Diabetes & Metabolism Journal

Original Article

Type 1 Diabetes
A New Tool to Identify Pediatric Patients with Atypical Diabetes Associated with Gene Polymorphisms: Sophie Welsch, Antoine Harvengt, Paola Gallo, Manon Martin, Dominique Beckers, Thierry Mouraux, Nicole Seret, Marie-Christine Lebrethon, Raphaël Helaers, Pascal Brouillard, Miikka Vikkula, Philippe A. Lysy; Received May 26, 2023 Accepted November 25, 2023 Published online March 22, 2024; DOI: https://doi.org/10.4093/dmj.2023.0166 [Epub ahead of print]

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Abstract PDF Supplementary Material PubReader ePub: Background
Recent diabetes subclassifications have improved the differentiation between patients with type 1 diabetes mellitus (T1DM) and type 2 diabetes mellitus despite several overlapping features, yet without considering genetic forms of diabetes. We sought to facilitate the identification of monogenic diabetes by creating a new tool that we validated in a pediatric maturity-onset diabetes of the young (MODY) cohort.
Methods
We first created the DIAgnose MOnogenic DIAbetes (DIAMODIA) criteria based on the pre-existing, but incomplete, MODY calculator. This new score is composed of four strong and five weak criteria, with patients having to display at least one weak and one strong criterion.
Results
The effectiveness of the DIAMODIA criteria was evaluated in two patient cohorts, the first consisting of patients with confirmed MODY diabetes (n=34) and the second of patients with T1DM (n=390). These DIAMODIA criteria successfully detected 100% of MODY patients. Multiple correspondence analysis performed on the MODY and T1DM cohorts enabled us to differentiate MODY patients from T1DM. The three most relevant variables to distinguish a MODY from T1DM profile were: lower insulin-dose adjusted A1c score ≤9, glycemic target-adjusted A1c score ≤4.5, and absence of three anti-islet cell autoantibodies.
Conclusion
We validated the DIAMODIA criteria, as it effectively identified all monogenic diabetes patients (MODY cohort) and succeeded to differentiate T1DM from MODY patients. The creation of this new and effective tool is likely to facilitate the characterization and therapeutic management of patients with atypical diabetes, and promptly referring them for genetic testing which would markedly improve clinical care and counseling, as well.

Brief Report

Genetics
Clinical Characteristics of Diabetes in People with Mitochondrial DNA 3243A>G Mutation in Korea: Eun Hoo Rho, Sang Ik Baek, Heerah Lee, Moon-Woo Seong, Jong-Hee Chae, Kyong Soo Park, Soo Heon Kwak; Received March 10, 2023 Accepted July 20, 2023 Published online February 1, 2024; DOI: https://doi.org/10.4093/dmj.2023.0078 [Epub ahead of print]

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Abstract PDF Supplementary Material PubReader ePub: Maternally inherited diabetes and deafness (MIDD) is a rare mitochondrial disorder primarily resulting from m.3243A>G mutation. The clinical characteristics of MIDD exhibit significant heterogeneity. Our study aims to delineate these characteristics and determine the potential correlation with m.3243A>G heteroplasmy levels. This retrospective, descriptive study encompassed patients with confirmed m.3243A>G mutation and diabetes mellitus at Seoul National University Hospital. Our cohort comprises 40 patients with MIDD, with a mean age at study enrollment of 33.3±12.9 years and an average % of heteroplasmy of 30.0%± 14.6% in the peripheral blood. The most prevalent comorbidity was hearing loss (90%), followed by albuminuria (61%), seizure (38%), and stroke (33%). We observed a significant negative correlation between % of heteroplasmy and age at diabetes diagnosis. These clinical features can aid in the suspicion of MIDD and further consideration of genetic testing for m.3243A>G mutation.

