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Open access

Ping Li, Fei Cheng, and Lei Xiu

Objective

This study sought to determine the effect of the recombinant human growth hormone (rhGH) treatment of Turner syndrome (TS) on height outcome.

Methods

We searched in MEDLINE, EMBASE and Cochrane Central Register of Controlled Trials and Cochrane Database of Systematic Reviews. A literature search identified 640 records. After screening and full-text assessment, 11 records were included in the systematic review. Methodological quality was assessed using the Cochrane Risk of Bias tool. RevMan 5.3 software was used for meta-analysis. We also assessed the quality of evidence with the GRADE system.

Results

Compared with controls, rhGH therapy led to increased final height (MD = 7.22 cm, 95% CI 5.27–9.18, P < 0.001, I2 = 4%; P = 0.18), height standard deviation (HtSDS) (SMD = 1.22, 95% CI 0.88–1.56, P < 0.001, I2 = 49%; P = 0.14) and height velocity (HV) (MD 2.68 cm/year; 95% CI 2.34, 3.02; P < 0.001, I2 = 0%; P = 0.72). There was a small increase in bone age (SMD 0.32 years; 95% CI 0.1, 0.54; P = 0.004, I2 = 73%; P = 0.02) after rhGH therapy for 12 months. What is more, the rhGH/oxandrolone combination therapy suggested greater final height (MD 2.46 cm; 95% CI 0.73, 4.18; P = 0.005, I2 = 32%; P = 0.22), increase and faster HV (SMD 1.67 cm/year; 95% CI 1.03, 2.31; P < 0.03, I2 = 80%; P < 0.001), with no significant increase in HtSDS and bone maturation compared with rhGH therapy alone.

Conclusions

For TS patients, rhGH alone or with concomitant use of oxandrolone treatment had advantages on final height.

Open access

Jun-Xin Yan, Bin-Jing Pan, Ping-Ping Zhao, Li-Ting Wang, Jing-Fang Liu, and Song-Bo Fu

Objective

Previous studies have shown the correlations between serum ferritin and non-alcoholic fatty liver disease (NAFLD) or diabetes. However, this relationship remains unclear in patients with type 2 diabetes (T2DM) with NAFLD. Therefore, this study aimed to elaborate the relationship between serum ferritin levels and NAFLD in middle-aged and older patients with T2DM and further explored the biomarkers for NAFLD in T2DM.

Methods

A total of 805 middle-aged and older patients with T2DM were divided into NAFLD and non-NAFLD groups, and their serum ferritin levels were compared. Next, NAFLD group were divided into five subgroups according to the quintile levels of serum ferritin, and the differences in the constituent ratios of NAFLD were analyzed. A logistic regression analysis was performed to determine the risk factors for NAFLD in patients with T2DM.

Results

The serum ferritin levels were significantly higher in T2DM patients with NAFLD (168.47 (103.78, 248.00) ng/mL) than in the non-NAFLD patients (121.19 (76.97, 208.39) ng/mL). The constituent ratios of NAFLD were significantly higher in the F5 and F4 groups than in the F2 or F1 groups (22.70 and 22.70% vs. 15.90 and 16.90%, respectively; P < 0.05). Binary logistic regression analysis showed that serum ferritin (P = 0.001) was an independent risk factor for NAFLD in patients with T2DM.

Conclusions

Serum ferritin levels were significantly increased in T2DM with NAFLD, and the constituent ratios of NAFLD increased gradually along with the increased levels of serum ferritin. Thus, serum ferritin is an independent risk factor for NAFLD in patients with T2DM.

