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Evaluation of the Influence of Genetic Variants ofSLC2A9(GLUT9) andSLC22A12(URAT1) on the Development of Hyperuricemia and Gout

The result's identifiers

  • Result code in IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216208%3A11110%2F20%3A10414620" target="_blank" >RIV/00216208:11110/20:10414620 - isvavai.cz</a>

  • Alternative codes found

    RIV/00216208:11320/20:10414620 RIV/00023728:_____/20:N0000029

  • Result on the web

    <a href="https://verso.is.cuni.cz/pub/verso.fpl?fname=obd_publikace_handle&handle=IX2aMviP5x" target="_blank" >https://verso.is.cuni.cz/pub/verso.fpl?fname=obd_publikace_handle&handle=IX2aMviP5x</a>

  • DOI - Digital Object Identifier

    <a href="http://dx.doi.org/10.3390/jcm9082510" target="_blank" >10.3390/jcm9082510</a>

Alternative languages

  • Result language

    angličtina

  • Original language name

    Evaluation of the Influence of Genetic Variants ofSLC2A9(GLUT9) andSLC22A12(URAT1) on the Development of Hyperuricemia and Gout

  • Original language description

    Urate transporters, which are located in the kidneys, significantly affect the level of uric acid in the body. We looked at genetic variants of genes encoding the major reabsorption proteins GLUT9 (SLC2A9) and URAT1 (SLC22A12) and their association with hyperuricemia and gout. In a cohort of 250 individuals with primary hyperuricemia and gout, we used direct sequencing to examine theSLC22A12andSLC2A9genes. Identified variants were evaluated in relation to clinical data, biochemical parameters, metabolic syndrome criteria, and our previous analysis of the major secretory urate transporter ABCG2. We detected seven nonsynonymous variants ofSLC2A9. There were no nonsynonymous variants ofSLC22A12. Eleven variants ofSLC2A9and two variants ofSLC22A12were significantly more common in our cohort than in the European population (p= 0), while variants p.V282I and c.1002+78A&gt;G had a low frequency in our cohort (p= 0). Since the association between variants and the level of uric acid was not demonstrated, the influence of variants on the development of hyperuricemia and gout should be evaluated with caution. However, consistent with the findings of other studies, our data suggest that p.V282I and c.1002+78A&gt;G (SLC2A9) reduce the risk of gout, while p.N82N (SLC22A12) increases the risk.

  • Czech name

  • Czech description

Classification

  • Type

    J<sub>imp</sub> - Article in a specialist periodical, which is included in the Web of Science database

  • CEP classification

  • OECD FORD branch

    30226 - Rheumatology

Result continuities

  • Project

  • Continuities

    V - Vyzkumna aktivita podporovana z jinych verejnych zdroju

Others

  • Publication year

    2020

  • Confidentiality

    S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Data specific for result type

  • Name of the periodical

    Journal of Clinical Medicine

  • ISSN

    2077-0383

  • e-ISSN

  • Volume of the periodical

    9

  • Issue of the periodical within the volume

    8

  • Country of publishing house

    CH - SWITZERLAND

  • Number of pages

    17

  • Pages from-to

    2510

  • UT code for WoS article

    000564675200001

  • EID of the result in the Scopus database