The gut microbiota have become a focal point of research for their involvement in the etiology of a number of diseases. Increasing evidence is defining a role for their involvement in the development and pathogenesis of diabetes and obesity.
The influence of the gut microbiota in modulating gene expression of intestinal epithelial cells has been recognised to be, in part responsible for effects to overall host metabolism. In particular, for their role in influencing intestinal epithelial cell gene expression, short chain fatty acids (SFCAs) - metabolites produced by specific bacteria following fermentation of foodstuff within the gut - have been investigated for their potential to improve host metabolism in the context of obesity and diabetes. For example, the presence of microbially derived butyrate in promoting the secretion of the incretin hormone, GLP-1, has recently been observed and attributed to affording advantageous metabolic effects in the face of high fat feeding in mice (1).
Our group has observed advantageous effects of SCFAs in influencing the expression of genes related to glucose-insulin metabolism in vitro. Similar alteration in expression of these genes in intestinal epithelial cells has also been observed in vivo, in mice implanted with osmotic pumps containing specific SCFAs.
Interestingly, small-RNA sequencing data from intestinal epithelial cells from these mice depicts differential expression of a number of micro RNAs upon SCFA exposure, when compared with a control set of mice. Bioinformatic analysis of these miRNA targets suggests that these differentially expressed miRNAs target pathways involved in glucose-insulin metabolism within intestinal epithelial cells. Here, we propose a novel interaction between the gut microbiota and host metabolism that is regulated and mediated by these small RNA elements.