adjustment for age and sex. IT increased serum SHBG levels from 26.5±14.5 to 33.2±15.0 nmol/l (P<0.001), increased by 25.2% (95% CI, 20.3 to 30.9%, P<0.001). In a multiple linear regression model adjusting for age, sex, BMI, and WC, the decreases in ΔALT (standardized regression coefficient β=−0.374, P=0.012) and ΔTG (β=−0.380, P=0.020) were independent contributors to the increase in ΔSHBG.


IT increases serum SHBG likely through improving insulin resistance and liver function.

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Fan Yang, Zhongyan Shan, Xiaochun Teng, Yushu Li, Haixia Guan, Wei Chong, Di Teng, Xiaohui Yu, Chenling Fan, Hong Dai, Yang Yu, Rong Yang, Jia Li, Yanyan Chen, Dong Zhao, Jinyuan Mao, and Weiping Teng

Objective: An increasing incidence of hyperthyroidism has been observed when iodine supplementation has been introduced to an iodine-deficient population. Moreover, the influence of chronic more than adequate or excessive iodine intake on the epidemiological features of hyperthyroidism has not been widely and thoroughly described. To investigate the influences of different iodine intake levels on the incidence of hyperthyroidism, we conducted a prospective community-based survey in three communities with mild-deficient, more than adequate (previously mild deficient iodine intake), and excessive iodine intake.

Subjects and methods: In three rural Chinese communities, a total of 3761 unselected inhabitants aged above 13 years participated in the original investigation and 3018 of them received identical examinations after 5 years. Thyroid function, levels of thyroid peroxidase antibody (TPOAb), thyroglobulin antibody and urinary iodine excretion were measured and thyroid ultrasound examination was also performed.

Results: In three communities, median urinary iodine excretion was 88, 214, and 634 μg/l (P<0.05) respectively. The cumulative incidence of hyperthyroidism was 1.4, 0.9, and 0.8% (P>0.05) respectively. Autoimmune hyperthyroidism was predominant in thyroid hyperfunction in all the three cohorts. Either positive TPOAb (>50 U/ml) or goiter in original healthy participants was associated with the occurrence of unsuspected hyperthyroidism in 5 years (logistic regression, OR=4.2 (95% CI 1.7–8.8) for positive TPOAb, OR=3.1 (95% CI 1.4–6.8) for goiter).

Conclusion: Iodine supplementation may not induce an increase in hyperthyroidism in a previously mildly iodine-deficient population. Chronic iodine excess does not apparently increase the risk of autoimmune hyperthyroidism, suggesting that excessive iodine intake may not be an environmental factor involved in the occurrence of autoimmune hyperthyroidism.

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Yanli Li, Ying Peng, Xiuli Jiang, Yulong Cheng, Weiwei Zhou, Tingwei Su, Jing Xie, Xu Zhong, Dalong Song, Luming Wu, Liwen Fan, Min Li, Jie Hong, Weiqing Wang, Guang Ning, and Yanan Cao


Thymic neuroendocrine tumor is the second-most prevalent cause of ectopic adrenocorticotropic hormone (ACTH) syndrome (EAS), which is a rare disease characterized by ectopic ACTH oversecretion from nonpituitary tumors. However, the genetic abnormalities of thymic neuroendocrine tumors with EAS remain largely unknown. We aim to elucidate the genetic abnormalities and identify the somatic mutations of potential tumor-related genes of thymic neuroendocrine tumors with EAS by whole exome sequencing.

Design and methods

Nine patients with thymic neuroendocrine tumors with EAS who were diagnosed at Shanghai Clinical Center for Endocrine and Metabolic Diseases in Ruijin Hospital between 2002 and 2014 were enrolled. We performed whole exome sequencing on the DNA obtained from thymic neuroendocrine tumors and matched peripheral blood using the Hiseq2000 platform.


We identified a total of 137 somatic mutations (median of 15.2 per tumor; range, 1–24) with 129 single-nucleotide mutations (SNVs). The predominant substitution in these mutations was C:G > T:A transition. Approximately 80% of detected mutations resulted in amino acid changes. However, we failed to discover any recurrent mutations in these nine patients. By functional predictions, HRAS, PAK1 and MEN1, previously reported in neuroendocrine tumors, were identified as candidate tumor-related genes associated with thymic neuroendocrine tumors.


Using whole exome sequencing, we identified genetic abnormalities in thymic neuroendocrine tumors with EAS. Thereby, this study acts as a further supplement of the genetic features of neuroendocrine tumors. Somatic mutations of three potential tumor-related genes (HRAS, PAK1 and MEN1) might contribute to the tumorigenesis of thymic neuroendocrine tumors with EAS.

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Weiwei Wang, Weiping Teng, Zhongyan Shan, Sen Wang, Jianxin Li, Lin Zhu, Jin Zhou, Jinyuan Mao, Xiaohui Yu, Jia Li, Yanyan Chen, Haibo Xue, Chenling Fan, Hong Wang, Hongmei Zhang, Chenyang Li, Weiwei Zhou, Bo Gao, Tao Shang, Jiaren Zhou, Bin Ding, Ying Ma, Ying Wu, Hui Xu, and Wei Liu


Maternal thyroid disorders during early pregnancy can influence pregnancy outcome and fetal development. The recent Endocrine Society Clinical Practice Guideline recommends a case-finding approach in which pregnant women who are at high risk for developing thyroid disease are tested.


The purpose of this study was to use the first trimester-specific reference intervals of thyroid-related hormones to explore the prevalence of thyroid dysfunction during early pregnancy and to analyze effectiveness of different screening strategies.


A multicenter cohort study.


A total of 2899 pregnant women were enrolled in this study during their first trimester of gestation. Levels of TSH, free thyroxine, free triiodothyronine, and thyroid peroxidase antibodies (TPOAb) were measured and thyroid disorders of pregnant women were diagnosed based on the first trimester-specific reference intervals.


The prevalence of hypothyroidism was significantly higher in the high-risk group than in the non-high-risk group (10.9 vs 7.0%, χ 2=7.1, P=0.008). The prevalence of hyperthyroidism was not significantly different between the high-risk group and the non-high-risk group (2.7 vs 1.6%, χ 2=2.27, P=0.13). Elevated levels of TPOAb and a personal history of thyroid disease increased the risk of thyroid dysfunction.


A case-finding strategy for screening thyroid function in the high-risk group would miss about 81.6% pregnant women with hypothyroidism and 80.4% pregnant women with hyperthyroidism.