Schugar et al. (2017) proposed that the TMA/FMO3/TMAO pathway is a microbe-to-host endocrine axis that mediates the crosstalk with adipose tissue, as deleting TMAO-producing Fmo3 increases browning of gonadal WAT and protects against obesity in mice. Complimentary mouse and human studies indicate a negative regulatory role for FMO3 in the browning of white adipose tissue (Ussar et al., 2014). Here, FMO3 is linked to obesity due to melanocortin 4 receptor deficiency.