<i>HHEX</i> gene polymorphisms and type 2 diabetes mellitus: A case‐control report from Iran

Galavi, Hamidreza; Mollashahee-Kohkan, Fatemeh; Saravani, Ramin; Sargazi, Saman; Noorzehi, Nafiseh; Shahraki, Hojat

doi:10.1002/jcb.28788

Cited by 15 publications

(7 citation statements)

References 23 publications

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“…Genome-wide association studies indicated that HHET rs1111875G/A and rs5015480C/T variants significantly increased the risk of T2DM. 27 Hamidreza Galavi et al found the SREBF-2 gene rs2267439C/T polymorphism increased T2DM susceptibility. 28 IGF2BP2 rs11705701 and rs1470579 gene polymorphisms may be associated with T2DM.…”

Section: Discussionmentioning

confidence: 99%

Association of CYP7A1 and CYP2E1 Polymorphisms with Type 2 Diabetes in the Chinese Han Populations

Zhang¹,

Tang²,

Wang³

et al. 2022

PGPM

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Background Type 2 diabetes mellitus (T2DM) is caused by diverse environmental and genetic risk factors. Previous studies have reported that cytochrome P450 ( CYP ) is a promising gene for T2DM. Therefore, we aimed to determine the effects of CYP7A1 and CYP2E1 polymorphisms on T2DM susceptibility among the Chinese Han population. Methods A case-control study was conducted to assess the potential relationship of four polymorphisms (rs8192879, rs12542233, rs2070672 and rs2515641) with T2DM susceptibility in the Chinese population, involving 512 T2DM patients and 515 age- and gender-matched healthy individuals. We used the Agena MassARRAY platform to detect CYP7A1 and CYP2E1 polymorphisms. The relationship between genetic polymorphisms and T2DM risk was evaluated using odds ratios (ORs) and 95% confidence intervals (CIs) in various genetic models. Results After adjusting for age and gender, rs12542233 in the CYP7A1 gene was significantly associated with decreased T2DM risk (recessive: OR = 0.67, 95% CI = 0.49–0.91, p = 0.012; after FDR correction, p = 0.048). The CYP7A1 rs12542233 was associated with a reduced risk of T2DM in people over 59 years of age ( p = 0.010). In the population with BMI ≤ 24 kg/m 2 , CYP7A1 rs12542233 was associated with an increased risk of T2DM ( p < 0.05). In the population with BMI > 24 kg/m 2 , CYP2E1 rs2515641 can significantly reduce the risk of T2DM ( p < 0.05). And rs8192879, rs2070672 and rs2515641 could significantly increase the risk of diabetes retinopathy in T2DM patients ( p < 0.05). Furthermore, the T rs8192879 C rs12542233 haplotype was significantly associated with T2DM ( p = 0.019). Conclusion CYP7A1 and CYP2E1 polymorphisms may contribute to T2DM susceptibility in the Chinese Han population, especially in stratified analysis.

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Section: Discussionmentioning

confidence: 99%

Association of CYP7A1 and CYP2E1 Polymorphisms with Type 2 Diabetes in the Chinese Han Populations

Zhang¹,

Tang²,

Wang³

et al. 2022

PGPM

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“…Other comprehensive studies must be performed in order to establish the effect of HHEX on CRC hazard, particularly in several populations [41]. HHEX rs1111875G/A and rs5015480C/T may contribute to the upgrade of T2D hazard in a test of the southeast Iranian population [42].…”

Section: Hhex (Hematopoietically-expressed Homeobox Protein)mentioning

confidence: 99%

Parental History of Type 2 Diabetes Mellitus: A Lurking Genetic Threat

Zano

Rubab

Baig

et al. 2020

JAMMR

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Type-2 Diabetes Mellitus (T2DM) is presently the fastest growing disease and has been recognized to be caused by a collision between inherited parental genes and the environment. The current prevalence in Pakistan of type-2 diabetes mellitus is 26.3%. Out of them 19.2% had disease two to three decades back while 7.1% are recently diagnosed cases. Worldwide burden of disease was 415 million in 2015 and this number will increase to 642 million by 2040. Parental history of diabetes mellitus is a chief reason for the development of T2DM in children, but whether this association derives from shared genetic or environmental factors is unclear. Persistent high blood glucose levels can result in drastic outcomes like Diabetic Ketoacidosis and Hyperosmolar non ketotic syndrome. Genome-wide association analyses have uncovered multiple genomic regions associated with T2DM, but identification of the causal variants remains a challenge. This review will discuss the approach of diagnosing T2DM by analyzing the association of gene variants and family history.

