Taurocholic acid, a primary 12α-hydroxylated bile acid, induces leakiness in the distal small intestine in rats

Liu, Hongxia; Kohmoto, Ohji; Sakaguchi, Ayana; Hori, Shigeaki; Tochigi, Misuzu; Tada, Koji; Lee, Yeonmi; Kikuchi, Keidai; Ishizuka, Satoshi

doi:10.1016/j.fct.2022.113136

Cited by 14 publications

(11 citation statements)

References 44 publications

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“…In addition, compared with MC_1 group, the total amount of primary bile acids in feces of MC_2 group was increased, including β-MCA, CA and CDCA contents. Previous studies had shown that a high-fat diet increased the secretion of 12α-hydroxyl bile acids and promoted fecal bile acids excretion [32,33]. In hyperlipidemic rats, the total amount of primary bile acids in feces of rats in MC_2 and MC_3 groups had no signi cant change.…”

Section: Effect Of Lrs On the Overall Distribution Of Fecal Bile Acidsmentioning

confidence: 84%

The dynamic revolution of intestinal flora and bile acids profiles revealed the hypolipidemic effect of lotus seed resistant starch

Lei,

Jiang,

Cai

et al. 2024

Preprint

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Our research group had shown that lotus seed resistant starch (LRS) had hypolipidemic effect, but its mechanism is still being studied. Bile acids are important metabolic pathway of cholesterol, accelerating the conversion of cholesterol into bile acids and excreting them in the fecal may be one of the effective ways to reduce cholesterol levels in the body. This study aimed to reveal the lipid-lowering effect of LRS from the perspectives of fecal microbiota and bile acids. Herein, a rat model of hyperlipidemia was established and intervened with LRS. Fecal samples from different periods were collected to study the changes in microbiota and bile acids, and the correlation network diagram was established to reveal the lipid-lowering mechanism of LRS. The results showed that LRS inhibited the growth of Prevotella and Allobaculum in hyperlipidemic rats. Meanwhile LRS promoted the excretion of cholic acid (CA), chenodeoxycholic acid (CDCA), alpha-muricholic acid (α-MCA), ursodeoxycholic acid (UDCA), ursocholic acid (UCA), 7-ketodeoxycholic acid (7-keto-DCA) in hyperlipidemic rats. Furthermore, total cholesterol (TCHO), low-density lipoprotein cholesterol (LDL-C) were negatively correlated with CA, CDCA, UDCA and UCA, and TCHO was positively correlated with Prevotella. Triglycerides (TG) was negatively correlated with CA, CDCA, 7-keto-DCA and UCA, while high-density lipoprotein cholesterol (HDL-C) was positively correlated with α-MCA. Regulating the gut microbiota such as Prevotella and accelerating the transformation of liver cholesterol into primary bile acids (CA, CDCA) for excretion from the body was one of the effective means for LRS to ameliorate blood lipid levels in hyperlipidemic rats.

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Section: Effect Of Lrs On the Overall Distribution Of Fecal Bile Acidsmentioning

confidence: 84%

The dynamic revolution of intestinal flora and bile acids profiles revealed the hypolipidemic effect of lotus seed resistant starch

Lei,

Jiang,

Cai

et al. 2024

Preprint

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“…Previous studies showed that the level of primary 12αOH BAs in the enterohepatic circulation was selectively increased by feeding an HFD [ 11 , 12 ], and the level of primary BAs in the small intestine has been shown to be higher than that of secondary BAs in the large intestine [ 12 ]. In rats on a CA-supplemented diet, VCM treatment increased the TCA concentration in the ileum [ 37 ], whereas DCA was almost undetectable at the same site, and fecal CA concentration was high in rats fed the CA with VCM treatment [ 37 ]. These data are similar to our present findings ( Figure 8 ) and confirm that VCM treatment suppressed the 7α-dehydroxylation of CA in the large intestine.…”

Section: Discussionmentioning

confidence: 99%

“…These data are similar to our present findings ( Figure 8 ) and confirm that VCM treatment suppressed the 7α-dehydroxylation of CA in the large intestine. Moreover, TCA selectively affects the gut permeability in the ileum, which is the site for reabsorbing conjugated BAs [ 37 ]. In addition, the effect of the TCA on ileal permeability is much stronger than that of DCA in the colon for gut leakiness [ 37 ].…”

