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    J Clin Invest. 2005 Dec;115(12):3400-3.

    Flushing out the role of GPR109A (HM74A) in the clinical efficacy of nicotinic acid.

    Pike NB.

    Source

    Atherosclerosis Department, GlaxoSmithKline, Stevenage, UK. Nick.B.Pike@gsk.com

    Abstract

    The recent discovery of the G(i) protein-coupled receptor GPR109A (HM74A in humans; PUMA-G in mice) as a receptor for nicotinic acid has provided the opportunity to gain greater understanding of the underlying biology contributing to the clinical efficacy (increases in HDL, decreases in VLDL, LDL, and triglycerides) and the characteristic side-effect profile of nicotinic acid. GPR109A has been proven to be the molecular target for the actions of nicotinic acid on adipose tissue, and in this issue of the JCI, Benyó et al. have confirmed the involvement of GPR109A in the nicotinic acid-induced flushing response, a common side effect. The involvement of GPR109A in both the desirable and undesirable clinical actions of nicotinic acid raises interesting questions regarding the function of this receptor.

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    PMID:
    16322787
    [PubMed - indexed for MEDLINE]
    PMCID:
    PMC1297267
    Free PMC Article

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