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“…This involved genes such as glucokinase (GCK) [ 6 ], hepatocyte nuclear factor 1 alpha (HNF1A) [ 7 ], hepatocyte nuclear factor 1 alpha (HNF4A) [ 8 ], hepatocyte nuclear factor 1 beta ( HNF1B ) [ 9 ], sulfonylurea receptor 1 (ABCC8) [ 10 ], Insulin (INS), Neuronal differentiation 1 (NEUROD1) [ 11 ], insulin gene promoter factor 1 (IPF1 or PDX1) [ 12 ], Paired box 4 (PAX4) [ 13 ], ATP-binding cassette sub-family C member 8 (ABCC8), GATA binding protein 4 (GATA4) [ 14 ] and GATA binding protein 6 (GATA6) [ 15 ]. Potassium inwardly rectifying channel, subfamily J, member 11 (KCNJ11) [ 16 ], kruppel-like factor 11 (KLF11) [ 17 ], carboxyl ester lipase (CEL) [ 18 ], B lymphoid tyrosine kinase (BLK) [ 19 ], Adaptor protein, phosphotyrosine interacting with PH domain and leucine zipper 1 (APPL1) [ 20 ] Previous human genetic studies have demonstrated a correlation between the genetic mutations and T2DM, such as lamin A/C mutations [ 21 ], glucokinase regulatory protein (GCKR) [ 22 ], fat mass and obesity-associated gene (FTO) [ 23 ], monocarboxylate transporter 11(SLC16A11) [ 24 ], hematopoietically-expressed homeobox (HHEX) gene [ 25 ], transcription factor 7-like 2 (TCF7L2) [ 26 ], Pro12Ala polymorphism in peroxisome proliferator-activated receptor- γ (PPAR- γ ) [ 27 ] and others. The role of single nucleotide polymorphisms in T2DM is also known.…”

Section: Introductionmentioning

confidence: 99%

Exploring histone deacetylases in type 2 diabetes mellitus: pathophysiological insights and therapeutic avenues

Kumar,

Aburawi,

Ljubisavljevic

et al. 2024

Clin Epigenet

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Diabetes mellitus is a chronic disease that impairs metabolism, and its prevalence has reached an epidemic proportion globally. Most people affected are with type 2 diabetes mellitus (T2DM), which is caused by a decline in the numbers or functioning of pancreatic endocrine islet cells, specifically the β-cells that release insulin in sufficient quantity to overcome any insulin resistance of the metabolic tissues. Genetic and epigenetic factors have been implicated as the main contributors to the T2DM. Epigenetic modifiers, histone deacetylases (HDACs), are enzymes that remove acetyl groups from histones and play an important role in a variety of molecular processes, including pancreatic cell destiny, insulin release, insulin production, insulin signalling, and glucose metabolism. HDACs also govern other regulatory processes related to diabetes, such as oxidative stress, inflammation, apoptosis, and fibrosis, revealed by network and functional analysis. This review explains the current understanding of the function of HDACs in diabetic pathophysiology, the inhibitory role of various HDAC inhibitors (HDACi), and their functional importance as biomarkers and possible therapeutic targets for T2DM. While their role in T2DM is still emerging, a better understanding of the role of HDACi may be relevant in improving insulin sensitivity, protecting β-cells and reducing T2DM-associated complications, among others.

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HHEX gene polymorphisms and type 2 diabetes mellitus: A case‐control report from Iran

Cited by 15 publications

References 23 publications

Association of CYP7A1 and CYP2E1 Polymorphisms with Type 2 Diabetes in the Chinese Han Populations

Association of CYP7A1 and CYP2E1 Polymorphisms with Type 2 Diabetes in the Chinese Han Populations

Parental History of Type 2 Diabetes Mellitus: A Lurking Genetic Threat

Exploring histone deacetylases in type 2 diabetes mellitus: pathophysiological insights and therapeutic avenues

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