Abstract
Butyrate and niacin are produced by gut microbiota, however butyrate has received most attention for its effects on colonic health. The present study aimed at exploring the effect of niacin on experimental colitis as well as throwing some light on the ability of niacin to modulate angiogenesis which plays a crucial role of in the pathogenesis of inflammatory bowel disease. Rats were given niacin for 2 weeks. On day 8, colitis was induced by intrarectal administration of iodoacetamide. Rats were sacrificed on day 15 and colonic damage was assessed macroscopically and histologically. Colonic myeloperoxidase (MPO), tumour necrosis factor (TNF)-α, interleukin (IL)-10, vascular endothelial growth factor (VEGF), angiostatin and endostatin levels were determined. Niacin attenuated the severity of colitis as demonstrated by a decrease in weight loss, colonic wet weight and MPO activity. Iodoacetamide-induced rise in the colonic levels of TNF-α, VEGF, angiostatin and endostatin was reversed by niacin. Moreover, niacin normalized IL-10 level in colon. Mepenzolate bromide, a GPR109A receptor blocker, abolished the beneficial effects of niacin on body weight, colon wet weight as well as colonic levels of MPO and VEGF. Therefore, niacin was effective against iodoacetamide-induced colitis through ameliorating pathologic angiogenesis and inflammatory changes in a GPR109A-dependent manner.
Highlights
Commensal microbiota in the gut have profound effects on human health[1, 2]
The cell-surface receptors identified for butyrate are GPR43 and GPR109A which is known as hydroxycarboxylic acid receptor 2 (HCA2 or HCAR2) or niacin receptor 1 (NIACR1)
The current study revealed that niacin protected against experimental colitis induced by iodoacetamide in rats by ameliorating colonic inflammation and pathologic angiogenesis
Summary
Commensal microbiota in the gut have profound effects on human health[1, 2]. They promote colonic health through production of the short-chain fatty acids (SCFAs) by fermentation of dietary fiber. Previous studies proved that butyrate attenuated colonic inflammation and stimulated colonic repair[4,5,6] It improved the efficacy of mesalazine in experimental colitis models and inflammatory bowel disease (IBD) patients[7,8,9]. The cell-surface receptors identified for butyrate are GPR43 and GPR109A which is known as hydroxycarboxylic acid receptor 2 (HCA2 or HCAR2) or niacin receptor 1 (NIACR1) These receptors are G-protein-coupled and are expressed in colonic epithelium, adipose tissue and immune cells[10, 11]. Niacin deficiency in humans results in pellagra, characterized by intestinal inflammation, diarrhea, dermatitis and dementia[14] Singh and his colleagues demonstrated that niacin protected antibiotic-treated mice from weight loss, diarrhea, bleeding and colon cancer induced by administration of azoxymethane (AOM) and DSS12. The role of GPR109A in mediating such beneficial effects of niacin was examined
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