The Uyghur population and genetic susceptibility to type 2 diabetes: potential role for variants in <scp>CAPN</scp>10,<scp>APM</scp>1 and <scp>FUT</scp>6 genes

Zhao, Fei; Mamatyusupu, Dolikun; Wang, Youxin; Fang, Honghong; Wang, Hao; Gao, Qing; Dong, Huijuan; Ge, Siqi; Yu, Xinwei; Zhang, Jie; Wu, Lijuan; Song, Manshu; Wang, Wei

doi:10.1111/jcmm.12911

Cited by 20 publications

(11 citation statements)

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“…H antigens are precursors of ABO and Lewis b histo-blood group antigens that are expressed on mucosal surfaces [ 5 ]. Recent studies have shown suggestive associations between variants of FUT2 with diabetes and body mass index [ 23 – 26 ].…”

Section: Co-factors or Regulators Of Co-factors Essential For The Tramentioning

confidence: 99%

An update on vitamin B12-related gene polymorphisms and B12 status

et al. 2018

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BackgroundVitamin B12 is an essential micronutrient in humans needed for health maintenance. Deficiency of vitamin B12 has been linked to dietary, environmental and genetic factors. Evidence for the genetic basis of vitamin B12 status is poorly understood. However, advancements in genomic techniques have increased the knowledge-base of the genetics of vitamin B12 status. Based on the candidate gene and genome-wide association (GWA) studies, associations between genetic loci in several genes involved in vitamin B12 metabolism have been identified.ObjectiveThe objective of this literature review was to identify and discuss reports of associations between single-nucleotide polymorphisms (SNPs) in vitamin B12 pathway genes and their influence on the circulating levels of vitamin B12.MethodsRelevant articles were obtained through a literature search on PubMed through to May 2017. An article was included if it examined an association of a SNP with serum or plasma vitamin B12 concentration. Beta coefficients and odds ratios were used to describe the strength of an association, and a P < 0.05 was considered as statistically significant. Two reviewers independently evaluated the eligibility for the inclusion criteria and extracted the data.ResultsFrom 23 studies which fulfilled the selection criteria, 16 studies identified SNPs that showed statistically significant associations with vitamin B12 concentrations. Fifty-nine vitamin B12-related gene polymorphisms associated with vitamin B12 status were identified in total, from the following populations: African American, Brazilian, Canadian, Chinese, Danish, English, European ancestry, Icelandic, Indian, Italian, Latino, Northern Irish, Portuguese and residents of the USA.ConclusionOverall, the data analyzed suggests that ethnic-specific associations are involved in the genetic determination of vitamin B12 concentrations. However, despite recent success in genetic studies, the majority of identified genes that could explain variation in vitamin B12 concentrations were from Caucasian populations. Further research utilizing larger sample sizes of non-Caucasian populations is necessary in order to better understand these ethnic-specific associations.

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Section: Co-factors or Regulators Of Co-factors Essential For The Tramentioning

confidence: 99%

An update on vitamin B12-related gene polymorphisms and B12 status

et al. 2018

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“…[ 7 , 19 , 23 ] The inherent genetic differences between ethnic group is to be responsible, just like the opposite trends of the calpain-10 rs3792267 allele and T2DM between the Uyghur and Chinese populations. [ 24 , 25 ] In 2011, Han et al [ 26 ] conducted a meta analysis to explore the association between SNPs of adiponectin gene and T2DM, and the results showed that the adiponectin rs266729 G allele was a risk factor for T2DM, with the pooled OR (95% CI) of 1.07 (1.03, 1.11, P = .001) for G versus C allele. However, the study did not provide the rs266729 genetic effect on the development of T2DM in different populations.…”

