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

1
Digestive Health Clinical Research Center, Division of Gastroenterology/Hepatology, Medical College of Georgia, Augusta University, 1120, 15th St, Augusta, GA 30912, USA
2
Center for Biotechnology and Genomic Medicine, Medical College of Georgia, Augusta University, 1120, 15th St, Augusta, GA 30912, USA
3
Department of Neuroscience, Medical College of Georgia, Augusta University, 1120, 15th St, Augusta, GA 30912, USA
4
Department of Obstetrics and Gynecology, Medical College of Georgia, Augusta University, 1120, 15th St, Augusta, GA 30912, USA
5
Department of Undergraduate Health Professionals, College of Allied Health Sciences, Augusta University, 1120, 15th St, Augusta, GA 30912, USA
6
Department of Physical Therapy, College of Allied Health Sciences, Augusta University, 1120, 15th St, Augusta, GA 30912, USA
*
Author to whom correspondence should be addressed.
Nutrients 2021, 13(1), 28; https://doi.org/10.3390/nu13010028
Received: 2 December 2020 / Revised: 18 December 2020 / Accepted: 21 December 2020 / Published: 23 December 2020
(This article belongs to the Special Issue Gut Microbiota in Cognition, Behaviour and Alzheimer's Disease)
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. View Full-Text
Keywords: Parkinson’s diseases; brain-gut axis; microbiome; intestinal barrier; permeability; leaky gut; niacin; butyrate; GPR109A; nutraceutical Parkinson’s diseases; brain-gut axis; microbiome; intestinal barrier; permeability; leaky gut; niacin; butyrate; GPR109A; nutraceutical
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MDPI and ACS Style

Karunaratne, T.B.; Okereke, C.; Seamon, M.; Purohit, S.; Wakade, C.; Sharma, A. Niacin and Butyrate: Nutraceuticals Targeting Dysbiosis and Intestinal Permeability in Parkinson’s Disease. Nutrients 2021, 13, 28. https://doi.org/10.3390/nu13010028

AMA Style

Karunaratne TB, Okereke C, Seamon M, Purohit S, Wakade C, Sharma A. Niacin and Butyrate: Nutraceuticals Targeting Dysbiosis and Intestinal Permeability in Parkinson’s Disease. Nutrients. 2021; 13(1):28. https://doi.org/10.3390/nu13010028

Chicago/Turabian Style

Karunaratne, Tennekoon B., Chijioke Okereke, Marissa Seamon, Sharad Purohit, Chandramohan Wakade, and Amol Sharma. 2021. "Niacin and Butyrate: Nutraceuticals Targeting Dysbiosis and Intestinal Permeability in Parkinson’s Disease" Nutrients 13, no. 1: 28. https://doi.org/10.3390/nu13010028

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