Evidence map›Paper›PMID 16322787›Full record

ArticleThe Journal of clinical investigation2005

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

Nicholas B Pike

Open access · bronzeAbstract readComment
In one paragraph

Article in The Journal of clinical investigation, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.3field-weighted citation impact, top 13% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

25 citing papers in PubMed, 71 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

1 author at 1 institution in 1 country.

Nicholas B PikeAtherosclerosis Department, GlaxoSmithKline, Stevenage, UK. Nick.B.Pike@gsk.com
GlaxoSmithKline (United Kingdom) · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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.

Indexed as

AdipocytesAnimalsHumansHypolipidemic AgentsLigandsLipoproteins, HDLLipoproteins, LDLMiceModels, BiologicalNiacinReceptors, G-Protein-CoupledReceptors, NicotinicHCAR2 protein, humanHCAR3 protein, humanHypolipidemic AgentsLigandsLipoproteins, HDLLipoproteins, LDLNiacinReceptors, G-Protein-CoupledReceptors, Nicotinic

Identifiers

PMID16322787
PMCPMC1297267
OpenAlexW1981002997

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.