Evidence mapPaperPMID 19627285Full record

ReviewBritish journal of pharmacology2009

Niacin: a re-emerging pharmaceutical for the treatment of dyslipidaemia.

Helen Vosper

2 registry-linked trialsAbstract readReview
In one paragraph

Review in British journal of pharmacology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to 2 registered trials, which are not on this map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
field-weighted citation impact
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.

NCT03973203 nacompletednot on this mapstarted 2014, after this paper: background citation

The Effect of Niacin Supplementation on Systemic Nicotinamide Adenine Dinucleotide (NAD+) Metabolism, Physiology and Muscle Performance in Healthy Controls and Mitochondrial Myopathy Patients

TypeinterventionalSponsorUniversity of HelsinkiRan2014 to 2018Enrolled15ConditionsMitochondrial MyopathiesArmsNiacin
NCT04538521 nacompletednot on this mapstarted 2019, after this paper: background citation

NiaMIT (NiaMIT_0001) Continuation for Early-stage Mitochondrial Myopathy Patients to Investigate the Effect of Niacin Supplementation on Systemic Nicotinamide Adenine Dinucleotide (NAD+) Metabolism, Physiology and Muscle Performance

TypeinterventionalSponsorUniversity of HelsinkiRan2019 to 2020Enrolled3ConditionsMitochondrial MyopathiesArmsNiacin
3 · Its place in the literature

Who cites it

18 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Treatment of dyslipidemia in allogeneic hematopoietic stem cell transplant patients.Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation · 2015
    Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

1 author.

Helen VosperSchool of Pharmacy and Life Sciences, The Robert Gordon University, Aberdeen, UK. h.vosper@rgu.ac.uk

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dyslipidaemias, particularly those characterized by the 'atherogenic profile' of high low-density lipoprotein-cholesterol and triglycerides and low high-density lipoprotein-cholesterol, are the major modifiable risk factor for atherosclerosis. The search for drugs to favourably alter such lipid profiles, reducing the associated morbidity and mortality, remains a major research focus. Niacin (nicotinic acid) is the most effective agent available for increasing high-density lipoprotein-cholesterol, but its use is associated with side effects that negatively affect patient compliance: these appear to arise largely as a result of production of prostaglandin D(2) and its subsequent activation of the DP(1) receptor. Desire to reduce the side effects (and improve pharmacokinetic parameters) has led to the development of a number of agonists that have differing effects, both in terms of clinical potency and the severity of adverse effects. The recent discovery of the niacin G-protein-coupled receptor HM74A (GPR109A) has clarified the distinction between the mechanism whereby niacin exerts its therapeutic effects and the mechanisms responsible for the generation of side effects. This has allowed the development of new drugs that show great potential for the treatment of dyslipidaemia. However, recent advances in understanding of the contribution of prostaglandin metabolism to vascular wall health suggest that some of the beneficial effects of niacin may well result from activation of the same pathways responsible for the adverse reactions. The purpose of this review is to emphasize that the search for agonists that show higher tolerability must take into account all aspects of signalling through this receptor.

Indexed as

AnimalsAtherosclerosisDrug DesignDyslipidemiasHumansHypolipidemic AgentsMedication AdherenceNiacinReceptors, G-Protein-CoupledReceptors, NicotinicRisk FactorsHCAR2 protein, humanHypolipidemic AgentsNiacinReceptors, G-Protein-CoupledReceptors, Nicotinic

Identifiers

PMID19627285
PMCPMC2757682

What Socratic holds

Texttitle and abstract
Read underepoch 390

Registered trials

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 Socratic graph.