Evidence map›Paper›PMID 33374784›Full record

ReviewNutrients2020

Niacin and Butyrate: Nutraceuticals Targeting Dysbiosis and Intestinal Permeability in Parkinson's Disease.

Tennekoon B Karunaratne, Chijioke Okereke, Marissa Seamon, Sharad Purohit, Chandramohan Wakade, Amol Sharma

Open access · goldAbstract readReview
In one paragraph

Review in Nutrients, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 1 pooled it
2.1field-weighted citation impact, top 10% 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

32 citing papers in PubMed, 1 synthesis or guideline pooled it, 49 citations in OpenAlex.

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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

6 authors at 1 institution in 1 country.

Tennekoon B KarunaratneDigestive Health Clinical Research Center, Division of Gastroenterology/Hepatology, Medical College of Georgia, Augusta University, 1120, 15th St, Augusta, GA 30912, USA.ORCID 0000-0002-5918-5738
Chijioke OkerekeDigestive Health Clinical Research Center, Division of Gastroenterology/Hepatology, Medical College of Georgia, Augusta University, 1120, 15th St, Augusta, GA 30912, USA.
Marissa SeamonCenter for Biotechnology and Genomic Medicine, Medical College of Georgia, Augusta University, 1120, 15th St, Augusta, GA 30912, USA.
Sharad PurohitCenter for Biotechnology and Genomic Medicine, Medical College of Georgia, Augusta University, 1120, 15th St, Augusta, GA 30912, USA.ORCID 0000-0003-0385-3829
Chandramohan WakadeCenter for Biotechnology and Genomic Medicine, Medical College of Georgia, Augusta University, 1120, 15th St, Augusta, GA 30912, USA.
Amol SharmaDigestive Health Clinical Research Center, Division of Gastroenterology/Hepatology, Medical College of Georgia, Augusta University, 1120, 15th St, Augusta, GA 30912, USA.
Augusta University · US

Funding

CSRD VA I01 CX001815Department of Veterans Affairs, Rehabilitation Research and Development Merit Review Award RX001613Parkinson's Disease Foundation PF-TRG-1730RRD VA I01 RX001613
6 · The paper itself

Abstract

Dysbiosis is implicated by many studies in the pathogenesis of Parkinson's disease (PD). Advances in sequencing technology and computing have resulted in confounding data regarding pathogenic bacterial profiles in conditions such as PD. Changes in the microbiome with reductions in short-chain fatty acid (SCFA)-producing bacteria and increases in endotoxin-producing bacteria likely contribute to the pathogenesis of PD. GPR109A, a G-protein coupled receptor found on the surface of the intestinal epithelium and immune cells, plays a key role in controlling intestinal permeability and the inflammatory cascade. The absence of GPR109A receptors is associated with decreased concentration of tight junction proteins, leading to increased intestinal permeability and susceptibility to inflammation. In inflammatory states, butyrate acts via GPR109A to increase concentrations of tight junction proteins and improve intestinal permeability. Niacin deficiency is exacerbated in PD by dopaminergic medications. Niacin supplementation has been shown to shift macrophage polarization from pro-inflammatory to an anti-inflammatory profile. Niacin and butyrate, promising nutrients and unique ligands for the G protein-coupled receptor GPR109A, are reviewed in this paper in detail.

Indexed as

Dietary SupplementsAnimalsButyratesDysbiosisGastrointestinal MicrobiomeHumansIntestinal MucosaNiacinParkinson DiseasePermeabilityButyratesNiacinbrain-gut axisbutyrateGPR109Aintestinal barrierleaky gutmicrobiomeniacinnutraceuticalparkinson’s diseasespermeability

Identifiers

PMID33374784
PMCPMC7824468
OpenAlexW3116741321

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.