Review

Complications
Peripheral Neuropathy Phenotyping in Rat Models of Type 2 Diabetes Mellitus: Evaluating Uptake of the Neurodiab Guidelines and Identifying Future Directions: Md Jakir Hossain, Michael D. Kendig, Meg E. Letton, Margaret J. Morris, Ria Arnold; Diabetes Metab J. 2022;46(2):198-221. Published online March 24, 2022; DOI: https://doi.org/10.4093/dmj.2021.0347

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Diabetic peripheral neuropathy (DPN) affects over half of type 2 diabetes mellitus (T2DM) patients, with an urgent need for effective pharmacotherapies. While many rat and mouse models of T2DM exist, the phenotyping of DPN has been challenging with inconsistencies across laboratories. To better characterize DPN in rodents, a consensus guideline was published in 2014 to accelerate the translation of preclinical findings. Here we review DPN phenotyping in rat models of T2DM against the ‘Neurodiab’ criteria to identify uptake of the guidelines and discuss how DPN phenotypes differ between models and according to diabetes duration and sex. A search of PubMed, Scopus and Web of Science databases identified 125 studies, categorised as either diet and/or chemically induced models or transgenic/spontaneous models of T2DM. The use of diet and chemically induced T2DM models has exceeded that of transgenic models in recent years, and the introduction of the Neurodiab guidelines has not appreciably increased the number of studies assessing all key DPN endpoints. Combined high-fat diet and low dose streptozotocin rat models are the most frequently used and well characterised. Overall, we recommend adherence to Neurodiab guidelines for creating better animal models of DPN to accelerate translation and drug development.

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Jing Yang, Zhuoying Yu, Ye Jiang, Zixian Zhang, Yue Tian, Jie Cai, Min Wei, Yanhan Lyu, Dongsheng Yang, Shixiong Shen, Guo‐Gang Xing, Min Li
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Compound Qiying Granules alleviates diabetic peripheral neuropathy by inhibiting endoplasmic reticulum stress and apoptosis
Yan Hu, Chen Chen, Zhengting Liang, Tao Liu, Xiaoling Hu, Guanying Wang, Jinxia Hu, Xiaolin Xie, Zhiyan Liu
Molecular Medicine.2023;[Epub] CrossRef
HCV affects KATP channels through GnT-IVa-mediated N-glycosylation of GLUT2 on the surface of pancreatic β-cells leading to impaired insulin secretion
Ben Niu, Lijing Ma, Lixuan Yao, Yating Zhang, Heng Su
Endocrine.2023;[Epub] CrossRef
Multimodal Comparison of Diabetic Neuropathy in Aged Streptozotocin-Treated Sprague–Dawley and Zucker Diabetic Fatty Rats
Annalisa Canta, Valentina A. Carozzi, Alessia Chiorazzi, Cristina Meregalli, Norberto Oggioni, Virginia Rodriguez-Menendez, Barbara Sala, Roberto Cosimo Melcangi, Silvia Giatti, Raffaella Lombardi, Roberto Bianchi, Paola Marmiroli, Guido Cavaletti
Biomedicines.2022; 11(1): 20. CrossRef

Original Articles

Basic Research
Sulforaphane Ameliorates Diabetes-Induced Renal Fibrosis through Epigenetic Up-Regulation of BMP-7: Lili Kong, Hongyue Wang, Chenhao Li, Huiyan Cheng, Yan Cui, Li Liu, Ying Zhao; Diabetes Metab J. 2021;45(6):909-920. Published online June 4, 2021; DOI: https://doi.org/10.4093/dmj.2020.0168

