The idea that the GM might act as a buffer regulating host metabolic response to infection by a pathogen has been partially explored by Khosravi et al. [32], who showed that Helicobacter pylori infection triggered a stronger host metabolic response (modification of insulin, ghrelin and leptin levels) in germ free mice than in conventional animals and that infection-induced decreased growth rate was only observed in absence of GM. Here, INS is linked to infection.