FIGURE 1: Mechanisms behind activation of thermogenesis by gut microbiota after bariatric surgery. The findings of Jin et al [15] and Yadav et al [16] demonstrate that the shifts in gut microbiota after RYGB and VSG lead to increased gut levels of butyrate and licoricidin, respectively. This then leads to activation of brown fat thermogenesis after RYGB, possibly via a mechanism involving monocarboxlate transporter 1 (MCT1)-mediated transport of circulating butyrate into brown adipocytes [25], and activation of subcutaneous white fat thermogenesis after VSG, possibly via a mechanism involving the positive modulation of beta-3 adrenergic receptor in white adipocytes by increased circulating licoricidin [15].