High-fat-induced intestinal permeability dysfunction associated with altered fecal bile acids

Stenman, Lotta K.; Holma, Reetta; Korpela, Riitta

doi:10.3748/wjg.v18.i9.923

Cited by 146 publications

(155 citation statements)

References 34 publications

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“…The concentration of DCA in feces of fat-fed mice varies from 1.4 to 3.0 mM and in control mice from 0.28 to 0.44 mM (19). Interestingly, in the present study DCA did not influence colonic barrier function at the lower fecal concentrations.…”

Section: Discussionmentioning

confidence: 45%

“…We have previously reported an inverse correlation between the proportion of fecal UDCA and intestinal permeability (19). Orally administered UDCA has shown barrier-protective effects also in experimentally induced ileitis in rats (2).…”

Section: Discussionmentioning

confidence: 99%

“…Fatty feed increased the fecal concentration of DCA whereas it decreased the proportion of the more hydrophilic, tertiary bile acid ursodeoxycholic acid (UDCA) (19), which is potentially cytoprotective (2,10,18). The decrease in the proportion of fecal UDCA was related to disruption of the intestinal barrier (19).…”

mentioning

confidence: 99%

“…We have previously shown in mice that a diet high in fat deteriorates gut barrier function and increases the fecal concentration of DCA nearly tenfold (19). The present study aimed to investigate whether bile acids have a role in the onset of barrier dysfunction related to a high-fat diet.…”

mentioning

confidence: 99%

“…total fecal bile acid concentration, a high-fat diet in mice modifies the fecal bile acid profile (19). Fatty feed increased the fecal concentration of DCA whereas it decreased the proportion of the more hydrophilic, tertiary bile acid ursodeoxycholic acid (UDCA) (19), which is potentially cytoprotective (2,10,18).…”

mentioning

confidence: 99%

See 4 more Smart Citations

A novel mechanism for gut barrier dysfunction by dietary fat: epithelial disruption by hydrophobic bile acids

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Eggert

et al. 2013

American Journal of Physiology-Gastrointestinal and Liver Physi

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Section: Discussionmentioning

confidence: 45%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

See 3 more Smart Citations

A novel mechanism for gut barrier dysfunction by dietary fat: epithelial disruption by hydrophobic bile acids

Stenman

Holma

Eggert

et al. 2013

American Journal of Physiology-Gastrointestinal and Liver Physi

178

137

View full text Add to dashboard Cite

show abstract

Adiponectin, bile acids, and burnt-out nonalcoholic steatohepatitis: New light on an old paradox

Claudel

Trauner

2013

Hepatology

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Gut microbial composition can differentially regulate bile acid synthesis in humanized mice

Kang

Hylemon

Gillevet

et al. 2017

Hepatology Communications

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We previously reported that alcohol drinkers with and without cirrhosis showed a significant increase in fecal bile acid secretion compared to nondrinkers. We hypothesized this may be due to activation by alcohol of hepatic cyclic adenosine monophosphate responsive element‐binding protein 3‐like protein 3 (CREBH), which induces cholesterol 7α‐hydroxylase (Cyp7a1). Alternatively, the gut microbiota composition in the absence of alcohol might increase bile acid synthesis by up‐regulating Cyp7a1. To test this hypothesis, we humanized germ‐free (GF) mice with stool from healthy human subjects (Ctrl‐Hum), human subjects with cirrhosis (Cirr‐Hum), and human subjects with cirrhosis and active alcoholism (Alc‐Hum). All animals were fed a normal chow diet, and none demonstrated cirrhosis. Both hepatic Cyp7a1 and sterol 12α‐hydroxylase (Cyp8b1) messenger RNA (mRNA) levels were significantly induced in the Alc‐Hum and Ctrl‐Hum mice but not in the Cirr‐Hum mice or GF mice. Liver bile acid concentration was correspondingly increased in the Alc‐Hum mice despite fibroblast growth factor 15, fibroblast growth receptor 4, and small heterodimer partner mRNA levels being significantly induced in the large bowel and liver of the Ctrl‐Hum mice and Alc‐Hum mice but not in the Cirr‐Hum mice or GF mice. This suggests that the normal pathways of Cyp7a1 repression were activated in the Alc‐Hum mice and Ctrl‐Hum mice. CREBH mRNA was significantly induced only in the Ctrl‐Hum mice and Alc‐Hum mice, possibly indicating that the gut microbiota up‐regulate CREBH and induce bile acid synthesis genes. Analysis of stool bile acids showed that the microbiota of the Cirr‐Hum and Alc‐Hum mice had a greater ability to deconjugate and 7α‐dehydroxylate primary bile acids compared to the microbiota of the Cirr‐Hum mice. 16S ribosomal RNA gene sequencing of the gut microbiota showed that the relative abundance of taxa that 7‐α dehydroxylate primary bile acids was higher in the Ctrl‐Hum and Alc‐Hum groups. Conclusion: The composition of gut microbiota influences the regulation of the rate‐limiting enzymes in bile acid synthesis in the liver. (Hepatology Communications 2017;1:61–70)

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High-fat-induced intestinal permeability dysfunction associated with altered fecal bile acids

Abstract: High-fat-feeding increased intestinal permeability, perhaps by a mechanism related to bile acid metabolism, namely a decreased proportion of fecal UDCA and increased FXR expression.

Cited by 146 publications

References 34 publications

A novel mechanism for gut barrier dysfunction by dietary fat: epithelial disruption by hydrophobic bile acids

A novel mechanism for gut barrier dysfunction by dietary fat: epithelial disruption by hydrophobic bile acids

Adiponectin, bile acids, and burnt-out nonalcoholic steatohepatitis: New light on an old paradox

Gut microbial composition can differentially regulate bile acid synthesis in humanized mice

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