scholarly journals Genetically obese mice do not show increased gut permeability or faecal bile acid hydrophobicity

2013 ◽  
Vol 110 (6) ◽  
pp. 1157-1164 ◽  
Author(s):  
Lotta K. Stenman ◽  
Reetta Holma ◽  
Helena Gylling ◽  
Riitta Korpela
Keyword(s):  
Bile Acid ◽  
Bile Acids ◽  
Intestinal Permeability ◽  
Low Grade ◽  
Obese Mice ◽  
Gut Permeability ◽  
Barrier Dysfunction ◽  
Gut Barrier ◽  
Genetic Obesity ◽  
Gut Barrier Function

Gut barrier dysfunction may lead to metabolic endotoxaemia and low-grade inflammation. Recent publications have demonstrated gut barrier dysfunction in obesity induced by a diet high in fat, and a pathogenetic role for luminal bile acids has been proposed. We aimed to investigate whether genetically obese mice develop increased gut permeability and alterations in luminal bile acids on a diet with a regular fat content. We used seven obese male ob/ob mice of C57BL/6J background and ten male wild-type (WT) mice of the same strain. Faeces were collected for bile acid analysis. Intestinal permeability was measured in an Ussing chamber upon euthanasia, using 4 kDa fluorescein isothiocyanate dextran, as per mille (‰, 1/1000) of translocated dextran. We analysed the liver expression of lipopolysaccharide-binding protein (LBP), as well as serum LBP (ELISA). Intestinal permeability was not affected by genetic obesity (jejunum: 0·234 (sem 0·04) ‰ for obese v. 0·225 (sem 0·03) ‰ for WT, P= 0·93; colon: 0·222 (sem 0·06) ‰ for obese v. 0·184 (sem 0·03) ‰ for WT, P= 0·86), nor was liver LBP expression (relative expression: 0·55 (sem 0·08) for obese v. 0·55 (sem 0·13) for WT, P= 0·70). Serum LBP was 2·5-fold higher in obese than in WT mice (P= 0·001). Obese mice had increased daily excretion of total bile acids, but their faecal bile acid hydrophobicity was unchanged. In conclusion, genetic obesity did not impair gut barrier function in mice on a regular chow diet, nor was faecal bile acid hydrophobicity affected.

Bofutsushosan Improves Gut Barrier Function with a Bloom of Akkermansia Muciniphila and Improves Glucose Metabolism in Diet-Induced Obese Mice

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 1990-P ◽  
Author(s):  
SHIHO FUJISAKA ◽  
ISAO USUI ◽  
ALLAH NAWAZ ◽  
YOSHIKO IGARASHI ◽  
TOMONOBU KADO ◽  
...  
Keyword(s):  
Glucose Metabolism ◽  
Barrier Function ◽  
Obese Mice ◽  
Gut Barrier ◽  
Akkermansia Muciniphila ◽  
Gut Barrier Function

scholarly journals Clinical Analysis of Gut Barrier Dysfunction in Patients with Advanced Colorectal Cancer Undergoing Cytoreductive Surgery and HIPEC

2021 ◽  
Author(s):  
Le lai Ping ◽  
Jiang xu Mian ◽  
Chen Wei
Keyword(s):  
Colorectal Cancer ◽  
Cytoreductive Surgery ◽  
Barrier Function ◽  
Intraperitoneal Injection ◽  
Advanced Colorectal Cancer ◽  
Patient Characteristics ◽  
Barrier Dysfunction ◽  
Large Area ◽  
Gut Barrier ◽  
Gut Barrier Function

Abstract Introduction: Hyperthermic intraperitoneal chemotherapy combinedwith cytoreductive surgery is a preferred treatment option for advanced colorectal cancer patients. However, little is known whether the HIPEC can cause the damage of gut barrier function.Methods: A total of 123 patients underwent surgical resection for advanced CRC. Sixty-five patients were treated HIPEC after cytoreductive surgery whereas 58 patients underwent surgery only. Gut barrier function were evaluated using the expression of serum DAO/D-la/ET on D1/D5/D10 after surgery. Both groups were compared for patient characteristics, perioperative data and gut barrier function. Moreover, rats received intraperitoneal injection of retetrexed to observe possible changes of colonic structure under optical microscope.Results: Both groups were comparable with respect to general patient characteristics and post-operative complications. The HIPEC+CRS group was associated with a higher postoperative serum level of DAO/D-la on D1/D5 (p < 0.05) and ET on D5 after surgery (p < 0.05) than that of the surgery only group. Ten days after surgery showed no statistical difference between the 2 groups (p > 0.05).A large area structure disorder, epithelial necrosis, glandular deformation and a large number of lymphocytes infiltration was found in the lamina propria in animals received intraperitoneal injection of retetrexed.Conclusion: In this study, CRS combined with HIPEC does have but only an irreversible impact on gut barrier for advanced CRC patients.

