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Zhao Z.-F.,Gongli Hospital | Zhao Y.-J.,Shanghai JiaoTong University | Gu M.-J.,Gongli Hospital | Cui J.-L.,Shanghai Institute of Endocrinology and Metabolism | Wang S.,Shanghai JiaoTong University
Journal of Shanghai Jiaotong University (Medical Science) | Year: 2013

Objective: To investigate the effect of Ganoderma lucidum polysaccharides on hyperthyroidism and liver injury in the mice model of Graves' disease (GD). Methods: GD mice model was constructed by immunizing BALB/c mice with thyroid stimulating hormone receptor-A (TSHR-A). Serum thyroxine (T4), thyroid stimulating hormone receptor antibody (TRAb), and liver function parameters were measured, and correlation analysis was performed. The mice were intragastrically managed with pure water, low-dose Ganoderma lucidum polysaccharides (100 mg·kg-1·d-1) and high-dose Ganoderma lucidum polysaccharides (400 mg·kg-1·d-1) respectively, and the change of serum T4, TRAb, alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (ALP) were determined. Results: Serum ALT, AST and ALP in mice with hyperthyroidism in model group were significantly higher than those in mice without hyperthyroidism in model group and mice in control group (P<0.05). Serum AST and ALP were positively significantly related to serum T4 (r=0.585, P<0.05; r=0.744, P<0.05), but were not related to serum TRAb (P>0.05). Serum T4 and TRAb in model mice were not significantly changed after treatment with Ganoderma lucidum polysaccharides (P>0.05). Serum ALT and ALP in mice with hyperthyroidism in model group treated with low-dose Ganoderma lucidum polysaccharides were significantly superior to those in pure water group (P<0.05). Conclusion: Ganoderma lucidum polysaccharides may not work on hyperthyroidism improvement in GD mice model, but can improve the liver injury caused by hyperthyroidism. Source

Zhan M.,State Key Laboratory of Medical Genomics and Shanghai Institute of Endocrinology and Metabolism | Chen G.,Fujian Medical University | Pan C.-M.,State Key Laboratory of Medical Genomics and | Gu Z.-H.,Shanghai Center for Systems Biomedicine | And 17 more authors.
Human molecular genetics | Year: 2014

Thyroid-stimulating hormone (TSH) is a sensitive indicator of thyroid function. High and low TSH levels reflect hypothyroidism and hyperthyroidism, respectively. Even within the normal range, small differences in TSH levels, on the order of 0.5-1.0 mU/l, are associated with significant differences in blood pressure, BMI, dyslipidemia, risk of atrial fibrillation and atherosclerosis. Most of the variance in TSH levels is thought to be genetically influenced. We conducted a genome-wide association study of TSH levels in 1346 Chinese Han individuals. In the replication study, we genotyped four candidate SNPs with the top association signals in an independent isolated Chinese She cohort (n = 3235). We identified a novel serum TSH susceptibility locus within XKR4 at 8q12.1 (rs2622590, Pcombined = 2.21 × 10(-10)), and we confirmed two previously reported TSH susceptibility loci near FOXE1 at 9q22.33 and near CAPZB at 1p36.13, respectively. The rs2622590_T allele at XKR4 and the rs925489_C allele near FOXE1 were correlated with low TSH levels and were found to be nominally associated to patients with papillary thyroid carcinoma (PTC) (OR = 1.41, P= 0.014 for rs2622590_T, and OR = 1.61, P= 0.030 for rs925489_C). The rs2622590 and rs925489 genotypes were also correlated with the expression levels of FOXE1 and XKR4, respectively, in PTC tissues (P = 2.41 × 10(-4) and P= 0.02). Our findings suggest that the SNPs in XKR4 and near FOXE1 are involved in the regulation of TSH levels. © The Author 2014. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oup.com. Source

Jiang H.,Shanghai Institute of Endocrinology and Metabolism | Ye X.-P.,Shanghai Institute of Endocrinology and Metabolism | Yang Z.-Y.,Shanghai JiaoTong University | Zhan M.,Shanghai Institute of Endocrinology and Metabolism | And 6 more authors.
Journal of Molecular Endocrinology | Year: 2013

