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We began analyzing https://link.springer.com/article/10.1007/s00125-007-0791-0, but it redirected us to https://link.springer.com/article/10.1007/s00125-007-0791-0. The analysis below is for the second page.

Title[redir]:
Selective increases of bifidobacteria in gut microflora improve high-fat-diet-induced diabetes in mice through a mechanism associated with endotoxaemia | Diabetologia
Description:
Aims/hypothesis Recent evidence suggests that a particular gut microbial community may favour occurrence of the metabolic diseases. Recently, we reported that high-fat (HF) feeding was associated with higher endotoxaemia and lower Bifidobacterium species (spp.) caecal content in mice. We therefore tested whether restoration of the quantity of caecal Bifidobacterium spp. could modulate metabolic endotoxaemia, the inflammatory tone and the development of diabetes. Methods Since bifidobacteria have been reported to reduce intestinal endotoxin levels and improve mucosal barrier function, we specifically increased the gut bifidobacterial content of HF-diet-fed mice through the use of a prebiotic (oligofructose [OFS]). Results Compared with normal chow-fed control mice, HF feeding significantly reduced intestinal Gram-negative and Gram-positive bacteria including levels of bifidobacteria, a dominant member of the intestinal microbiota, which is seen as physiologically positive. As expected, HF-OFS-fed mice had totally restored quantities of bifidobacteria. HF-feeding significantly increased endotoxaemia, which was normalised to control levels in HF-OFS-treated mice. Multiple-correlation analyses showed that endotoxaemia significantly and negatively correlated with Bifidobacterium spp., but no relationship was seen between endotoxaemia and any other bacterial group. Finally, in HF-OFS-treated-mice, Bifidobacterium spp. significantly and positively correlated with improved glucose tolerance, glucose-induced insulin secretion and normalised inflammatory tone (decreased endotoxaemia, plasma and adipose tissue proinflammatory cytokines). Conclusions/interpretation Together, these findings suggest that the gut microbiota contribute towards the pathophysiological regulation of endotoxaemia and set the tone of inflammation for occurrence of diabetes and/or obesity. Thus, it would be useful to develop specific strategies for modifying gut microbiota in favour of bifidobacteria to prevent the deleterious effect of HF-diet-induced metabolic diseases.

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Keywords {🔍}

mice, pubmed, article, gut, google, scholar, cas, diet, endotoxaemia, glucose, insulin, plasma, bifidobacteria, spp, bacteria, microbiota, fig, metabolic, dietary, hfofs, bifidobacterium, intestinal, fed, control, weight, hfcell, content, prebiotic, data, adipose, diabetes, inflammatory, bacterial, inflammation, obesity, fibre, cani, highfat, levels, increased, compared, significantly, correlated, body, prebiotics, nutr, group, tolerance, increase, fat,

Topics {✒️}

tumor necrosis factor-alpha hf-cell high-fat diet bio-breeding diabetes-prone rat hf-ofs high-fat diet hf-ofs-fed mice exhibit hf-cell mice showed hf-diet-induced metabolic disorders short-chain fatty acids hf-diet-induced metabolic diseases multiple-correlation analyses showed proglucagon mrna precursor hf high-fat diet high-fat hf-cell glucose-induced insulin secretion trans-epithelial electrical resistance ob/ob mice treated gram-negative bacteria present obesity-induced insulin resistance hf-diet-induced inflammation hf-diet-treated mice cytophaga–flavobacter–bacteroides phylum phylum cytophaga–flavobacter–bacteroides gram-negative bacteroides mib hf-diet-induced obesity [9] hf diet-induced obesity hf-ofs-treated mice hf-ofs-treated-mice microcrystalline cellulose [hf-cell] hf-ofs mice impacted gut-derived bacterial translocation hf-diet-fed mice hf-cell-fed mice low-grade inflammatory tone hf-ofs-fed mice hf-ofs fed mice body weight gain hf-cell mice compared hf-fed mice compared hotamisligil gs gram-negative bacteria gut microbial community microbial ecology obesity-linked insulin resistance high-fat diet gram-positive bacteria murine intestinal microflora colonic proglucagon mrna major gram-positive high-fat feeding endotoxaemia article published

Questions {❓}

  • Is the gut flora involved in the development of type 1 diabetes?

