2017
DOI: 10.1016/j.imlet.2017.08.005
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Sodium butyrate ameliorates S100/FCA-induced autoimmune hepatitis through regulation of intestinal tight junction and toll-like receptor 4 signaling pathway

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Cited by 31 publications
(28 citation statements)
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“…Butyrate is an important energy source for gut enterocytes (Chen et al, 2018), and it is mainly from butyric acid-producing bacteria in gut (Hamer et al, 2008). Lack of butyric acid can result in gut permeability increase (Wu et al, 2017). In this experiment, the gut permeability was significantly increased, and butyrate content was sharply decreased due to the reduction in the relative abundance of butyric acid producing bacteria.…”
Section: Discussionmentioning
confidence: 73%
“…Butyrate is an important energy source for gut enterocytes (Chen et al, 2018), and it is mainly from butyric acid-producing bacteria in gut (Hamer et al, 2008). Lack of butyric acid can result in gut permeability increase (Wu et al, 2017). In this experiment, the gut permeability was significantly increased, and butyrate content was sharply decreased due to the reduction in the relative abundance of butyric acid producing bacteria.…”
Section: Discussionmentioning
confidence: 73%
“…The maintenance of the intestinal epithelial barrier is critical to reducing systemic inflammation as evidenced by the emerging association between obesity and increased intestinal permeability [7,107]. Recent studies have suggested that SCFAs enhance the expression of epithelial barrier-forming molecules and mucin production, which are partly mediated by 5′ adenosine monophosphate-activated protein kinase (AMPK) activation, HDACi activity and TLR4 pathway [108,109,110,111]. It is known that SCFAs activate several cell surface G-protein-coupled receptors (GPCRs), such as GPR43, GPR41, GPR109A, and Olfr78 [112,113,114].…”
Section: The Role Of Secondary Bas and Scfas In Colonic Inflammationmentioning
confidence: 99%
“…Obese, diabetic models in a simplistic context exhibit fatty, insulin resistant livers due to increased triglyceride content and decreased β oxidation within the tissue, which is also associated a pro-inflammatory state. Supplementation of butyrate or butyrogenic bacterial strains is associated with the reduction of ectopic lipids in hepatic tissue [ 172 , 173 , 174 , 175 ]. For example, Jin et al assessed the effect of oral sodium butyrate supplementation (0.6 g/kg body weight/day) in female C57BL/6J mice fed either a liquid control (12% energy from fat) or Westernized diet (25% energy from fat, 50% w/w sucrose supplementation) for 6 weeks [ 172 ].…”
Section: Butyrate and Peripheral Tissuesmentioning
confidence: 99%
“…Additionally butyrate-supplemented rats exhibited significantly increased hepatic peroxisome proliferator-activated receptor γ coactivator 1-α (PGC-1α), a transcriptional coactivator important in increasing mitochondrial biogenesis and function, expression [ 173 ]. In a murine model of autoimmune hepatitis induced by Freund’s complete adjuvant, male C57BL/6 mice receiving 300 mg/kg sodium butyrate as a daily gavage for 3 weeks exhibited reduced mRNA and protein content of NF-κB, IL-6 and TNF-α relative to the hepatitis controls [ 174 ]. Finally, Liu and colleagues administered C. butyricum (5 × 10 8 CFU) intragastrically in male ICR mice for 5 days prior to acute liver injury induced via carbon tetrachloride (CCl 4 ) intraperitoneal injection [ 175 ].…”
Section: Butyrate and Peripheral Tissuesmentioning
confidence: 99%