A new article published in the Journal of Molecular Biology reported that alterations of both ecology and functions of gut microbiota are conspicuous traits of several inflammatory pathologies, notably metabolic diseases such as obesity and type-2 diabetes. It was also stated that the proliferation of enterobacteria, subdominant members of the intestinal microbial ecosystem, has been shown to be favored by western diet – the strongest inducer of metabolic diseases and gut microbiota dysbiosis. Meanwhile, the in vitro interdependence between the host and the gut microbiota is based on a number of molecular mechanisms by which host and intestinal microbes modify each other. These mechanisms were enlisted, vis: the well-known metabolic impact of short chain fatty acids, produced by microbial fermentation of complex carbohydrates from plants; a mutual modulation of miRNAs expression, both on the eukaryotic (host) and prokaryotic (gut microbes) side; the production by enterobacteria of virulence factors such as the genotoxin colibactin, shown to alter the integrity of host genome and induce a senescence-like phenotype, in vitro; and the microbial excretion of outer membrane vesicles, which, in addition to other functions, may act as a carrier for multiple molecules such as toxins to be delivered to target cells. In summary, this review described the major molecular mechanisms by which gut microbes exert their metabolic impact at a multi-organ level and support the emerging triad of metabolic diseases, gut microbiota dysbiosis, and enterobacterial infections.