Section: Discussionmentioning

confidence: 99%

“…Moreover, TCA selectively affects the gut permeability in the ileum, which is the site for reabsorbing conjugated BAs [ 37 ]. In addition, the effect of the TCA on ileal permeability is much stronger than that of DCA in the colon for gut leakiness [ 37 ]. Therefore, we suggest that the iHFC diet with VCM treatment may disrupt gut permeability by increasing TCA levels in the small intestine and induce liver inflammation by enterohepatic circulation in our mouse NASH model.…”

Section: Discussionmentioning

confidence: 99%

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Impact of Vancomycin Treatment and Gut Microbiota on Bile Acid Metabolism and the Development of Non-Alcoholic Steatohepatitis in Mice

Kasai

Igarashi

Tada

et al. 2023

IJMS

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The potential roles of the gut microbiota in the pathogenesis of non-alcoholic fatty liver disease, including non-alcoholic steatohepatitis (NASH), have attracted increased interest. We have investigated the links between gut microbiota and NASH development in Tsumura-Suzuki non-obese mice fed a high-fat/cholesterol/cholate-based (iHFC) diet that exhibit advanced liver fibrosis using antibiotic treatments. The administration of vancomycin, which targets Gram-positive organisms, exacerbated the progression of liver damage, steatohepatitis, and fibrosis in iHFC-fed mice, but not in mice fed a normal diet. F4/80+-recruited macrophages were more abundant in the liver of vancomycin-treated iHFC-fed mice. The infiltration of CD11c+-recruited macrophages into the liver, forming hepatic crown-like structures, was enhanced by vancomycin treatment. The co-localization of this macrophage subset with collagen was greatly augmented in the liver of vancomycin-treated iHFC-fed mice. These changes were rarely seen with the administration of metronidazole, which targets anaerobic organisms, in iHFC-fed mice. Finally, the vancomycin treatment dramatically modulated the level and composition of bile acid in iHFC-fed mice. Thus, our data demonstrate that changes in inflammation and fibrosis in the liver by the iHFC diet can be modified by antibiotic-induced changes in gut microbiota and shed light on their roles in the pathogenesis of advanced liver fibrosis.

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“…Liu H. et al. studied the effects of CA supplementation on intestinal barrier integrity in rats ( 125 ). There was an accumulation of TCA at the ileum and subsequently found that TCA at concentrations found in CA fed mice increased ileal permeability in a Ussing chamber but not in other regions of the intestine.…”

Section: Bile Acids and Barrier Function/intestinal Permeabilitymentioning

confidence: 99%

Bile acids as inflammatory mediators and modulators of intestinal permeability

et al. 2022

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Bile acids are critical for the digestion and absorption of lipids and fat-soluble vitamins; however, evidence continues to emerge supporting additional roles for bile acids as signaling molecules. After they are synthesized from cholesterol in the liver, primary bile acids are modified into secondary bile acids by gut flora contributing to a diverse pool and making the composition of bile acids highly sensitive to alterations in gut microbiota. Disturbances in bile acid homeostasis have been observed in patients with Inflammatory Bowel Diseases (IBD). In fact, a decrease in secondary bile acids was shown to occur because of IBD-associated dysbiosis. Further, the increase in luminal bile acids due to malabsorption in Crohn’s ileitis and ileal resection has been implicated in the induction of diarrhea and the exacerbation of inflammation. A causal link between bile acid signaling and intestinal inflammation has been recently suggested. With respect to potential mechanisms related to bile acids and IBD, several studies have provided strong evidence for direct effects of bile acids on intestinal permeability in porcine and rodent models as well as in humans. Interestingly, different bile acids were shown to exert distinct effects on the inflammatory response and intestinal permeability that require careful consideration. Such findings revealed a potential effect for changes in the relative abundance of different bile acids on the induction of inflammation by bile acids and the development of IBD. This review summarizes current knowledge about the roles for bile acids as inflammatory mediators and modulators of intestinal permeability mainly in the context of inflammatory bowel diseases.

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Taurocholic acid, a primary 12α-hydroxylated bile acid, induces leakiness in the distal small intestine in rats

Cited by 14 publications

References 44 publications

The dynamic revolution of intestinal flora and bile acids profiles revealed the hypolipidemic effect of lotus seed resistant starch

The dynamic revolution of intestinal flora and bile acids profiles revealed the hypolipidemic effect of lotus seed resistant starch

Impact of Vancomycin Treatment and Gut Microbiota on Bile Acid Metabolism and the Development of Non-Alcoholic Steatohepatitis in Mice

Bile acids as inflammatory mediators and modulators of intestinal permeability

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