<i> <b>Phascolarctobacterium faecium</b> </i> <b>reduces food intake via PYY signaling, contributing to the mitigation of body weight gain in diet-induced obese mice</b>

Excess energy intake contributes to adiposity in obesity. We investigated whether the human intestinal bacterium <i>Phascolarctobacterium faecium</i> could prevent obesity <i>via</i> enteroendocrine pathways in a mouse model of diet-induced obesity (DIO). Daily administration of <i>P. faecium</i> (2 × 10⁹ cells/mouse) reduced food intake through the early overproduction of the satiety hormone peptide YY (PYY) compared to untreated DIO mice. Moreover, <i>P. faecium</i> increased the intestinal levels of branched-chain amino acids, which, in turn, stimulated PYY secretion in neuroendocrine cell cultures and also modified gut microbiota composition. A pair-feeding study demonstrated that the anorexigenic effect of <i>P. faecium</i> contributes to its effects in attenuating body weight gain in DIO mice, but that other mechanisms are also involved in its metabolic benefits. Specifically, <i>P. faecium</i> accelerated gut transit and serum lipid clearance, thereby limiting adiposity independently of food intake. This study identifies the mode of action of a human intestinal bacterium recently linked to obesity protection, providing valuable insights into host-microbe interactions governing body weight.