Open access

Lei Lei, Yi-Hua Bai, Hong-Ying Jiang, Ting He, Meng Li, and Jia-Ping Wang

N6-methyladenosine (m6A) methylation has been reported to play a role in type 2 diabetes (T2D). However, the key component of m6A methylation has not been well explored in T2D. This study investigates the biological role and the underlying mechanism of m6A methylation genes in T2D. The Gene Expression Omnibus (GEO) database combined with the m6A methylation and transcriptome data of T2D patients were used to identify m6A methylation differentially expressed genes (mMDEGs). Ingenuity pathway analysis (IPA) was used to predict T2D-related differentially expressed genes (DEGs). Gene ontology (GO) term enrichment and the Kyoto Encyclopedia of Genes and Genomes (KEGG) were used to determine the biological functions of mMDEGs. Gene set enrichment analysis (GSEA) was performed to further confirm the functional enrichment of mMDEGs and determine candidate hub genes. The least absolute shrinkage and selection operator (LASSO) regression analysis was carried out to screen for the best predictors of T2D, and RT-PCR and Western blot were used to verify the expression of the predictors. A total of 194 overlapping mMDEGs were detected. GO, KEGG, and GSEA analysis showed that mMDEGs were enriched in T2D and insulin signaling pathways, where the insulin gene (INS), the type 2 membranal glycoprotein gene (MAFA), and hexokinase 2 (HK2) gene were found. The LASSO regression analysis of candidate hub genes showed that the INS gene could be invoked as a predictive hub gene for T2D. INS, MAFA,and HK2 genes participate in the T2D disease process, but INS can better predict the occurrence of T2D.

Open access

Ju-shuang Li, Tao Wang, Jing-jing Zuo, Cheng-nan Guo, Fang Peng, Shu-zhen Zhao, Hui-hui Li, Xiang-qing Hou, Yuan Lan, Ya-ping Wei, Chao Zheng, and Guang-yun Mao

Diabetic retinopathy (DR), the most common microvascular complication of diabetes and leading cause of visual impairment in adults worldwide, is suggested to be linked to abnormal lipid metabolism. The present study aims to comprehensively investigate the relationship between n-6 polyunsaturated fatty acids (PUFAs) and DR. This was a propensity score matching based case–control study, including 69 pairs of DR patients and type 2 diabetic patients without DR with mean age of 56.7 ± 9.2 years. Five n-6 PUFAs were determined by UPLC-ESI-MS/MS system. Principle component regression (PCR) and multiple conditional logistic regression models were used to investigate the association of DR risk with n-6 PUFAs depending on independent training and testing sets, respectively. According to locally weighted regression model, we observed obvious negative correlation between levels of five n-6 PUFAs (linoleic acid, γ-linolenic acid, eicosadienoic acid, dihomo-γ-linolenic acid and arachidonicacid) and DR. Based on multiple PCR model, we also observed significant negative association between the five n-6 PUFAs and DR with adjusted OR (95% CI) as 0.62 (0.43,0.87). When being evaluated depending on the testing set, the association was still existed, and PCR model had excellent classification performance, in which area under the curve (AUC) was 0.88 (95% CI: 0.78, 0.99). In addition, the model also had valid calibration with a non-significant Hosmer–Lemeshow Chi-square of 9.44 (P = 0.307) in the testing set. n-6 PUFAs were inversely associated with the presence of DR, and the principle component could be potential indicator in distinguishing DR from other T2D patients.

Open access

Yanmei Lou, Yanyan Zhang, Ping Zhao, Pei Qin, Changyi Wang, Jianping Ma, Xiaolin Peng, Hongen Chen, Dan Zhao, Shan Xu, Li Wang, Ming Zhang, Dongsheng Hu, and Fulan Hu

We aimed to assess the association between fasting plasma glucose (FPG) change trajectory and incident hypertension among Chinese population. This cohort study included 11,791 adults aged 18–80 years without hypertension at first entry and who completed at least four follow-ups between 2009 and 2016. Logistic regression was used to estimate odds ratios (ORs) and 95% CIs for the association between FPG change trajectory and probability of hypertension. During a median follow-up of 5.10 years (total person–years 61,887.76), hypertension developed in 2177 participants. After adjusting for baseline potential confounders, the probability of hypertension increased with the increasing FPG change trajectory (adjusted OR (aOR) 1.22, 95% CI 1.07–1.40), bell-shape trajectory (aOR 1.15, 95% CI 1.02–1.30) and other-shape trajectory (aOR 1.13, 95% CI 1.02–1.25) which showed a higher variability of FPG compared to the decreasing group. In addition, the increasing FPG change trajectory was associated with a higher probability of hypertension compared with the decreasing group regardless of age and BMI but was only significant in males and in those with normal FPG at baseline. Our study indicates that the increasing FPG change trajectory determines the highest risk of hypertension, demonstrating the importance of maintaining low and stable levels of FPG, especially in males and in those with normal FPG.