There is a high incidence of metabolic syndrome among patients with primary aldosteronism PA, which has recently been associated with an unfavorable cardiometabolic profile. However, the underlying mechanisms have not been clarified in detail. Characterizing aldosterone Ald target genes in adipocytes will help us to elucidate the deleterious effects associated with excess Ald. Apelin, a novel adipokine, exerts beneficial effects on obesityassociated disorders and cardiovascular homeostasis. The objective of this study was to investigate the effects of high Ald levels on apelin expression and secretion and the underlying mechanisms involved in adipocytes. In vivo, a single-dose Ald injection acutely decreased apelin serum levels and adipose tissue apelin production, which demonstrates a clear inverse relationship between the levels of plasma Ald and plasma apelin. Experiments using 3T3-L1 adipocytes showed that Ald decreased apelin expression and secretion in a time- and dose-dependent manner. This effect was reversed by glucocorticoid receptor GR antagonists or GR NR3C1 knockdown; furthermore, putative HREs were identified in the apelin promoter. Subsequently, we verified that both glucocorticoids and mineralocorticoids regulated apelin expression through GR activation, although no synergistic effect was observed. Additionally, detailed potential mechanisms involved a p38 MAPK signaling pathway. In conclusion, our findings strengthen the fact that there is a direct interaction between Ald and apelin in adipocytes, which has important implications for hyperaldosteronism or PA-associated cardiometabolic syndrome and hoists apelin on the list of potent therapeutic targets for PA. © 2013 Society for Endocrinology. Source

Du W.,Linyi Peoples Hospital | Du W.,CAS Shenyang Institute of Metal Research | Liang C.,Linyi Peoples Hospital | Che F.,CAS Shenyang Institute of Metal Research | And 16 more authors.
International Journal of Clinical and Experimental Medicine | Year: 2014

This study is to evaluate the association of 9 single nucleotide polymorphisms (SNPs) with Graves’ disease (GD) in different homogenous samples of the Chinese Han population. A total of 2,865 unrelated individuals were enrolled from Linyi City, Shandong Province, China, including 1,139 patients of GD and 1,726 controls. All 9 SNPs showed significant associations with GD (P < 1.3×10-4, Bonferroni corrected Pc < 0.001). The most significant asso­ciation was detected at rs2281388 at the HLA-DPB1 locus (P=1.3×10-21; OR=1.62, 95% CI: 1.47-1.79). After adjusting for gender and age, 7 SNPs remained significantly associated with GD (P < 3.4×10-4, Pc < 0.003). The risk of GD caused by any of these SNPs was not significantly different between female and male participants (Phet > 0.15). Four SNPs located in MHC regions were significantly associated with GD in different ages (P < 8.4×10-4, Pc < 0.04). The risks of any SNP leading to the development of GD did not differ significantly in different ages (P_trend > 0.02, Pc > 0.18). The rs6457617 at the HLA-DR-DQ locus was significantly correlated with gender in GD patients (P=0.004, Pc=0.04). No significant correlation was found between any SNP and age of diagnosis in GD patients (P > 0.02, Pc > 0.17). The 9 previously identified SNPs are associated with GD in the Chinese Han population. And, gender and age may not influence the associations between the 9 SNPs and GD. © 2014, E-Century Publishing Corporation. All Rights Reserved. Source

Hong J.,Shanghai Institute of Endocrinology and Metabolism | Shi J.,Shanghai Institute of Endocrinology and Metabolism | Qi L.,Brigham and Womens Hospital | Cui B.,Shanghai JiaoTong University | And 12 more authors.
International Journal of Obesity | Year: 2013

Objective:Birth weight reflects prenatal metabolic adaption and has been related to later-life obesity risk. This study aimed to evaluate whether birth weight modifies the effect of genetic susceptibility on obesity risk in young Chinese.Methods:We recruited 540 young (14-30 years) and obese patients (body mass index, BMI≥30 kg m -2), and 500 age- and sex-matched normal-weight healthy individuals (BMI<23 kg m -2). We genotyped 23 BMI-associated genetic variants identified from recent genome-wide association studies (GWAS) in Caucasians with European ancestry with minor allele frequency>0.05 in HapMap Han Chinese in Beijing, China.Results:Six loci, including SEC16B, GNPDA2, BDNF, FTO, MC4R and TMEM160, were significantly associated with obesity risk, with odds ratio from 1.314 to 1.701. The 23 risk loci accounted for 6.38% of the genetic variance in obesity. We created two genetic risk scores (GRSs) by summing the risk alleles of all 23 (GRS1) and 6 obesity-associated (GRS2) genetic variants. Prediction of obesity was significantly improved (P<0.001) when the GRS1 and GRS2 were added to a model with age and gender, with improvement of discrimination for obesity by 0.8% and 2.7%, respectively. In addition, we found that the two GRSs interacted with birth weight in relation to obesity (P interaction <0.001). The genetic effect appeared to be more pronounced in individuals with normal range of birth weight (25-75%) than those with either low (<25%) or high (>75%) birth weight.Conclusion:We confirmed the associations of the single-nucleotide polymorphism tagging six loci reported in recent GWAS with obesity in young Chinese. Our data also suggest birth weight may significantly modify genetic susceptibility to obesity risk. © 2013 Macmillan Publishers Limited. Source

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