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The rs2304256 Polymorphism in TYK2 Gene Is Associated with Protection for Type 1 Diabetes Mellitus
Felipe Mateus Pellenz, Cristine Dieter, Guilherme Coutinho Kullmann Duarte, Luís Henrique Canani, Bianca Marmontel de Souza, Daisy Crispim
Diabetes Metab J. 2021;45(6):899-908.   Published online May 24, 2021
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  • 159 Download
  • 3 Web of Science
  • 3 Crossref
Graphical AbstractGraphical Abstract AbstractAbstract PDFPubReader   ePub   
Tyrosine kinase 2 (TYK2) is a candidate gene for type 1 diabetes mellitus (T1DM) since it plays an important role in regulating apoptotic and pro-inflammatory pathways in pancreatic β-cells through modulation of the type I interferon signaling pathway. The rs2304256 single nucleotide polymorphism (SNP) in TYK2 gene has been associated with protection for different autoimmune diseases. However, to date, only two studies have evaluated the association between this SNP and T1DM, with discordant results. This study thus aimed to investigate the association between the TYK2 rs2304256 SNP and T1DM in a Southern Brazilian population.
This case-control study comprised 478 patients with T1DM and 518 non-diabetic subjects. The rs2304256 (C/A) SNP was genotyped by real-time polymerase chain reaction technique using TaqMan minor groove binder (MGB) probes.
Genotype and allele frequencies of the rs2304256 SNP differed between T1DM patients and non-diabetic subjects (P<0.0001 and P=0.001, respectively). Furthermore, the A allele was associated with protection against T1DM under recessive (odds ratio [OR], 0.482; 95% confidence interval [CI], 0.288 to 0.806) and additive (OR, 0.470; 95% CI, 0.278 to 0.794) inheritance models, adjusting for human leukocyte antigen (HLA) DR/DQ genotypes, gender, and ethnicity.
The A/A genotype of TYK2 rs2304256 SNP is associated with protection against T1DM in a Southern Brazilian population.


Citations to this article as recorded by  
  • Associations of genetic variants within TYK2 with pulmonary tuberculosis among Chinese population
    Mingwu Zhang, Zhengwei Liu, Yelei Zhu, Kunyang Wu, Lin Zhou, Ying Peng, Junhang Pan, Bin Chen, Xiaomeng Wang, Songhua Chen
    Molecular Genetics & Genomic Medicine.2024;[Epub]     CrossRef
  • Host genetic variants associated with COVID-19 reconsidered in a Slovak cohort
    Maria Skerenova, Michal Cibulka, Zuzana Dankova, Veronika Holubekova, Zuzana Kolkova, Vincent Lucansky, Dana Dvorska, Andrea Kapinova, Michaela Krivosova, Martin Petras, Eva Baranovicova, Ivana Baranova, Elena Novakova, Peter Liptak, Peter Banovcin, Anna
    Advances in Medical Sciences.2024; 69(1): 198.     CrossRef
  • Cross-Domain Text Mining of Pathophysiological Processes Associated with Diabetic Kidney Disease
    Krutika Patidar, Jennifer H. Deng, Cassie S. Mitchell, Ashlee N. Ford Versypt
    International Journal of Molecular Sciences.2024; 25(8): 4503.     CrossRef
Article image
Association of Combined TCF7L2 and KCNQ1 Gene Polymorphisms with Diabetic Micro- and Macrovascular Complications in Type 2 Diabetes Mellitus
Rujikorn Rattanatham, Nongnuch Settasatian, Nantarat Komanasin, Upa Kukongviriyapan, Kittisak Sawanyawisuth, Phongsak Intharaphet, Vichai Senthong, Chatri Settasatian
Diabetes Metab J. 2021;45(4):578-593.   Published online March 22, 2021
  • 5,940 View
  • 148 Download
  • 8 Web of Science
  • 7 Crossref
AbstractAbstract PDFSupplementary MaterialPubReader   ePub   
Vascular complications are the major morbid consequences of type 2 diabetes mellitus (T2DM). The transcription factor 7-like 2 (TCF7L2), potassium voltage-gated channel subfamily Q member 1 (KCNQ1), and inwardly-rectifying potassium channel, subfamily J, member 11 gene (KCNJ11) are common T2DM susceptibility genes in various populations. However, the associations between polymorphisms in these genes and diabetic complications are controversial. This study aimed to investigate the effects of combined gene-polymorphisms within TCF7L2, KCNQ1, and KCNJ11 on vascular complications in Thai subjects with T2DM.
We conducted a case-control study comprising 960 T2DM patients and 740 non-diabetes controls. Single nucleotide polymorphisms in TCF7L2, KCNQ1, and KCNJ11 were genotyped and evaluated for their association with diabetic vascular complications.
The gene variants TCF7L2 rs290487-T, KCNQ1 rs2237892-C, and KCNQ1 rs2237897-C were associated with increased risk of T2DM. TCF7L2 rs7903146-C, TCF7L2 rs290487-C, KCNQ1 rs2237892-T, and KCNQ1 rs2237897-T revealed an association with hypertension. The specific combination of risk-alleles that have effects on T2DM and hypertension, TCF7L2 rs7903146-C, KCNQ1 rs2237892-C, and KCNQ1 rs2237897-T, as genetic risk score (GRS), pronounced significant association with coronary artery disease (CAD), cumulative nephropathy and CAD, and cumulative microvascular and macrovascular complications (respective odds ratios [ORs] with 95% confidence interval [95% CI], comparing between GRS 2–3 and GRS 5–6, were 7.31 [2.03 to 26.35], 3.92 [1.75 to 8.76], and 2.33 [1.13 to 4.79]).
This study demonstrated, for the first time, the effect conferred by specific combined genetic variants in TCF7L2 and KCNQ1 on diabetic vascular complications, predominantly with nephropathy and CAD. Such a specific pattern of gene variant combination may implicate in the progression of T2DM and life-threatening vascular complications.