scholarly journals 2’-fucosyllactose (2’-FL) Supplementation Improves Gut Barrier Function and Lipid Metabolism in HF-fed Mice

2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 425-425
Author(s):  
Sunhye Lee ◽  
Michael Goodson ◽  
Wendie Vang ◽  
Karen Kalanetra ◽  
Daniela Barile ◽  
...  
Keyword(s):  
Body Weight ◽  
Lipid Metabolism ◽  
Intestinal Permeability ◽  
Barrier Function ◽  
Intestinal Barrier ◽  
Intestinal Barrier Function ◽  
Gut Barrier ◽  
Low Fat ◽  
Barrier Integrity ◽  
Gut Barrier Function

Abstract Objectives 2’-fucosyllactose (2’-FL), the most predominant oligosaccharide found in human milk, acts as a prebiotic with beneficial effects on the host. The aim of this study was to determine the beneficial effect of 2’-FL on intestinal barrier integrity and metabolic functions in low-fat (LF)- and high-fat (HF)-fed mice. Methods Male C57/BL6 mice (n = 32, 8/group; 6 weeks old, JAX, CA) were counter-balanced into four weight-matched groups and fed either a low-fat (LF; 10% kcal fat with 7% kcal sucrose) or HF (45% kcal fat with 17% kcal sucrose) with or without supplementation of 2’-FL in the diet [10% (w/w), 8 weeks; LF/2’-FL or HF/2’-FL; BASF, Germany]. General phenotypes (body weight, energy intake, fat and lean mass), intestinal permeability (ex vivo in Ussing chambers), lipid profiles, and microbial metabolites were assessed. Results 2’-FL significantly attenuated the HF-induced increase in body fat mass with a trend to decrease body weight gain. 2’-FL significantly decreased intestinal permeability in LF-fed mice with a trend for a decrease in HF-fed mice. This was associated with a significant increase in interleukin-22, a cytokine known to have a protective role in intestinal barrier function. Visceral adipocyte size was significantly decreased by 2’-FL in both LF- and HF-fed mice. 2’-FL suppressed HF-induced upregulation of adipogenic transcription factors peroxisome proliferator-activated receptor gamma and sterol regulatory element binding protein-1c in the liver. Lastly, 2’-FL supplementation led to a significant elevation of lactic acid concentration in the cecum of HF-fed mice, which is known to be a product from beneficial microbes. Conclusions 2’-FL supplementation improved gut barrier integrity and lipid metabolism in mice with and without the metabolic challenge of HF feeding. These findings support the use of 2’-FL in the control of gut barrier function and metabolic homeostasis under normal and abnormal physiological conditions. Funding Sources BASF (Germany).

scholarly journals Role of Gut Barrier Function in the Pathogenesis of Nonalcoholic Fatty Liver Disease

2015 ◽  
Vol 2015 ◽  
pp. 1-6 ◽  
Author(s):  
Xin Dai ◽  
Bangmao Wang
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Barrier Function ◽  
Fatty Liver Disease ◽  
Barrier Dysfunction ◽  
Gut Barrier ◽  
Nonalcoholic Fatty Liver ◽  
Gut Barrier Function

Nonalcoholic fatty liver disease (NAFLD) is one of the most common forms of chronic liver disease, and its incidence is increasing year by year. Many efforts have been made to investigate the pathogenesis of this disease. Since 1998 when Marshall proposed the conception of “gut-liver axis,” more and more researchers have paid close attention to the role of gut barrier function in the pathogenesis of NAFLD. The four aspects of gut barrier function, including physical, chemical, biological, and immunological barriers, are interrelated closely and related to NAFLD. In this paper, we present a summary of research findings on the relationship between gut barrier dysfunction and the development of NAFLD, aiming at illustrating the role of gut barrier function in the pathogenesis of this disease.

