Association between functional variants of the ICAM1 and CRP genes and metabolic syndrome in Taiwanese subjects

Hsu, Lung‐An; Chang, Chi-Jen; Wu, Semon; Teng, Ming‐Sheng; Chou, Hsin-Hua; Chang, Hsin-Yu; Ko, Yu‐Lin

doi:10.1016/j.metabol.2010.04.004

Cited by 20 publications

(27 citation statements)

References 29 publications

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“…Several studies subsequently narrowed down the genetic determinants of circulating sICAM1 levels to the ICAM cluster on chromosome 19 with a heritability estimate from 0.34 to 0.59 [7, 8], and many single nucleotide polymorphisms (SNPs) in the vicinity of the ICAM1 locus were identified to associate with sICAM1 levels [7, 9–11]. We have previously reported that the ICAM1 SNP rs5491 was associated with sICAM1 levels and metabolic syndrome in a Taiwanese population [12]. This SNP, also named ICAM1 Kilifi (rs5491), lies in a loop close to the N-terminus of the ICAM1 protein critical to its binding to the malaria parasite Plasmodium falciparum , human rhinovirus, lymphocyte function–associated antigen–1 (LFA-1), and fibrinogen [13–15], and is likely a result of evolutionary adaptation.…”

Section: Introductionmentioning

confidence: 99%

Association between NF-κB Pathway Gene Variants and sICAM1 Levels in Taiwanese

Teng

et al. 2017

PLoS ONE

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Intercellular adhesion molecule–1 (ICAM1) is crucial to the development and progression of atherosclerosis. Recent genome-wide association studies (GWAS) have revealed that single nucleotide polymorphisms (SNPs) in two of the nuclear factor-κB (NF-κB) pathway genes, NFKBIK and RELA, are associated with soluble ICAM1 (sICAM1) levels. However, neither of these two gene variants is found in the Asian populations. This study aimed to elucidate whether other candidate gene variants involved in the NF-κB pathway may be associated with sICAM1 levels in Taiwanese. After excluding carriers of the ICAM1 rs5491-T allele, three SNPs in the ICAM1 gene and eight SNPs in six of the NF-κB pathway genes (NFKB1, PDCD11, TNFAIP3, NKAPL, IKBKE, and PRKCB) were analyzed for their association with sICAM1 levels in 480 individuals. Our data showed that two SNPs, rs5498 of ICAM1 and rs1635 of NKAPL, were significantly associated with sICAM1 levels (P = 0.002 and 0.004, respectively) in the Taiwanese population. Using a multivariate analysis, rs5498 and rs1635 as well as the previously reported ABO genotypes and rs12051272 of the CDH13 gene were independently associated with sICAM1 levels (P = 0.001, 0.001, 0.006 and 0.031, respectively). An analysis with combined risk alleles of four candidate SNPs in the ICAM1, NKAPL, ABO, and CDH13 genes showed an increase in sICAM1 levels with added numbers of risk alleles and weighted genetic risk score. Our findings thus expanded the repertoire of gene variants responsible for the regulation of sICAM1 levels in the Asian populations.

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Section: Introductionmentioning

confidence: 99%

Association between NF-κB Pathway Gene Variants and sICAM1 Levels in Taiwanese

Teng

et al. 2017

PLoS ONE

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“…The T allele of rs5491 encodes a lysine to methionine substitution in exon 2 in the N-terminal domain of ICAM-1 and results in a protein that is unable to bind to fibrinogen and has a decreased affinity for T cells at lower ICAM-1 concentrations compared to wild-type ICAM-1 (Craig et al 2000). This lead to increased circulating levels of sICAM-1 and an association with insulin resistance and the metabolic syndrome (Hsu et al 2010). …”

Section: Clinical Significancementioning

confidence: 99%

Genetic basis of interindividual susceptibility to cancer cachexia: selection of potential candidate gene polymorphisms for association studies

Johns

Tan

Macmillan

et al. 2014

J Genet

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Cancer cachexia is a complex and multifactorial disease. Evolving definitions highlight the fact that a diverse range of biological processes contribute to cancer cachexia. Part of the variation in who will and who will not develop cancer cachexia may be genetically determined. As new definitions, classifications and biological targets continue to evolve, there is a need for reappraisal of the literature for future candidate association studies. This review summarizes genes identified or implicated as well as putative candidate genes contributing to cachexia, identified through diverse technology platforms and model systems to further guide association studies. A systematic search covering 1986-2012 was performed for potential candidate genes / genetic polymorphisms relating to cancer cachexia. All candidate genes were reviewed for functional polymorphisms or clinically significant polymorphisms associated with cachexia using the OMIM and GeneRIF databases. Pathway analysis software was used to reveal possible network associations between genes. Functionality of SNPs/genes was explored based on published literature, algorithms for detecting putative deleterious SNPs and interrogating the database for expression of quantitative trait loci (eQTLs). A total of 154 genes associated with cancer cachexia were identified and explored for functional polymorphisms. Of these 154 genes, 119 had a combined total of 281 polymorphisms with functional and/or clinical significance in terms of cachexia associated with them. Of these, 80 polymorphisms (in 51 genes) were replicated in more than one study with 24 polymorphisms found to influence two or more hallmarks of cachexia (i.e., inflammation, loss of fat mass and/or lean mass and reduced survival). Selection of candidate genes and polymorphisms is a key element of multigene study design. The present study provides a contemporary basis to select genes and/or polymorphisms for further association studies in cancer cachexia, and to develop their potential as susceptibility biomarkers of cachexia.

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“…130 These high correlations seem to be attributable to the enhanced production of inflammatory cytokines derived from visceral fat cells. 131 Macrophages are known to infiltrate adipose tissues, including the vascular walls and visceral fat tissues. 132 In addition to the overloaded visceral fat cells, these infiltrating, activated macrophages themselves are a major source of the generation of inflammatory cyto kines, including TNF-α and interleukin 6, which further exacerbate metabolic abnormalities.…”

Section: Visceral Obesity and Metabolic Syndromementioning

confidence: 99%

Visceral adiposity and cardiometabolic risks: epidemic of abdominal obesity in North America

Wimalawansa¹

2013

RRED

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Association between functional variants of the ICAM1 and CRP genes and metabolic syndrome in Taiwanese subjects

Cited by 20 publications

References 29 publications

Association between NF-κB Pathway Gene Variants and sICAM1 Levels in Taiwanese

Association between NF-κB Pathway Gene Variants and sICAM1 Levels in Taiwanese

Genetic basis of interindividual susceptibility to cancer cachexia: selection of potential candidate gene polymorphisms for association studies

Visceral adiposity and cardiometabolic risks: epidemic of abdominal obesity in North America

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