# Phascolarctobacterium faecium reduces food intake via PYY signaling, contributing to the mitigation of body weight gain in diet-induced obese mice

## TL;DR

A gut bacterium called Phascolarctobacterium faecium helps reduce food intake and body weight in obese mice through a hormone called PYY.

## Contribution

The study reveals how P. faecium mitigates obesity via PYY signaling and gut microbiota modulation in a mouse model.

## Key findings

- P. faecium reduces food intake by increasing early PYY hormone production in diet-induced obese mice.
- The bacterium modifies gut microbiota and increases branched-chain amino acids, which stimulate PYY secretion.
- P. faecium also accelerates gut transit and lipid clearance, reducing adiposity independently of food intake.

## Abstract

Excess energy intake contributes to adiposity in obesity. We investigated whether the human intestinal bacterium Phascolarctobacterium faecium could prevent obesity via enteroendocrine pathways in a mouse model of diet-induced obesity (DIO). Daily administration of P. faecium (2 × 109 cells/mouse) reduced food intake through the early overproduction of the satiety hormone peptide YY (PYY) compared to untreated DIO mice. Moreover, P. faecium 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 P. faecium contributes to its effects in attenuating body weight gain in DIO mice, but that other mechanisms are also involved in its metabolic benefits. Specifically, P. faecium 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.