Fig. 2. Proposed mechanism for modulation of host insulin sensitivity by Bacteroides acidifaciens (BA). The selected commensal bacterium (i.e., BA) causes intestinal epithelial cells to secrete lower amounts of dipeptidyl peptidase-4 (DPP-4) in the gut and increased levels of glucagon-like peptide-1 (GLP-1), which may contribute to glucose homeostasis. At the same time, increased levels of bile acids (i.e., cholate and taurine) may contribute to GLP-1 activation in the intestine and to peroxisome proliferator-activated receptor α (PPARα) activation through TGR5 in adipose tissues, ultimately resulting in fat oxidation and improved insulin sensitivity.