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- 저자 : Amanda. J. Cox (검색결과 2 건)
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Megan E. Rudock,Amanda. J. Cox,Julie T. Ziegler,Allison B. Lehtinen,Jessica J. Connelly,Barry I. Freedman,J. Jeffrey Carr,Elizabeth R. Hauser,Benjamin D. Horne,Donald W. Bowden 한국유전학회 2011 Genes & Genomics Vol.33 No.5
All manifestations of cardiovascular disease (CVD) are substantially more common in patients with type 2 diabetes mellitus (T2DM) than in non-diabetic individuals. The current study evaluated KALRN, a gene previously linked to CVD, as a contributor to CVD in a sample enriched for T2DM. Specifically,the potential modifying effect of cigarette smoking was examined. A total of 28 SNPs in KALRN were genotyped in 1001 European Americans from 369 Diabetes Heart Study (DHS) families, as well as 762 population-based controls. The association between each SNP and both qualitative and quantitative CVD disease phenotypes was determined using generalized estimating equations and variance component models,respectively. Selected KALRN SNPs were found to be associated with both the qualitative (T2DM, CVD, metabolic syndrome)and quantitative traits (C-reactive protein and abdominal aortic calcified plaque). Interaction analysis and stratification were then used to test whether smoking modulates the genetic effects of KALRN. The strongest evidence of a modifying effect of smoking status was observed for rs9289231 and intima-media thickness (p=9.0x10^(-4)) and abdominal aortic calcified plaque (p=3.0x10^(-4)). Overall, following stratification by smoking status, the evidence of association with quantitative traits was more pronounced in smokers compared to non-smokers. The strongest association for smokers was between rs1720960 and abdominal aortic calcified plaque (p=2.6x10^(-5)), while in non-smokers there was no observed association. KALRN variants are associated with measures of CVD and T2DM in the DHS sample with smoking status observed to have a significant modifying effect on these associations.
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Kyle M. Hatton-Jones,Nicholas P. West,Mike W.C. Thang,Pin-Yen Chen,Peter Davoren,Allan W. Cripps,Amanda J. Cox 대한비만학회 2024 Journal of obesity & metabolic syndrome Vol.33 No.1
Background: The contributions of the gut microbiota to obesity and metabolic disease represent a potentially modifiable factor that may explain variation in risk between individuals. This study aimed to explore relationships among microbial composition and imputed functional attributes, a range of soluble metabolic and immune indices, and gene expression markers in males with or without evidence of metabolic dysregulation (MetDys). Methods: This case-control study included healthy males (n=15; 41.9±11.7 years; body mass index [BMI], 22.9±1.2 kg/m2) and males with evidence of MetDys (n=14; 46.6±10.0 years; BMI, 35.1±3.3 kg/m2) who provided blood and faecal samples for assessment of a range of metabolic and immune markers and microbial composition using 16S rRNA gene sequencing. Metagenomic functions were imputed from microbial sequence data for analysis. Results: In addition to elevated values in a range of traditional metabolic, adipokine and inflammatory indices in the MetDys group, 23 immunomodulatory genes were significantly altered in the MetDys group. Overall microbial diversity did not differ between groups; however, a trend for a higher relative abundance of the Bacteroidetes (P=0.06) and a lower relative abundance of the Verrucomicrobia (P=0.09) phyla was noted in the MetDys group. Using both family- and genera-level classifications, a partial least square discriminant analysis revealed unique microbial signatures between the groups. Conclusion: These findings confirm the need for ongoing investigations in human clinical cohorts to further resolve the relationships between the gut microbiota and metabolic and immune markers and risk for metabolic disease.
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