The present study aimed to investigate the contribution of DNA methylation of the protein tyrosine phosphatase, non-receptor type 1 (PTPN1) gene to the susceptibility to type 2 diabetes (T2D). Peripheral blood mononuclear cells (PBMCs) were collected from 97 patients with T2D and 97 age- and gender-matched controls. DNA methylation of the PTPN1 gene promoter was evaluated by bisulfite pyrosequencing. Independent sample t-tests were used to compare the differences in the PTPN1 promoter and other phenotypes between the patients with T2D and the controls. The results indicated a significant correlation between PTPN1 promoter methylation and the risk of T2D. Additionally, a breakdown analysis by gender revealed that PTPN1 methylation was associated with an increased risk of T2D in females. Furthermore, low-density lipoprotein (r=-0.183, P=0.046) and total cholesterol (r=-0.310, P=0.001) were inversely associated with PTPN1 methylation in females. In conclusion, the results indicate that elevated PTPN1 promoter methylation is a risk factor for T2D in the female Chinese population.
Objective To study the relationship between the prevalence of thyroid dysfunction and components of metabolic syndrome.Methods A total of 10 461 working and retired employees aged 20 to 90 years in a Petrochemical Corporation in Ningbo were included.Body mass index ( BMI),waist circumference,blood pressure,fasting blood glucose,blood lipid profile,serum thyroid-stimulating hormone (TSH),free thyroxine ( FT4 ),and free triiodothyronine (FT3 ) were measured in all subjects. Metabolic syndrome was diagnosed according to the International Diabetes Federation(IDF) criteria.Results ( 1 ) The prevalences of metabolic syndrome and overall thyroid dysfunction were 10.2％ and 4.6％,respectively. ( 2 ) 18.1％ petrochemical employees had abdominal obesity with at least one component of metabolic syndrome.( 3 ) There was no significant difference in the prevalence of metabolic syndrome among the groups with lowered,normal,and elevated TSH. (4) Logistic regression analysis revealed that lowered high density lipoprotein cholesterol ( HDL-C ) was associated with lowered TSH ( OR =0.313,95％ CI 0.184-0.530 ),and raised triglyceride was associated with elevated TSH ( OR =0.767,95％ CI 0.595-0.991 ). ( 5 ) There were significant associations between serum TSH levels and lipid parameters such as total cholesterol in males,triglyceride and low density lipoprotein cholesterol in females,and HDL-C in both genders.Conclusion The prevalence of thyroid dysfunction was not associated with central obesity,hypertension,and hyperglycemia.Lipid disorder was correlated with serum TSH levels.
Key words:
Thyroid dysfunction; Metabolic Syndrome; Epidemiology
The goal of our study is to investigate the associations between 18 candidate genetic markers and overweight/obesity.A total of 72 eligible articles were retrieved from literature databases including PubMed, Embase, SpingerLink, Web of Science, Chinese National Knowledge Infrastructure (CNKI), and Wanfang. Meta-analyses of 18 genetic markers among 56,738 controls and 48,148 overweight/obese persons were done by Review Manager 5.0.Our results showed that SH2B1 rs7498665 polymorphism was significantly associated with the risk of overweight/obesity (overall odds ratio (OR) = 1.21, 95% confidence interval (CI) = 1.09-1.34, P = 0.0004). Increased risk of overweight/obesity was also observed in FAIM2 rs7138803 polymorphism (overall OR = 1.11, 95% CI = 1.01-1.22, P = 0.04).Our meta-analyses have shown the important role of 2 polymorphisms (SH2B1 rs7498665 and FAIM2 rs7138803) in the development of overweight/obesity. This study highlighted the importance of above two candidate genes (SH2B1 and FAIM2) in the risk of overweight/obesity.The virtual slide(s) for this article can be found here: http://www.diagnosticpathology.diagnomx.eu/vs/2785487401176182.
Type 2 diabetes mellitus (T2DM) is a glucose metabolic disorder driven by both genetic and environmental factors. Recent DNA methylation studies have established that T2DM may be contributed by environmental factors through the regulation of DNA methylation. Human and animal model studies have made much progress on the interaction between DNA methylation of T2DM genes and environmental factors in multiple tissues. Current studies on DNA methylation of T2DM genes mainly focus on glucose and energy metabolism, inflammation, and so on. This review comprehensively introduces the DNA methylation studies for the genes involved in T2DM and its related environmental factors.
