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      Analysis of gender-specific associations between aldehyde dehydrogenase 2 ( ALDH2) rs671 genetic polymorphisms and serum uric acid levels in Han Chinese

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          Abstract

          Background

          Serum uric acid (SUA) is influenced by lifestyle and genetics, and unbalanced SUA levels are linked to various common disorders. While the aldehyde dehydrogenase 2 (ALDH2) rs671 polymorphism appears to be associated with SUA levels, the evidence remains inconclusive. The aim of this study was to examine the distribution of the ALDH2 rs671 polymorphism among Han Chinese in Beijing and determine the association between this polymorphism and SUA.

          Methods

          A total of 6,461 randomized healthy individuals were included in the study. Biochemical indicators were tested and ALDH2 rs671 polymorphism testing was conducted for subjects enrolled in the study. The distribution of the ALDH2 rs671 polymorphism and the relationship between genotype and the levels of serum lipids and uric acid (UA) were analyzed.

          Results

          The ALDH2 rs671 genotype frequencies were 68.1% (G/G), 29.3% (G/A), and 2.6% (A/A). There was no significant difference in allele distribution between males and females. In males, different ALDH2 genotypes exhibited significant differences in several biochemical analytes, including body mass index (BMI), blood glucose (Glu), total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), UA, glutamyl transpeptidase (GGT), and creatinine (Cr) (P<0.05). No such differences were found in females. SUA levels in G/A and A/A-carrying males were significantly lower than those of G/G-carrying males. The effect of the ALDH2 polymorphism on UA was still significant after further adjustment for factors including BMI, Glu, TC, HDL-C, Cr, and GGT.

          Conclusions

          The ALDH2 polymorphism is related to SUA in Beijing males, and A allele-carrying males have lower SUA levels.

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          Most cited references26

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          Uric acid and cardiovascular risk.

          Daniel Feig, Duk-Hee Kang, Richard J. Johnson (2008)
          Article 0 comments Cited 309 times – based on 0 reviews     Review now
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            Association of three genetic loci with uric acid concentration and risk of gout: a genome-wide association study.

            Abbas Dehghan, Anna Köttgen, Qiong Yang … (2008)
            Hyperuricaemia, a highly heritable trait, is a key risk factor for gout. We aimed to identify novel genes associated with serum uric acid concentration and gout. Genome-wide association studies were done for serum uric acid in 7699 participants in the Framingham cohort and in 4148 participants in the Rotterdam cohort. Genome-wide significant single nucleotide polymorphisms (SNPs) were replicated in white (n=11 024) and black (n=3843) individuals who took part in the study of Atherosclerosis Risk in Communities (ARIC). The SNPs that reached genome-wide significant association with uric acid in either the Framingham cohort (p<5.0 x 10(-8)) or the Rotterdam cohort (p<1.0 x 10(-7)) were evaluated with gout. The results obtained in white participants were combined using meta-analysis. Three loci in the Framingham cohort and two in the Rotterdam cohort showed genome-wide association with uric acid. Top SNPs in each locus were: missense rs16890979 in SLC2A9 (p=7.0 x 10(-168) and 2.9 x 10(-18) for white and black participants, respectively); missense rs2231142 in ABCG2 (p=2.5 x 10(-60) and 9.8 x 10(-4)), and rs1165205 in SLC17A3 (p=3.3 x 10(-26) and 0.33). All SNPs were direction-consistent with gout in white participants: rs16890979 (OR 0.59 per T allele, 95% CI 0.52-0.68, p=7.0 x 10(-14)), rs2231142 (1.74, 1.51-1.99, p=3.3 x 10(-15)), and rs1165205 (0.85, 0.77-0.94, p=0.002). In black participants of the ARIC study, rs2231142 was direction-consistent with gout (1.71, 1.06-2.77, p=0.028). An additive genetic risk score of high-risk alleles at the three loci showed graded associations with uric acid (272-351 mumol/L in the Framingham cohort, 269-386 mumol/L in the Rotterdam cohort, and 303-426 mumol/L in white participants of the ARIC study) and gout (frequency 2-13% in the Framingham cohort, 2-8% in the Rotterdam cohort, and 1-18% in white participants in the ARIC study). We identified three genetic loci associated with uric acid concentration and gout. A score based on genes with a putative role in renal urate handling showed a substantial risk for gout.
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              The molecular physiology of uric acid homeostasis.

              Asim K. Mandal, David Mount (2015)
              Uric acid, generated from the metabolism of purines, has proven and emerging roles in human disease. Serum uric acid is determined by production and the net balance of reabsorption or secretion by the kidney and intestine. A detailed understanding of epithelial absorption and secretion of uric acid has recently emerged, aided in particular by the results of genome-wide association studies of hyperuricemia. Novel genetic and regulatory networks with effects on uric acid homeostasis have also emerged. These developments promise to lead to a new understanding of the various diseases associated with hyperuricemia and to novel, targeted therapies for hyperuricemia.
              Article 0 comments Cited 162 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): Ann Transl Med
                Journal ID (iso-abbrev): Ann Transl Med
                Journal ID (publisher-id): ATM
                Title: Annals of Translational Medicine
                Publisher: AME Publishing Company
                ISSN (Print): 2305-5839
                ISSN (Electronic): 2305-5847
                Publication date (Print and electronic): May 2021
                Publication date (Print): May 2021
                Volume: 9
                Issue: 9
                Electronic Location Identifier: 772
                Affiliations
                [1 ]deptDepartment of Laboratory Medicine, Peking Union Medical College Hospital , Peking Union Medical College & Chinese Academy of Medical Science , Beijing, China;
                [2 ]deptDepartment of Health Care , Peking Union Medical College and Chinese Academy of Medical Science , Beijing, China
                Author notes

                Contributions: (I) Conception and design: J Wu, C Ma; (II) Administrative support: L Qiu, T Xu; (III) Provision of study materials or patients: J Yi, Y Chen, A Ye, L Kong; (IV) Collection and assembly of data: J Wu, C Ma; (V) Data analysis and interpretation: C Ma, J Wu; (VI) Manuscript writing: All authors; (VII) Final approval of manuscript: All authors.

                [#]

                These authors contributed equally to this work.

                Correspondence to: Prof. Ling Qiu. Department of Laboratory Medicine, Peking Union Medical College Hospital, Peking Union Medical College & Chinese Academy of Medical Science, Beijing 100730, China. Email: lingqiubj@ 123456163.com ; Prof. Tengda Xu. Department of Health Care, Peking Union Medical College and Chinese Academy of Medical Science, Beijing 100730, China. Email: Xutd@ 123456pumch.cn .
                Article
                Publisher ID: atm-09-09-772
                DOI: 10.21037/atm-20-7113
                PMC ID: 8246195
                PubMed ID: 34268385
                SO-VID: 3bb0b9a7-bf06-4cfa-b2d5-a924f978a17e
                Copyright © 2021 Annals of Translational Medicine. All rights reserved.
                License:

                Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0.

                History
                Date received : 25 October 2020
                Date accepted : 28 February 2021
                Categories
                Subject: Original Article

                Keywords: aldehyde dehydrogenase 2 (aldh2),gene polymorphism,uric acid (ua)
                Data availability:
                Keywords: aldehyde dehydrogenase 2 (aldh2), gene polymorphism, uric acid (ua)

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