Citations to this article as recorded by  
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    Amal F. Alshammary, Malak Mohammed Al-Hakeem, Imran Ali Khan
    Genes.2023; 14(4): 924.     CrossRef
  • Association between KCNJ11 E23K polymorphism and the risk of type 2 diabetes mellitus: A global meta-analysis
    Yaxuan Ren, Wenfei Zhu, Jikang Shi, Aiyu Shao, Yi Cheng, Yawen Liu
    Journal of Diabetes and its Complications.2022; 36(5): 108170.     CrossRef
  • Association between carotid atherosclerosis and presence of intracranial atherosclerosis using three-dimensional high-resolution vessel wall magnetic resonance imaging in asymptomatic patients with type 2 diabetes
    Ji Eun Jun, You-Cheol Hwang, Kyu Jeong Ahn, Ho Yeon Chung, Geon-Ho Jahng, Soonchan Park, In-Kyung Jeong, Chang-Woo Ryu
    Diabetes Research and Clinical Practice.2022; 191: 110067.     CrossRef
  • Multiple Single Nucleotide Polymorphism Testing Improves the Prediction of Diabetic Retinopathy Risk with Type 2 Diabetes Mellitus
    Yu-Ting Hsiao, Feng-Chih Shen, Shao-Wen Weng, Pei-Wen Wang, Yung-Jen Chen, Jong-Jer Lee
    Journal of Personalized Medicine.2021; 11(8): 689.     CrossRef
  • Oxidative Stress Genes in Diabetes Mellitus Type 2: Association with Diabetic Kidney Disease
    Athanasios Roumeliotis, Stefanos Roumeliotis, Fotis Tsetsos, Marianthi Georgitsi, Panagiotis I. Georgianos, Aikaterini Stamou, Anna Vasilakou, Kalliopi Kotsa, Xanthippi Tsekmekidou, Peristera Paschou, Stylianos Panagoutsos, Vassilios Liakopoulos, Elena Az
    Oxidative Medicine and Cellular Longevity.2021; 2021: 1.     CrossRef
  • Analysis of the association of polymorphisms of genes markers functions of endothelium and vascular-plate hemostasis with development of diabetic foot syndrome
    N. I. Troitskaya, K. G. Shapovalov, V. A. Mudrov
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Resistin in Rodents and Humans
Hyeong Kyu Park, Rexford S. Ahima
Diabetes Metab J. 2013;37(6):404-414.   Published online December 12, 2013
  • 5,863 View
  • 55 Download
  • 122 Crossref
AbstractAbstract PDFPubReader   

Obesity is characterized by excess accumulation of lipids in adipose tissue and other organs, and chronic inflammation associated with insulin resistance and an increased risk of type 2 diabetes. Obesity, type 2 diabetes, and cardiovascular diseases are major health concerns. Resistin was first discovered as an adipose-secreted hormone (adipokine) linked to obesity and insulin resistance in rodents. Adipocyte-derived resistin is increased in obese rodents and strongly related to insulin resistance. However, in contrast to rodents, resistin is expressed and secreted from macrophages in humans and is increased in inflammatory conditions. Some studies have also suggested an association between increased resistin levels and insulin resistance, diabetes and cardiovascular disease. Genetic studies have provided additional evidence for a role of resistin in insulin resistance and inflammation. Resistin appears to mediate the pathogenesis of atherosclerosis by promoting endothelial dysfunction, vascular smooth muscle cell proliferation, arterial inflammation, and formation of foam cells. Indeed, resistin is predictive of atherosclerosis and poor clinical outcomes in patients with coronary artery disease and ischemic stroke. There is also growing evidence that elevated resistin is associated with the development of heart failure. This review will focus on the biology of resistin in rodents and humans, and evidence linking resistin with type 2 diabetes, atherosclerosis, and cardiovascular disease.


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    Alan Chait, Laura J. den Hartigh
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Sulwon Lecture 2011
Post-Renal Transplant Diabetes Mellitus in Korean Subjects: Superimposition of Transplant-Related Immunosuppressant Factors on Genetic and Type 2 Diabetic Risk Factors
Hyun Chul Lee
Diabetes Metab J. 2012;36(3):199-206.   Published online June 14, 2012
  • 3,703 View
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AbstractAbstract PDFPubReader   

Postrenal transplantation diabetes mellitus (PTDM), or new-onset diabetes after organ transplantation, is an important chronic transplant-associated complication. Similar to type 2 diabetes, decreased insulin secretion and increased insulin resistance are important to the pathophysiologic mechanism behind the development of PTDM. However, β-cell dysfunction rather than insulin resistance seems to be a greater contributing factor in the development of PTDM. Increased age, family history of diabetes, ethnicity, genetic variation, obesity, and hepatitis C are partially accountable for an increased underlying risk of PTDM in renal allograft recipients. In addition, the use of and kinds of immunosuppressive agents are key transplant-associated risk factors. Recently, a number of genetic variants or polymorphisms susceptible to immunosuppressants have been reported to be associated with calcineurin inhibition-induced β-cell dysfunction. The identification of high risk factors of PTDM would help prevent PTDM and improve long-term patient outcomes by allowing for personalized immunosuppressant regimens and by managing cardiovascular risk factors.


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