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Background
The dietary agent sulforaphane (SFN) has been reported to reduce diabetes-induced renal fibrosis, as well as inhibit histone deacetylase (HDAC) activity. Bone morphologic protein 7 (BMP-7) has been shown to reduce renal fibrosis induced by transforming growth factor-beta1. The aim of this study was to investigate the epigenetic effect of SFN on BMP-7 expression in diabetes-induced renal fibrosis.
Methods
Streptozotocin (STZ)-induced diabetic mice and age-matched controls were subcutaneously injected with SFN or vehicle for 4 months to measure the in vivo effects of SFN on the kidneys. The human renal proximal tubular (HK11) cell line was used to mimic diabetic conditions in vitro. HK11 cells were transfected to over-express HDAC2 and treated with high glucose/palmitate (HG/Pal) to explore the epigenetic modulation of BMP-7 in SFN-mediated protection against HG/Pal-induced renal fibrosis.
Results
SFN significantly attenuated diabetes-induced renal fibrosis in vivo. Among all of the HDACs we detected, HDAC2 activity was markedly elevated in the STZ-induced diabetic kidneys and HG/Pal-treated HK11 cells. SFN inhibited the diabetes-induced increase in HDAC2 activity which was associated with histone acetylation and transcriptional activation of the BMP-7 promoter. HDAC2 over-expression reduced BMP-7 expression and abolished the SFN-mediated protection against HG/Pal-induced fibrosis in vitro.
Conclusion
Our study demonstrates that the HDAC inhibitor SFN protects against diabetes-induced renal fibrosis through epigenetic up-regulation of BMP-7.

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Patrícia dos Santos Azeredo, Daping Fan, E. Angela Murphy, Wayne E. Carver
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Christodoula Kourtidou, Konstantinos Tziomalos
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Da-Wei Lin, Yung-Chien Hsu, Cheng-Chih Chang, Ching-Chuan Hsieh, Chun-Liang Lin
International Journal of Molecular Sciences.2023; 24(7): 6053. CrossRef
Beneficial Effects of Sulforaphane on Diabetes and Its Complications via Both Nrf2-Dependent and Independent Mechanisms
Minhyuk Kim, Joo Young Lee
Food Supplements and Biomaterials for Health.2023;[Epub] CrossRef
Sulforaphane exhibits potent renoprotective effects in preclinical models of kidney diseases: A systematic review and meta-analysis
Elisa B. Monteiro, Matheus Ajackson, Milena B. Stockler-Pinto, Fitsum Guebre-Egziabher, Julio B. Daleprane, Christophe O. Soulage
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Integrated single-cell RNA-seq analysis revealed podocyte injury through activation of the BMP7/AMPK/mTOR mediated autophagy pathway
Hongzhou Lin, Huihui Chen, Rengcheng Qian, Guoqi Tang, Yinjuan Ding, Yalan Jiang, Congde Chen, Dexuan Wang, Maoping Chu, Xiaoling Guo
Chemico-Biological Interactions.2023; 382: 110559. CrossRef
Underlying mechanisms and molecular targets of genistein in the management of type 2 diabetes mellitus and related complications
Tao Jiang, Yuhe Dong, Wanying Zhu, Tong Wu, Linyan Chen, Yuantong Cao, Xi Yu, Ye Peng, Ling Wang, Ying Xiao, Tian Zhong
Critical Reviews in Food Science and Nutrition.2023; : 1. CrossRef
Sulforaphane: A nutraceutical against diabetes-related complications
Sinenhlanhla X.H. Mthembu, Sithandiwe E. Mazibuko-Mbeje, Marakiya T. Moetlediwa, Ndivhuwo Muvhulawa, Sonia Silvestri, Patrick Orlando, Bongani B. Nkambule, Christo J.F. Muller, Duduzile Ndwandwe, Albertus K. Basson, Luca Tiano, Phiwayinkosi V. Dludla
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Emad H.M. Hassanein, Islam M. Ibrahim, Esraa K. Abd-alhameed, Zeina W. Sharawi, Fatima A. Jaber, Hanan S. Althagafy
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Neda Mohamadi, Vafa Baradaran Rahimi, Mohammad Reza Fadaei, Fatemeh Sharifi, Vahid Reza Askari
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Jiayu Wang, Jiaxing Li, Xin Zhang, Min Zhang, Xiaopeng Hu, Hang Yin
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Genetics
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; DOI: https://doi.org/10.4093/dmj.2020.0194

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Background
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.
Methods
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.
Results
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.
Conclusion
The A/A genotype of TYK2 rs2304256 SNP is associated with protection against T1DM in a Southern Brazilian population.