Section: Discussionmentioning

confidence: 99%

The polymorphism of rs266729 in adiponectin gene and type 2 diabetes mellitus

Sun

Liu

Chen³

et al. 2017

Medicine

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Genome-wide association studies and meta-analyses indicate that the polymorphism of rs266729 in adiponectin gene increases the risk of type 2 diabetes mellitus (T2DM); however, these study methods have not been able to identify the underlying genetic effect on the development of T2DM. A genetic model-free approach was conducted to determine the underlying genetic model of inheritance of T2DM because of rs266729 in adiponectin gene.We searched available studies on the association between the rs266729 in adiponectin gene and T2DM in accordance with the inclusion and exclusion criteria. Based on the information extracted from the studies, generalized odds ratio value (GOR) was used to evaluate whether the rs266729 polymorphism was a risk factor for T2DM. The parameter λ was calculated to estimate the genetic model, which was defined as the quotient of natural logarithm odds ratio of GC to CC divided by the natural logarithm odds ratio of GG to CC. Finally, binary logistic regression analysis was used to calculate the genetic effect of rs266729 on T2DM.Data from 7 studies were included in this meta-analysis. The total number of subjects was 12,323, comprising 5,948 cases and 6,395 controls. Mean (standard deviation) age of cases was 59.50 (11.53), and that of the controls was 53.80 (11.65), whereas the proportion of male was 40.9 and 50.0%, respectively. GOR was 1.13 (1.02, 1.25) and λ was 0.47 (0.29, 0.64). The result of logistic regression indicated that the G allele influenced the development of T2DM in the additive model, whereas the genetic effect was 1.13 (1.06, 1.19). Sources of control populations were the cause of between-study heterogeneity; nonetheless, there was no publication bias among studies.The G allele of rs266729 in adiponectin gene increases the risk of T2DM through an additive genetic model with an effect of 1.13 (1.06, 1.19).

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“…is particularly interesting given its controversial association with T2D risk. It was the first T2D susceptibility gene identified in linkage studies (HORIKAWA et al 2000), with multiple subsequent GWAS or candidate gene studies having also identified an association between variants near CAPN10 and T2D risk and other diabetes-related phenotypes (BAIER et al 2000;EVANS et al 2001;OROZCO et al 2014;IBRAHIM et al 2015;CUI et al 2016;ZHAO et al 2016;BAYRAMCI et al 2017;HOU et al 2017;CASTRO-MARTINEZ et al 2018). However, many other studies failed to replicate these findings (HEGELE et al 2001;TSAI et al 2001;KHAN et al 2014;AL-SINANI et al 2015;PLENGVIDHYA et al 2015;ZHANG et al 2019).…”

Section: Among the Most Significant Genes Whose Expression Is Regulatmentioning

confidence: 99%

A novel mapping strategy utilizing mouse chromosome substitution strains identifies multiple epistatic interactions that regulate complex traits

Miller

Chen

Bartlett

et al. 2020

Preprint

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The genetic contribution of additive versus non-additive (epistasis) effects in the regulation of hematologic and other complex traits is unclear. While genome-wide association studies typically ignore gene-gene interactions, in part because of the lack of statistical power for detecting them, mouse chromosome substitution strains (CSSs) represent an alternate and powerful model for detecting epistasis given their limited allelic variation. Therefore, we utilized CSSs to identify and map both additive and epistatic loci that regulate a range of hematologic-and metabolism-related traits, as well as hepatic gene expression. Quantitative trait loci (QTLs) were identified using a modified backcross strategy involving the segregation of variants on the A/J-derived substituted chromosomes 4 and 6 on an otherwise C57BL/6J genetic background. By analyzing the transcriptomes of offspring from this cross, we identified and mapped additive QTLs regulating the expression of 768 genes, and epistatic QTL pairs for 519 genes. Similarly, we identified additive QTLs for fat pad weight, platelets, and the percentage of granulocytes in blood, as well as epistatic QTL pairs controlling the percentage of lymphocytes in blood and red cell distribution width. The variance attributed to the epistatic QTLs was approximately equal to that of the additive QTLs, demonstrating the importance of identifying genetic interactions to understand the genetic architecture of complex traits. Of particular note, even the epistatic QTLs that accounted for the largest variances were undetected in our single loci GWAS-like association analyses, highlighting the need to account for epistasis in association studies.

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The Uyghur population and genetic susceptibility to type 2 diabetes: potential role for variants in CAPN10,APM1 and FUT6 genes

Cited by 20 publications

References 49 publications

An update on vitamin B12-related gene polymorphisms and B12 status

An update on vitamin B12-related gene polymorphisms and B12 status

The polymorphism of rs266729 in adiponectin gene and type 2 diabetes mellitus

A novel mapping strategy utilizing mouse chromosome substitution strains identifies multiple epistatic interactions that regulate complex traits

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