Independent effects of ADH1B and ALDH2 common dysfunctional variants on gout risk

Abstract Gout is caused by hyperuricemia, with alcohol consumption being an established risk factor. Alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH) are crucial enzymes for alcohol metabolism. We recently performed a genome-wide association study of gout and a subsequent fine-mapping s...

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Autores principales:	Masayuki Sakiyama, Hirotaka Matsuo, Airi Akashi, Seiko Shimizu, Toshihide Higashino, Makoto Kawaguchi, Akiyoshi Nakayama, Mariko Naito, Sayo Kawai, Hiroshi Nakashima, Yutaka Sakurai, Kimiyoshi Ichida, Toru Shimizu, Hiroshi Ooyama, Nariyoshi Shinomiya
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2017
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/fc32a65889214026935183695432fcf6
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spelling	oai:doaj.org-article:fc32a65889214026935183695432fcf62021-12-02T11:41:10ZIndependent effects of ADH1B and ALDH2 common dysfunctional variants on gout risk10.1038/s41598-017-02528-z2045-2322https://doaj.org/article/fc32a65889214026935183695432fcf62017-05-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-02528-zhttps://doaj.org/toc/2045-2322Abstract Gout is caused by hyperuricemia, with alcohol consumption being an established risk factor. Alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH) are crucial enzymes for alcohol metabolism. We recently performed a genome-wide association study of gout and a subsequent fine-mapping study which identified rs671 of ALDH2 as a gout locus. However, the association between gout and common variants of ADH1B has hitherto remained unreported, prompting us to investigate the association between gout and common dysfunctional variants of ADH1B (rs1229984) and ALDH2 (rs671). We used 1,048 clinically defined gout cases and 1,334 controls of Japanese male. The “His carrier” (His/His or His/Arg) of rs1229984 (His48Arg) of ADH1B significantly increased gout risk (P = 4.3 × 10−4, odds ratio = 1.76), as did the “non-Lys carrier (Glu/Glu)” of rs671 (Glu504Lys) of ALDH2. Furthermore, common variants of ADH1B and ALDH2 are independently associated with gout. Our findings likewise suggest that genotyping these variants can be useful for the evaluation of gout risk.Masayuki SakiyamaHirotaka MatsuoAiri AkashiSeiko ShimizuToshihide HigashinoMakoto KawaguchiAkiyoshi NakayamaMariko NaitoSayo KawaiHiroshi NakashimaYutaka SakuraiKimiyoshi IchidaToru ShimizuHiroshi OoyamaNariyoshi ShinomiyaNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-6 (2017)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Masayuki Sakiyama Hirotaka Matsuo Airi Akashi Seiko Shimizu Toshihide Higashino Makoto Kawaguchi Akiyoshi Nakayama Mariko Naito Sayo Kawai Hiroshi Nakashima Yutaka Sakurai Kimiyoshi Ichida Toru Shimizu Hiroshi Ooyama Nariyoshi Shinomiya Independent effects of ADH1B and ALDH2 common dysfunctional variants on gout risk
description	Abstract Gout is caused by hyperuricemia, with alcohol consumption being an established risk factor. Alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH) are crucial enzymes for alcohol metabolism. We recently performed a genome-wide association study of gout and a subsequent fine-mapping study which identified rs671 of ALDH2 as a gout locus. However, the association between gout and common variants of ADH1B has hitherto remained unreported, prompting us to investigate the association between gout and common dysfunctional variants of ADH1B (rs1229984) and ALDH2 (rs671). We used 1,048 clinically defined gout cases and 1,334 controls of Japanese male. The “His carrier” (His/His or His/Arg) of rs1229984 (His48Arg) of ADH1B significantly increased gout risk (P = 4.3 × 10−4, odds ratio = 1.76), as did the “non-Lys carrier (Glu/Glu)” of rs671 (Glu504Lys) of ALDH2. Furthermore, common variants of ADH1B and ALDH2 are independently associated with gout. Our findings likewise suggest that genotyping these variants can be useful for the evaluation of gout risk.
format	article
author	Masayuki Sakiyama Hirotaka Matsuo Airi Akashi Seiko Shimizu Toshihide Higashino Makoto Kawaguchi Akiyoshi Nakayama Mariko Naito Sayo Kawai Hiroshi Nakashima Yutaka Sakurai Kimiyoshi Ichida Toru Shimizu Hiroshi Ooyama Nariyoshi Shinomiya
author_facet	Masayuki Sakiyama Hirotaka Matsuo Airi Akashi Seiko Shimizu Toshihide Higashino Makoto Kawaguchi Akiyoshi Nakayama Mariko Naito Sayo Kawai Hiroshi Nakashima Yutaka Sakurai Kimiyoshi Ichida Toru Shimizu Hiroshi Ooyama Nariyoshi Shinomiya
author_sort	Masayuki Sakiyama
title	Independent effects of ADH1B and ALDH2 common dysfunctional variants on gout risk
title_short	Independent effects of ADH1B and ALDH2 common dysfunctional variants on gout risk
title_full	Independent effects of ADH1B and ALDH2 common dysfunctional variants on gout risk
title_fullStr	Independent effects of ADH1B and ALDH2 common dysfunctional variants on gout risk
title_full_unstemmed	Independent effects of ADH1B and ALDH2 common dysfunctional variants on gout risk
title_sort	independent effects of adh1b and aldh2 common dysfunctional variants on gout risk
publisher	Nature Portfolio
publishDate	2017
url	https://doaj.org/article/fc32a65889214026935183695432fcf6
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Independent effects of ADH1B and ALDH2 common dysfunctional variants on gout risk

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