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Genetics
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; DOI: https://doi.org/10.4093/dmj.2020.0101

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Background
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.
Methods
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.
Results
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]).
Conclusion
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.

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Aleena Shujaat Ali, Cecilia Pham, Grant Morahan, Elif Ilhan Ekinci
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Amal F. Alshammary, Malak Mohammed Al-Hakeem, Imran Ali Khan
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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
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Review

Genetics
Update on Monogenic Diabetes in Korea: Ye Seul Yang, Soo Heon Kwak, Kyong Soo Park; Diabetes Metab J. 2020;44(5):627-639. Published online October 21, 2020; DOI: https://doi.org/10.4093/dmj.2020.0214

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Monogenic diabetes, including maturity-onset diabetes of the young, neonatal diabetes, and other rare forms of diabetes, results from a single gene mutation. It has been estimated to represent around 1% to 6% of all diabetes. With the advances in genome sequencing technology, it is possible to diagnose more monogenic diabetes cases than ever before. In Korea, 11 studies have identified several monogenic diabetes cases, using Sanger sequencing and whole exome sequencing since 2001. The recent largest study, using targeted exome panel sequencing, found a molecular diagnosis rate of 21.1% for monogenic diabetes in clinically suspected patients. Mutations in glucokinase (GCK), hepatocyte nuclear factor 1α (HNF1A), and HNF4A were most commonly found. Genetic diagnosis of monogenic diabetes is important as it determines the therapeutic approach required for patients and helps to identify affected family members. However, there are still many challenges, which include a lack of simple clinical criterion for selecting patients for genetic testing, difficulties in interpreting the genetic test results, and high costs for genetic testing. In this review, we will discuss the latest updates on monogenic diabetes in Korea, and suggest an algorithm to screen patients for genetic testing. The genetic tests and non-genetic markers for accurate diagnosis of monogenic diabetes will be also reviewed.

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Original Articles

Genetics
Exome Chip Analysis of 14,026 Koreans Reveals Known and Newly Discovered Genetic Loci Associated with Type 2 Diabetes Mellitus: Seong Beom Cho, Jin Hwa Jang, Myung Guen Chung, Sang Cheol Kim; Diabetes Metab J. 2021;45(2):231-240. Published online July 28, 2020; DOI: https://doi.org/10.4093/dmj.2019.0163

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Background

Most loci associated with type 2 diabetes mellitus (T2DM) discovered to date are within noncoding regions of unknown functional significance. By contrast, exonic regions have advantages for biological interpretation.

Methods

We analyzed the association of exome array data from 14,026 Koreans to identify susceptible exonic loci for T2DM. We used genotype information of 50,543 variants using the Illumina exome array platform.

Results

In total, 7 loci were significant with a Bonferroni adjusted P=1.03×10⁻⁶. rs2233580 in paired box gene 4 (PAX4) showed the highest odds ratio of 1.48 (P=1.60×10⁻¹⁰). rs11960799 in membrane associated ring-CH-type finger 3 (MARCH3) and rs75680863 in transcobalamin 2 (TCN2) were newly identified loci. When we built a model to predict the incidence of diabetes with the 7 loci and clinical variables, area under the curve (AUC) of the model improved significantly (AUC=0.72, P<0.05), but marginally in its magnitude, compared with the model using clinical variables (AUC=0.71, P<0.05). When we divided the entire population into three groups—normal body mass index (BMI; <25 kg/m²), overweight (25≤ BMI <30 kg/m²), and obese (BMI ≥30 kg/m²) individuals—the predictive performance of the 7 loci was greatest in the group of obese individuals, where the net reclassification improvement was highly significant (0.51; P=8.00×10⁻⁵).

Conclusion

We found exonic loci having a susceptibility for T2DM. We found that such genetic information is advantageous for predicting T2DM in a subgroup of obese individuals.

