Bifidobacterium strains have been reported to be very good at hydrolyzing high amylose starch (type 3 RS).[36] Bifidobacteria have novel metabolic pathways that utilize human milk Fulvestrant oligosaccharides and host glycoproteins.[37]

Bifidobacterium longum and Bifidobacterium adolescentis produce acetate from glucose[38] while the former has an ATP-binding cassette-type carbohydrate transporter that also allows it to use fructose to produce acetate. Studies in an in vitro human colon model suggested that R. bromii and related species were the primary starch degraders in most cases, but metabolic cross-feeding of Prevotella species, B. adolescentis, and E. rectale occurred resulting in fermentation to acetate, butyrate, and propionate.[39] The need for a consortium of bacteria to complete these processes is further illustrated by the fact that members of Clostridium cluster XIVa convert lactate produced by several microbial species from

carbohydrate to butyrate while members of Clostridium cluster IX convert lactate to propionate.[28] The role of gut microbiota in regulating body weight originated from studies in germ-free mice, which are typically lean, where transplanting gut flora from conventional mice resulted in greater than 50% increase in body weight.[40] Subsequent studies Decitabine datasheet indicated that obesity is in an animal model was associated with characteristic changes in gut microbiota composition.

Microbiota analysis in obese (ob)/ob mice, lacking the leptin gene, indicated that there was a marked predominance of phylum Firmicutes compared with phylum Bacteroidetes.[41] This was accompanied by increased expression of microbial genes coding for enzymes involved in the breakdown of complex carbohydrate, and in sugar and SCFA metabolism.[42] These mice also had higher cecal concentrations of SCFA and lower fecal energy losses than conventional animals. This suggested that the ob/ob mice were absorbing more energy from medchemexpress their dietary carbohydrate, which could be a contributing factor to obesity. Further, these investigators showed that germ-free conventional mice developed obesity when inoculated with the gut microbiota from ob/ob mice, indicating important microbial contributions to energy conservation and obesity. Obese fatty (fa)/fa rats, with mutations in the leptin receptor genes, had relatively higher urinary leucine, isoleucine, and acetate and higher plasma low density and very low density lipoprotein compared with wild-type rats.[43] Their gut microbiota showed reduced abundance of bifidobacteria with the presence of Halomonas and Sphingomonas in the cecum that were likely to be involved in energy conservation from carbohydrate that was not digested in the small bowel.