The association studies ofADIPOQwith type 2 diabetes mellitus in Chinese populations

2012 ◽  
Vol 28 (7) ◽  
pp. 551-559 ◽  
Author(s):  
Yiping Li ◽  
Ying Yang ◽  
Li Shi ◽  
Xianli Li ◽  
Ying Zhang ◽  
...  
2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
Ming-Kai Tsai ◽  
Hui-Min David Wang ◽  
Jeng-Chuan Shiang ◽  
I-Hung Chen ◽  
Chih-Chiang Wang ◽  
...  

Diabetes is a serious global health problem. Large-scale genome-wide association studies identified loci for type 2 diabetes mellitus (T2DM), including adiponectin (ADIPOQ) gene and transcription factor 7-like 2 (TCF7L2), but few studies clarified the effect of genetic polymorphisms ofADIPOQandTCF7L2on risk of T2DM. We attempted to elucidate association between T2DM and polymorphic variations of both in Taiwan’s Chinese Han population, with our retrospective case-control study genotyping single nucleotide polymorphisms (SNPs) inADIPOQandTCF7L2genes both in 149 T2DM patients and in 139 healthy controls from Taiwan. Statistical analysis gauged association of these polymorphisms with risk of T2DM to showADIPOQrs1501299 polymorphism variations strongly correlated with T2DM risk(P=0.042), with rs2241766 polymorphism being not associated with T2DM(P=0.967). However, both polymorphisms rs7903146 and rs12255372 ofTCF7L2were rarely detected in Taiwanese people. This study avers thatADIPOQrs1501299 polymorphism contributes to risk of T2DM in the Taiwanese population.


2015 ◽  
Vol 2015 ◽  
pp. 1-7 ◽  
Author(s):  
Habiba Alsafar ◽  
Ahmed Hassoun ◽  
Shaikha Almazrouei ◽  
Wala Kamal ◽  
Mustafa Almaini ◽  
...  

The association of Angiotensin Converting Enzyme (ACE) insertion-deletion (I/D) polymorphism with Type 2 Diabetes Mellitus (T2DM) and hypertension has been extensively studied throughout various ethnic populations but largely with inconsistent findings. We investigated these associations in Emirati population and their interaction with obesity status. Saliva samples were collected from a total of 564 Emiratis (277 T2DM and 297 healthy). DNA was extracted and the samples were genotyped forACEI/D polymorphism by a PCR based method followed by gel electrophoresis. Upon evaluation of theACEI/D polymorphism amongst all T2DM, hypertensive patients, and respective controls regardless of obesity status,ACEDD genotype was not found to be associated with either T2DM [odds ratio (OR) = 1.34,p=0.086] or hypertension [odd ratio (OR) = 1.02,p=0.93]. When the genetic variants amongst the nonobese and obese population were analyzed separately, the risk genotypeACEDD conferred significantly increased risk of hypertension in nonobese population [odds ratio (OR) = 1.80,p=0.02] but was found to be protective against the hypertension in the obese group ((OR) = 0.54,p=0.01). However, there was no effect of obesity status on the association ofACEgenotypes with T2DM. The risk of hypertension associated withACEDD is modulated by obesity status and hence future genetic association studies should take obesity into account for the interpretation of data. We also confirmed thatACEI/D polymorphism is not associated with T2DM risk in Emirati population.


Author(s):  
Angela W.S. Lee ◽  
Roger D. Cox

The use of mouse models in medical research has greatly contributed to our understanding of the development of type 2 diabetes mellitus and the mechanisms of disease progression in the context of insulin resistance and β-cell dysfunction. Maintenance of glucose homeostasis involves a complex interplay of many genes and their actions in response to exogenous stimuli. In recent years, the availability of large population-based cohorts and the capacity to genotype enormous numbers of common genetic variants have driven various large-scale genome-wide association studies, which has greatly accelerated the identification of novel genes likely to be involved in the development of type 2 diabetes. The increasing demand for verifying novel genes is met by the timely development of new mouse resources established as various collaborative projects involving major transgenic and phenotyping centres and laboratories worldwide. The surge of new data will ultimately enable translational research into potential improvement and refinement of current type 2 diabetes therapy options, and hopefully restore quality of life for patients.


2018 ◽  
Vol 17 (1) ◽  
pp. 16-24 ◽  
Author(s):  
Sara Mankoč Ramuš ◽  
Daniel Petrovič

Atherosclerosis and its cardiovascular complications are the main cause of death in diabetic patients. Patients with diabetes mellitus have a greater than 10-fold risk of cardiovascular disease in their lifetime. The carotid Intima-Media Thickness (cIMT), a surrogate marker for the presence and progression of atherosclerosis, predicts future cardiovascular events in asymptomatic subjects with Type 2 Diabetes Mellitus (T2DM). This review focuses on genetic variants that contribute to the pathobiology of subclinical atherosclerosis in the setting of T2DM. Specifically, we devoted our attention to wellstudied genes selected for their relevance for atherosclerosis. These include: The Renin-Angiotensin- Aldosterone System (RAAS), Apolipoprotein E (ApoE), Methylenetetrahydrofolate Reductase (MTHFR) and pro-inflammatory genes. </P><P> The ever-growing availability of advanced genotyping technologies has made Genome-Wide Association Studies (GWAS) possible. Although several bioinformatics tools have been developed to manage and interpret the huge amounts of data produced, there has been limited success in the many attempts to uncover the biological meaning of the novel susceptibility loci for atherosclerosis.


2021 ◽  
Author(s):  
Raymond Noordam ◽  
Kristi Läll ◽  
Roelof AJ Smit ◽  
Triin Laisk ◽  
Ruth JF Loos ◽  
...  

<a>The pathogenesis of type 2 diabetes mellitus (T2D) might change with increasing age. Here, we used a stratification based on age of diagnosis, to gain insight in the genetics and causal risk factors of T2D across different age groups. </a>We performed genome-wide association studies (GWAS) on T2D and T2D subgroups based on age of diagnosis (<50 years, 50-60, 60-70, and >70 years; total of 24,986 cases). As controls, we used participants who were at least 70 years of age at the end of follow-up without developing T2D (N = 187,130). GWAS identified 208 independent lead SNPs mapping to 69 loci associated with T2D (p<1.0e-8). Among others, SNPs mapped to <i>CDKN2B-AS1</i> and multiple independent SNPs mapped to <i>TCF7L2</i> were more strongly associated to cases diagnosed after age 70 years than to cases diagnosed before age 50 years. Based on the different case groups, we performed two-sample Mendelian Randomization.<b> </b>Most notably, we observed that of the investigated risk factors the association between body mass index and T2D attenuated with increasing age of diagnosis. Collectively, stratification of T2D based on age of diagnosis reveals subgroup-specific genetics and causal determinants, supporting the hypothesis that the pathogenesis of T2D changes with increasing age.


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