Imidacloprid disturbed the gut barrier function and interfered with bile acids metabolism in mice

2020 ◽  
Vol 266 ◽  
pp. 115290
Author(s):  
Guiling Yang ◽  
Xianling Yuan ◽  
Cuiyuan Jin ◽  
Dou Wang ◽  
Yanhua Wang ◽  
...  
Keyword(s):  
Bile Acids ◽  
Barrier Function ◽  
Gut Barrier ◽  
Gut Barrier Function ◽  
Bile Acids Metabolism

The gut: central organ in nutrient requirements and metabolism

1994 ◽  
Vol 72 (3) ◽  
pp. 260-265 ◽  
Author(s):  
Michael L. McBurney
Keyword(s):  
Metabolic Response ◽  
Short Chain Fatty Acids ◽  
The Body ◽  
Whole Body ◽  
Nutrient Requirements ◽  
Barrier Dysfunction ◽  
Gut Barrier ◽  
Accidental Injury ◽  
Gut Barrier Function ◽  
Whole Body Metabolism

The gut is an important organ, which not only digests and absorbs food but selectively excludes bacteria and toxins from entering the body. It has one of the highest rates of protein turnover of any tissue in the body. Maintenance of epithelial cell proliferation and secretory, digestive, and gut-associated lymphatic tissues (GALT) function requires a constant supply of substrates. A primary feature of the metabolic response to fasting, accidental injury, or surgery is accelerated skeletal muscle proteolysis and translocation of amino acids from the periphery to visceral organs. Nevertheless, the serosal supply of nutrients may be inadequate to maintain normal gut barrier function. The following factors influencing gut nutrient requirements and the effect of the gut on the whole-body metabolism are discussed: (i) diet composition and gut mass, (ii) physiological and pathologic nutrient requirements of epithelial and GALT cells, (iii) route of nutrition (enteral versus parenteral), and (iv) nutrient inadequancy and gut barrier dysfunction (structural or immune mediated).Key words: gastrointestine, metabolism, gut-associated lymph tissue, glutamine, short-chain fatty acids.

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

2013 ◽  
Vol 304 (3) ◽  
pp. G227-G234 ◽  
Author(s):  
Lotta K. Stenman ◽  
Reetta Holma ◽  
Ariane Eggert ◽  
Riitta Korpela
Keyword(s):  
Bile Acids ◽  
Dietary Fat ◽  
Barrier Function ◽  
High Fat Diet ◽  
High Fat ◽  
Barrier Dysfunction ◽  
Gut Barrier ◽  
Epithelial Integrity

Impairment of gut barrier is associated with a fat-rich diet, but mechanisms are unknown. We have earlier shown that dietary fat modifies fecal bile acids in mice, decreasing the proportion of ursodeoxycholic acid (UDCA) vs. deoxycholic acid (DCA). To clarify the potential role of bile acids in fat-induced barrier dysfunction, we here investigated how physiological concentrations of DCA and UDCA affect barrier function in mouse intestinal tissue. Bile acid experiments were conducted in vitro in Ussing chambers using 4- and 20-kDa FITC-labeled dextrans. Epithelial integrity and inflammation were assayed by histology and Western blot analysis for cyclooxygenase-2. LPS was studied in DCA-induced barrier dysfunction. Finally, we investigated in a 10-wk in vivo feeding trial in mice the barrier-disrupting effect of a diet containing 0.1% DCA. DCA disrupted epithelial integrity dose dependently at 1–3 mM, which correspond to physiological concentrations on a high-fat diet. Low-fat diet-related concentrations of DCA had no effect. In vivo, the DCA-containing diet increased intestinal permeability 1.5-fold compared with control ( P = 0.016). Hematoxylin-eosin staining showed a clear disruption of the epithelial barrier by 3 mM DCA in vitro. A short-term treatment by DCA did not increase cyclooxygenase-2 content in colon preparations. UDCA did not affect barrier function itself, but it ameliorated DCA-induced barrier disruption at a 0.6 mM concentration. LPS had no significant effect on barrier function at 0.5–4.5 μg/ml concentrations. We suggest a novel mechanism for barrier dysfunction on a high-fat diet involving the effect of hydrophobic luminal bile acids.

