Of most interest, it was noted that transplanting the

gut microbiota of kwashiorkor children into gnotobiotic mice, along with feeding of a Malawian diet to these animals, resulted in marked weight loss and disturbances in amino acid and carbohydrate metabolism in the treated animals. Thus, there appears to be a role for the gut microbiome also in the development of malnutrition. A number of other associations exist between the gut microbiota and human nutrition. Thus, studies in iron-deficient individuals show that the gut microbiota is relatively depleted of lactobacilli in individuals with iron-deficiency Selleckchem Crenolanib anemia.[72] It is not clear whether decrease in abundance of lactobacilli contributes Napabucasin in vitro to iron deficiency or whether iron deficiency is responsible for the reduction in lactobacilli. Lactobacilli have a major growth requirement for iron and may therefore be reduced in numbers in the gut of iron-deficient individuals. On the other hand, carbohydrate-fermenting

bacteria produce SCFA and reduce the luminal pH in the right colon, effects that stimulate the absorption of divalent cations through transporters in the cecum.[73, 74] Although the primary site for iron absorption is the duodenum, it is now clear that the enterocyte transporters involved in iron transport are also expressed in the cecum and right colon. In animal models, colonic absorption of iron is promoted by the presence of easily fermented carbohydrates that stimulate the growth of bacteria, which produce propionic acid.[75] As lactobacilli are involved in the conversion of lactate to propionate in fermentation systems,[35] this provides a plausible Chloroambucil explanation for a causal link between reduction of lactobacilli and iron-deficiency anemia. A role for the gut microbiota has been postulated

in the development of type 2 diabetes. Changes that have been demonstrated include decreased phosphorylation of the insulin receptor, insulin receptor substrate (IRS), and Akt, along with increased inhibitory serine phosphorylation of IRS-1, leading to impaired insuling signaling.[76] In TLR2 knockout mice, metabolic syndrome was induced and associated with marked increase in the Firmicutes and mild increase in Bacteroides.[77] An increase in the abundance of E. rectale-C. coccoides belonging to phylum Firmicutes has been noted in women with metabolic syndrome, where this population correlated with the metabolic dysfunction.[78] In an interesting randomized trial, intestinal infusions of microbiota from lean donors (or patient’s own microbiota as control) were given to male recipients with metabolic syndrome.