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Genetics
Enhancer-Gene Interaction Analyses Identified the Epidermal Growth Factor Receptor as a Susceptibility Gene for Type 2 Diabetes Mellitus: Yang Yang, Shi Yao, Jing-Miao Ding, Wei Chen, Yan Guo; Diabetes Metab J. 2021;45(2):241-250. Published online June 10, 2020; DOI: https://doi.org/10.4093/dmj.2019.0204

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Background

Genetic interactions are known to play an important role in the missing heritability problem for type 2 diabetes mellitus (T2DM). Interactions between enhancers and their target genes play important roles in gene regulation and disease pathogenesis. In the present study, we aimed to identify genetic interactions between enhancers and their target genes associated with T2DM.

Methods

We performed genetic interaction analyses of enhancers and protein-coding genes for T2DM in 2,696 T2DM patients and 3,548 controls of European ancestry. A linear regression model was used to identify single nucleotide polymorphism (SNP) pairs that could affect the expression of the protein-coding genes. Differential expression analyses were used to identify differentially expressed susceptibility genes in diabetic and nondiabetic subjects.

Results

We identified one SNP pair, rs4947941×rs7785013, significantly associated with T2DM (combined P=4.84×10⁻¹⁰). The SNP rs4947941 was annotated as an enhancer, and rs7785013 was located in the epidermal growth factor receptor (EGFR) gene. This SNP pair was significantly associated with EGFR expression in the pancreas (P=0.033), and the minor allele “A” of rs7785013 decreased EGFR gene expression and the risk of T2DM with an increase in the dosage of “T” of rs4947941. EGFR expression was significantly upregulated in T2DM patients, which was consistent with the effect of rs4947941×rs7785013 on T2DM and EGFR expression. A functional validation study using the Mouse Genome Informatics (MGI) database showed that EGFR was associated with diabetes-relevant phenotypes.

Conclusion

Genetic interaction analyses of enhancers and protein-coding genes suggested that EGFR may be a novel susceptibility gene for T2DM.

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Reviews

Basic Research
Role of CRTC2 in Metabolic Homeostasis: Key Regulator of Whole-Body Energy Metabolism?: Hye-Sook Han, Yongmin Kwon, Seung-Hoi Koo; Diabetes Metab J. 2020;44(4):498-508. Published online March 5, 2020; DOI: https://doi.org/10.4093/dmj.2019.0200

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Cyclic adenosine monophosphate (cAMP) signaling is critical for regulating metabolic homeostasis in mammals. In particular, transcriptional regulation by cAMP response element-binding protein (CREB) and its coactivator, CREB-regulated transcription coactivator (CRTC), is essential for controlling the expression of critical enzymes in the metabolic process, leading to more chronic changes in metabolic flux. Among the CRTC isoforms, CRTC2 is predominantly expressed in peripheral tissues and has been shown to be associated with various metabolic pathways in tissue-specific manners. While initial reports showed the physiological role of CRTC2 in regulating gluconeogenesis in the liver, recent studies have further delineated the role of this transcriptional coactivator in the regulation of glucose and lipid metabolism in various tissues, including the liver, pancreatic islets, endocrine tissues of the small intestines, and adipose tissues. In this review, we discuss recent studies that have utilized knockout mouse models to delineate the role of CRTC2 in the regulation of metabolic homeostasis.

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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; DOI: https://doi.org/10.4093/dmj.2013.37.6.404

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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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Original Article

Association of Estrogen Receptor α Genes PvuII and XbaI Polymorphisms with Type 2 Diabetes Mellitus in the Inpatient Population of a Hospital in Southern Iran: Farzaneh Mohammadi, Mohammad Pourahmadi, Mohadeseh Mosalanejad, Houshang Jamali, Mohamed Amin Ghobadifar, Saeideh Erfanian; Diabetes Metab J. 2013;37(4):270-277. Published online August 14, 2013; DOI: https://doi.org/10.4093/dmj.2013.37.4.270

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Abstract PDF PubReader

Background

Estrogen plays a fundamental role in the pathogenesis of type 2 diabetes mellitus (T2DM). Very few studies have shown the association between estrogen receptor α (ERα), PvuII and XbaI gene polymorphisms with T2DM in both men and women. We evaluated the hypothesis that PvuII and XbaI polymorphisms of ERα gene may be associated with T2DM in adult.