scholarly journals The contribution of bile acid metabolism to the pathogenesis of Clostridioides difficile infection

2021 ◽  
Vol 14 ◽  
pp. 175628482110177
Author(s):  
Benjamin H. Mullish ◽  
Jessica R. Allegretti
Keyword(s):  
Bile Acid ◽  
Bile Acids ◽  
Gut Microbiome ◽  
Acid Metabolism ◽  
Disease Process ◽  
Farnesoid X Receptor ◽  
Bile Acid Metabolism ◽  
Clostridioides Difficile ◽  
Gut Barrier Function ◽  
Clostridioides Difficile Infection

Clostridioides difficile infection (CDI) remains a major global cause of gastrointestinal infection, with significant associated morbidity, mortality and impact upon healthcare system resources. Recent antibiotic use is a key risk factor for the condition, with the marked antibiotic-mediated perturbations in gut microbiome diversity and composition that underpin the pathogenesis of CDI being well-recognised. However, only relatively recently has further insight been gained into the specific mechanistic links between these gut microbiome changes and CDI, with alteration of gut microbial metabolites – in particular, bile acid metabolism – being a particular area of focus. A variety of in vitro, ex vivo, animal model and human studies have now demonstrated that loss of gut microbiome members with bile-metabolising capacity (including bile salt hydrolases, and 7-α-dehydroxylase) – with a resulting alteration of the gut bile acid milieu – contributes significantly to the disease process in CDI. More specifically, this microbiome disruption results in the enrichment of primary conjugated bile acids (including taurocholic acid, which promotes the germination of C. difficile spores) and loss of secondary bile acids (which inhibit the growth of C. difficile, and may bind to and limit activity of toxins produced by C. difficile). These bile acid changes are also associated with reduced activity of the farnesoid X receptor pathway, which may exacerbate C. difficile colitis throughout its impact upon gut barrier function and host immune/inflammatory response. Furthermore, a key mechanism of efficacy of faecal microbiota transplant (FMT) in treating recurrent CDI has been shown to be restoration of gut microbiome bile metabolising functionality; ensuring the presence of this functionality among defined microbial communities (and other ‘next generation’ FMT products) designed to treat CDI may be critical to their success.

scholarly journals Methionine Restriction Improves Gut Barrier Function by Reshaping Diurnal Rhythms of Inflammation-Related Microbes in Aged Mice

2021 ◽  
Vol 8 ◽  
Author(s):  
Bo Ren ◽  
Luanfeng Wang ◽  
Aiziguli Mulati ◽  
Yan Liu ◽  
Zhigang Liu ◽  
...  
Keyword(s):  
Gut Microbiome ◽  
Diurnal Rhythms ◽  
Inflammatory Factors ◽  
Protective Effects ◽  
Barrier Dysfunction ◽  
Gut Barrier ◽  
Aged Mice ◽  
Gut Barrier Function ◽  
Age Related ◽  
Methionine Restriction

Age-related gut barrier dysfunction and dysbiosis of the gut microbiome play crucial roles in human aging. Dietary methionine restriction (MR) has been reported to extend lifespan and reduce the inflammatory response; however, its protective effects on age-related gut barrier dysfunction remain unclear. Accordingly, we focus on the effects of MR on inflammation and gut function. We found a 3-month methionine-restriction reduced inflammatory factors in the serum of aged mice. Moreover, MR reduced gut permeability in aged mice and increased the levels of the tight junction proteins mRNAs, including those of occludin, claudin-1, and zona occludens-1. MR significantly reduced bacterial endotoxin lipopolysaccharide concentration in aged mice serum. By using 16s rRNA sequencing to analyze microbiome diurnal rhythmicity during 24 h, we found MR moderately recovered the cyclical fluctuations of the gut microbiome which was disrupted in aged mice, leading to time-specific enhancement of the abundance of short-chain fatty acid-producing and lifespan-promoting microbes. Moreover, MR dampened the oscillation of inflammation-related TM7-3 and Staphylococcaceae. In conclusion, the effects of MR on the gut barrier were likely related to alleviation of the oscillations of inflammation-related microbes. MR can enable nutritional intervention against age-related gut barrier dysfunction.

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