Retrograde ejaculation (RE), known as one of the late complications of diabetes mellitus, is rarely a presenting symptom in the diagnosis of diabetes. A 30-year-old male presented with a progressive decline in ejaculate over 2-month. Lab results revealed a high random blood glucose level (425 mg/dL). A substantial number of sperm were found in the post-ejaculate urine specimens, confirming a diagnosis of RE. Further lab tests revealed an hemoglobin-A1c (HbA1c) of 12.7%, with negative results for antibodies to glutamic acid decarboxylase, insulin antigen-2, insulin receptor and islet cell, consistent with a diagnosis of type 2 diabetes mellitus (T2DM). Insulin glargine and oral anti-hyperglycemic agents were initiated. Also, imipramine and pseudoephedrine were prescribed for 4-week and then discontinued, as no positive effect on ejaculation was seen. At the 36-month follow-up, the patient had a normal glucose level with HbA1c <6.5%. However, RE persisted. RE is commonly seen as a late-stage complication among T2DM. We presented a rare case where RE was the first referred symptom of T2DM and RE persisted even after adequate control of glycemia.
Background . Controversy remains for the association between hepatocyte nuclear factor 4α ( HNF-4α ) P2 promoter polymorphism rs1884613 and type 2 diabetes (T2D). There was no association test of this polymorphism with prediabetes and T2D in the Chinese population. Moreover, an updated meta-analysis in various ethnic groups is needed to establish the contribution of rs1884613 to T2D risk. Methods . Using the Sequenom MassARRAY platform approach, we genotyped rs1884613 of HNF-4α in the P2 promoter region among 490 T2D patients, 471 individuals with prediabetes, and 575 healthy controls. All the individuals were recruited from 16 community health service centers in Nanshan district in Shenzhen province. Using STATA 11.0 software, meta-analysis was performed to summarize the overall contribution of rs1884613 to T2D risk. Results . Polymorphism rs1884613 was associated with genetic susceptibility to prediabetes in the whole samples (OR = 1.40, 95% CI = 1.16–1.68,P=0.0001) and the female subgrouped samples (OR = 1.48, 95% CI = 1.14–1.92,P=0.003) after adjusting for age and body mass index (BMI). In contrast, there was no association of rs1884613 with T2D in the whole samples and male in our case-control study and meta-analysis. Conclusions . Our results suggest that rs1884613 contributes to susceptibility to prediabetes, whereas this polymorphism may not play an important role in the development of T2D.
The correlation between diabetes and systematic well-being on human life has long established. As a common complication of diabetes, the prevalence of diabetic nephropathy (DN) has been increasing globally. DN is known to be a major cause of end-stage kidney disease (ESKD). Till now, the molecular mechanisms for DN have not been fully explored and the effective therapies are still lacking. Noncoding RNAs are a class of RNAs produced by genome transcription that cannot be translated into proteins. It has been documented that ncRNAs participate in the pathogenesis of DN by regulating inflammation, apoptosis, autophagy, cell proliferation, and other pathological processes. In this review, the pathological roles and diagnostic and therapeutic potential of three types of ncRNAs (microRNA, long noncoding RNA, and circular RNA) in the progression of DN are summarized and illustrated.
The association of the fat mass and obesity-associated gene (FTO) rs11642015 polymorphism with prediabetes, type 2 diabetes and obesity in certain populations has not been previously reported. A population-based study was conducted that included 490 type 2 diabetic, 471 prediabetic and 575 normal subjects. The main outcomes of the study were prediabetes, type 2 diabetes and obesity. Binary logistic regression was performed to estimate the association of FTO rs11642015 with the risk of prediabetes, type 2 diabetes and obesity following adjustment for the corresponding confounders. A meta-analysis was also conducted to evaluate the association between FTO rs11642015 and obesity. FTO rs11642015 was significantly associated with prediabetes in the whole sample under the additive model [odds ratio (OR), 1.50; 95% confidence interval (CI), 1.17-1.93; P=0.002], particularly in females. The polymorphism remained consistently significant following adjustment for age and body mass index (BMI), showing an increased prediabetes risk with an additive effect (OR, 1.55; 95% CI, 1.19-2.01; P=0.001). In addition, a significant association was found for rs11642015 with prediabetes and type 2 diabetes under the dominant model. However, under the stringent Bonferroni's correction there was no evidence of positive associations for FTO rs11642015 with obesity in the whole sample, females or males. Findings of the meta-analysis showed that FTO rs11642015 was not predisposed to obesity. In conclusion, the T allele of FTO rs11642015 is positively associated with an increased risk of prediabetes, even after adjustment for age and BMI, particularly in females. Subjects carrying the CT + TT genotype are predisposed to prediabetes and type 2 diabetes. Therefore, results of the population-based study and follow-up meta-analysis suggested that FTO rs11642015 is not significantly associated with susceptibility to obesity.
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