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] Related Links [The relationship between intestinal bifidobacteria and bacteria/endotoxin translocation in scalded rats] [Zhonghua Shao Shang Za Zhi. 2002] PMID:12641990 The role of bifidobacteria in gut barrier function after thermal injury in rats. [J Trauma. 2006] PMID:16967002 Adipose tissue inflammation induced by high-fat diet in obese diabetic mice is prevented by n-3 polyunsaturated fatty acids. [Diabetologia. 2006] PMID:16783472 A low-fat diet has a higher potential than energy restriction to improve high-fat diet-induced insulin resistance in mice. [Metabolism. 2002] PMID:12037721 Dietary cholate increases plasma levels of apolipoprotein B in mice by posttranscriptional mechanisms. [Int J Biochem Cell Biol. 2001] PMID:11606258