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

Research output: Contribution to journalReview articlepeer-review

12 Scopus citations


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 ex-acerbated 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.

Original languageEnglish (US)
Article number28
Pages (from-to)1-13
Number of pages13
Issue number1
StatePublished - Jan 2021


  • Brain-gut axis
  • Butyrate
  • GPR109A
  • Intestinal barrier
  • Leaky gut
  • Microbiome
  • Niacin
  • Nutraceutical
  • Parkinson’s diseases
  • Permeability

ASJC Scopus subject areas

  • Food Science
  • Nutrition and Dietetics


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