Methods

From spring of 2010 to the fall of 2011, a case-control study was performed at clinical centers of Jahrom University of Medical Sciences. We included 174 patients with T2DM including men and women and 174 age, sex, and body mass index frequency-matched health controls. We analyzed the PvuII and XbaI polymorphisms of ERα by using the polymerase chain reaction-based restriction fragment length polymorphism method.

Results

No significant differences between demographic characteristics of control and patients groups were observed. Allele frequencies of both PvuII and XbaI polymorphisms were significantly different between patients and control subjects (P=0.014 vs. P=0.002, respectively). When the group was separated into women and men, logistic regression analysis of genotype distribution of PvuII (pp vs. Pp+PP) in both sexes revealed that there was no significant association of PvuII genotype with men (odds ratio [OR], 1.67; confidence interval [CI], 0.86 to 3.28; P=0.89) and women (OR, 0.96; CI, 0.53 to 1.74; P=0.12).

Conclusion

PvuII and XbaI polymorphisms in ERα are related with T2DM in the inpatient population.

Citations

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Single-nucleotide polymorphisms as important risk factors of diabetes among Middle East population
Iman Akhlaghipour, Amir Reza Bina, Mohammad Reza Mogharrabi, Ali Fanoodi, Amir Reza Ebrahimian, Soroush Khojasteh Kaffash, Atefeh Babazadeh Baghan, Mohammad Erfan Khorashadizadeh, Negin Taghehchian, Meysam Moghbeli
Human Genomics.2022;[Epub] CrossRef
Estrogen receptor 1 gene polymorphisms (PvuII and XbaI) are associated with type 2 diabetes in Palestinian women
Suheir Ereqat, Stéphane Cauchi, Khaled Eweidat, Muawiyah Elqadi, Abedelmajeed Nasereddin
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Genetic polymorphism of estrogen receptor alpha gene in Egyptian women with type II diabetes mellitus
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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; DOI: https://doi.org/10.4093/dmj.2012.36.3.199

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Abstract PDF PubReader

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.

Citations

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Reviews

Challenges in Diagnosing Type 1 Diabetes in Different Populations: Marian Rewers; Diabetes Metab J. 2012;36(2):90-97. Published online April 17, 2012; DOI: https://doi.org/10.4093/dmj.2012.36.2.90

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Diabetes affects today an estimated 366 million people world-wide, including 20 million to 40 million of patients with type 1 diabetes (T1D). While T1D accounts for 5% to 20% of those with diabetes, it is associated with higher morbidity, mortality and health care cost than the more prevalent type 2 diabetes. Patients with T1D require exogenous insulin for survival and should be identified as soon as possible after diagnosis to avoid high morbidity due to a delay in insulin treatment. It is also important to present to the patient correct prognosis that differs by the type of diabetes. From the research point of view, correct classification should help to identify the etiologies and to develop specific prevention for T1D. This review summarizes evidence that may be helpful in diagnosing T1D in various ethnic groups. Challenges in interpretation of results commonly used to determine the type of diabetes are highlighted.

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The Importance of Global Studies of the Genetics of Type 2 Diabetes: Mark I. McCarthy; Diabetes Metab J. 2011;35(2):91-100. Published online April 30, 2011; DOI: https://doi.org/10.4093/dmj.2011.35.2.91

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Genome wide association analyses have revealed large numbers of common variants influencing predisposition to type 2 diabetes and related phenotypes. These studies have predominantly featured European populations, but are now being extended to samples from a wider range of ethnic groups. The transethnic analysis of association data is already providing insights into the genetic, molecular and biological causes of diabetes, and the relevance of such studies will increase as human discovery genetics increasingly moves towards sequencing-based approaches and a focus on low frequency and rare variants.

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