1: Diabetologia. 2007 Nov;50(11):2374-83. Epub 2007 Sep 6.

Selective increases of bifidobacteria in gut microflora improve
high-fat-diet-induced diabetes in mice through a mechanism associated with
endotoxaemia.

Cani PD, Neyrinck AM, Fava F, Knauf C, Burcelin RG, Tuohy KM, Gibson GR, Delzenne
NM.

Unit of Pharmacokinetics, Metabolism, Nutrition and Toxicology, Université
catholique de Louvain, Av. E. Mounier, 73/69, 1200, Brussels, Belgium,
patrice.cani@uclouvain.be.

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.

PMID: 17823788 [PubMed - in process]

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