We are analyzing https://link.springer.com/article/10.1007/s00125-007-0791-0.

Title:
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?

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         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.
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