We suggest that several potential mechanisms can be involved, such as the activation of a gut-brain axis via the release of GLP-1 and the maintenance of a healthy and functional enteric nervous system.31 Also, a stimulation of TGR5 can impact host physiology through the modulation of intestinal permeability32 33 as well as immune cell function by increasing anti-inflammatory cells.34 This might limit endotoxemia, which is associated with obesity and metabolic disturbance developments.35 The gene discussed is GPBAR1; the disease is obesity disorder.