Schema {🗺️}

WebPage:
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         headline:Selective increases of bifidobacteria in gut microflora improve high-fat-diet-induced diabetes in mice through a mechanism associated with endotoxaemia
         description:Recent evidence suggests that a particular gut microbial community may favour occurrence of the metabolic diseases. Recently, we reported that high-fat (HF) feeding was associated with higher endotoxaemia and lower Bifidobacterium species (spp.) caecal content in mice. We therefore tested whether restoration of the quantity of caecal Bifidobacterium spp. could modulate metabolic endotoxaemia, the inflammatory tone and the development of diabetes. Since bifidobacteria have been reported to reduce intestinal endotoxin levels and improve mucosal barrier function, we specifically increased the gut bifidobacterial content of HF-diet-fed mice through the use of a prebiotic (oligofructose [OFS]). Compared with normal chow-fed control mice, HF feeding significantly reduced intestinal Gram-negative and Gram-positive bacteria including levels of bifidobacteria, a dominant member of the intestinal microbiota, which is seen as physiologically positive. As expected, HF-OFS-fed mice had totally restored quantities of bifidobacteria. HF-feeding significantly increased endotoxaemia, which was normalised to control levels in HF-OFS-treated mice. Multiple-correlation analyses showed that endotoxaemia significantly and negatively correlated with Bifidobacterium spp., but no relationship was seen between endotoxaemia and any other bacterial group. Finally, in HF-OFS-treated-mice, Bifidobacterium spp. significantly and positively correlated with improved glucose tolerance, glucose-induced insulin secretion and normalised inflammatory tone (decreased endotoxaemia, plasma and adipose tissue proinflammatory cytokines). Together, these findings suggest that the gut microbiota contribute towards the pathophysiological regulation of endotoxaemia and set the tone of inflammation for occurrence of diabetes and/or obesity. Thus, it would be useful to develop specific strategies for modifying gut microbiota in favour of bifidobacteria to prevent the deleterious effect of HF-diet-induced metabolic diseases.
         datePublished:2007-09-06T00:00:00Z
         dateModified:2007-09-06T00:00:00Z
         pageStart:2374
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         sameAs:https://doi.org/10.1007/s00125-007-0791-0
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            Bifidobacteria
            Diabetes
            Endotoxin
            GLP-1
            Glucagon-like peptide-1
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            Inflammation
            Obesity
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            Metabolic Diseases
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      headline:Selective increases of bifidobacteria in gut microflora improve high-fat-diet-induced diabetes in mice through a mechanism associated with endotoxaemia
      description:Recent evidence suggests that a particular gut microbial community may favour occurrence of the metabolic diseases. Recently, we reported that high-fat (HF) feeding was associated with higher endotoxaemia and lower Bifidobacterium species (spp.) caecal content in mice. We therefore tested whether restoration of the quantity of caecal Bifidobacterium spp. could modulate metabolic endotoxaemia, the inflammatory tone and the development of diabetes. Since bifidobacteria have been reported to reduce intestinal endotoxin levels and improve mucosal barrier function, we specifically increased the gut bifidobacterial content of HF-diet-fed mice through the use of a prebiotic (oligofructose [OFS]). Compared with normal chow-fed control mice, HF feeding significantly reduced intestinal Gram-negative and Gram-positive bacteria including levels of bifidobacteria, a dominant member of the intestinal microbiota, which is seen as physiologically positive. As expected, HF-OFS-fed mice had totally restored quantities of bifidobacteria. HF-feeding significantly increased endotoxaemia, which was normalised to control levels in HF-OFS-treated mice. Multiple-correlation analyses showed that endotoxaemia significantly and negatively correlated with Bifidobacterium spp., but no relationship was seen between endotoxaemia and any other bacterial group. Finally, in HF-OFS-treated-mice, Bifidobacterium spp. significantly and positively correlated with improved glucose tolerance, glucose-induced insulin secretion and normalised inflammatory tone (decreased endotoxaemia, plasma and adipose tissue proinflammatory cytokines). Together, these findings suggest that the gut microbiota contribute towards the pathophysiological regulation of endotoxaemia and set the tone of inflammation for occurrence of diabetes and/or obesity. Thus, it would be useful to develop specific strategies for modifying gut microbiota in favour of bifidobacteria to prevent the deleterious effect of HF-diet-induced metabolic diseases.
      datePublished:2007-09-06T00:00:00Z
      dateModified:2007-09-06T00:00:00Z
      pageStart:2374
      pageEnd:2383
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      keywords:
         Bifidobacteria
         Diabetes
         Endotoxin
         GLP-1
         Glucagon-like peptide-1
         Gut microflora
         Inflammation
         Obesity
         Prebiotics
         Internal Medicine
         Metabolic Diseases
         Human Physiology
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                     name:Food Microbial Sciences Unit, Department of Food Biosciences, The University of Reading, Reading, UK
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            type:Person
            name:G. R. Gibson
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                  name:The University of Reading
                  address:
                     name:Food Microbial Sciences Unit, Department of Food Biosciences, The University of Reading, Reading, UK
                     type:PostalAddress
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      name:Unit of Pharmacokinetics, Metabolism, Nutrition and Toxicology, Université catholique de Louvain, Brussels, Belgium
      name:Unit of Pharmacokinetics, Metabolism, Nutrition and Toxicology, Université catholique de Louvain, Brussels, Belgium
      name:Food Microbial Sciences Unit, Department of Food Biosciences, The University of Reading, Reading, UK
      name:Rangueil Institute of Molecular Medicine, I2MR, IFR31, Toulouse, France
      name:Rangueil Institute of Molecular Medicine, I2MR, IFR31, Toulouse, France
      name:Food Microbial Sciences Unit, Department of Food Biosciences, The University of Reading, Reading, UK
      name:Food Microbial Sciences Unit, Department of Food Biosciences, The University of Reading, Reading, UK
      name:Unit of Pharmacokinetics, Metabolism, Nutrition and Toxicology, Université catholique de Louvain, Brussels, Belgium

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