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SAA1 genetic polymorphisms are associated with plasma glucose concentration in non-diabetic subjects

  • Xiang Xie , Yi-Tong Ma EMAIL logo , Yi-Ning Yang , Xiao-Mei Li , Ying-Ying Zheng , Zhen-Yan Fu , Xiang Ma , Fen Liu , Ying Huang and Bang-Dang Chen
Published/Copyright: August 13, 2013
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Clinical Chemistry and Laboratory Medicine (CCLM)
From the journal Clinical Chemistry and Laboratory Medicine (CCLM) Volume 51 Issue 12

Abstract

Background: Serum amyloid A (SAA) was reported to be associated with insulin resistance and type-2 diabetes. The present study aimed to investigate the association of SAA genetic polymorphisms with plasma glucose levels in non-diabetic subjects.

Methods: All participants (n=1220) were selected from subjects participating in the Cardiovascular Risk Survey (CRS) study. Five single-nucleotide polymorphisms (SNPs) (rs2229338, rs12218, rs4638289, rs7131332 and rs11603089) of SAA gene were genotyped using polymerase chain reaction (PCR)-restriction fragment length polymorphism (RFLP) analysis.

Results: In the present study, we found rs2229338, rs4638289 and rs12218 were significantly associated with plasma glucose levels in a dominate model, recessive model or additive model before and after multivariate adjustment (all p<0.05). These associations were not found in rs7131332 and rs11603089 before and after adjustment of key co-variants.

Conclusions: The genetic polymorphisms of SAA1 were associated with plasma glucose levels in non-diabetic subjects.

Keywords: genetic polymorphism; serum amyloid A; type 2 diabetes
Corresponding author: Yi-Tong Ma, Department of Cardiology, First Affiliated Hospital of Xinjiang Medical University, Urumqi, 830054 P.R. China, Phone: +86 991 4366169, Fax: +86 991 4366169, +86 991 4364303, E-mail: ;

This work was supported financially by grants from Natural Science Foundation of Xinjiang (2011211B32).

Conflict of interest statement

Authors’ conflict of interest disclosure: The authors stated that there are no conflicts of interest regarding the publication of this article. Research support played no role in thestudy design; in the collection, analysis, and interpretationof data; in the writing of the report; or in the decision tosubmit the report for publication.

Research funding: None declared.

Employment or leadership: None declared.

Honorarium: None declared.

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Received: 2013-02-15
Accepted: 2013-07-19
Published Online: 2013-08-13
Published in Print: 2013-12-01

©2013 by Walter de Gruyter Berlin Boston

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https://doi.org/10.1515/cclm-2013-0097
Keywords for this article
genetic polymorphism; serum amyloid A; type 2 diabetes

Articles in the same Issue

  1. Letters to the Editor
  2. The addition of MESNA in vitro prolongs prothrombin time similar to N-acetyl cysteine
  3. Detection of unknown β-thalassemia cases from atypical HbA1c chromatograms
  4. Analytical study of a new turbidimetric assay for urinary neutrophil gelatinase-associated lipocalin (NGAL) determination
  5. The rare bipolar-contracted red cell significance and correlation with red cell volume
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  7. PBMC expressed adiponectin mRNA is predictive of survival in patients with gastric cancer
  8. Comparison study of two commercially available methods for the determination of infliximab, adalimumab, etanercept and anti-drug antibody levels
  9. Development and validation of a rapid and reliable high-performance liquid chromatography method for methadone quantification in human plasma and saliva
  10. Reply to Ruiz-Argüello et al.: Comparison study of two commercially available methods for the determination of infliximab, adalimumab, etanercept and anti-drug antibody levels
  11. Still more discussion on the journal impact factor
  12. The order of draw, myth or science
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  34. Longitudinal evaluation of thyroid autoimmunity and function in pregnant Korean women
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  38. Double heterozygosity in the BRCA1 and BRCA2 genes in Italian family
  39. Quantification of EGFR autoantibodies in the amplification phenomenon of HER2 in breast cancer
  40. Diabetes
  41. SAA1 genetic polymorphisms are associated with plasma glucose concentration in non-diabetic subjects
  42. Acknowledgment
  43. Acknowledgment
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