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

Daily administration of P. faecium reduced food intake in diet-induced obese mice through early overproduction of the satiety hormone PYY.

• P. faecium was administered at a dose of 2 × 10⁹ cells/mouse daily.
• The anorexigenic effect was mediated by the early overproduction of peptide YY (PYY) compared to untreated DIO mice.
• The study used a mouse model of diet-induced obesity (DIO).
• The reduction in food intake was confirmed to contribute to attenuation of body weight gain via a pair-feeding study.

P. faecium increased intestinal levels of branched-chain amino acids, which stimulated PYY secretion in neuroendocrine cell cultures.

• Branched-chain amino acids (BCAAs) were elevated in the intestine following P. faecium administration.
• Elevated BCAAs were shown to stimulate PYY secretion using neuroendocrine cell cultures.
• This identifies a mechanistic link between P. faecium, BCAA production, and enteroendocrine signaling.

A pair-feeding study demonstrated that the anorexigenic effect of P. faecium only partially explains its attenuation of body weight gain, indicating additional food-intake-independent mechanisms.

• The pair-feeding study was designed to isolate the contribution of reduced food intake from other metabolic effects of P. faecium.
• Results showed that food intake reduction contributes to attenuating body weight gain but that other mechanisms are also involved in its metabolic benefits.
• P. faecium accelerated gut transit and serum lipid clearance as additional mechanisms limiting adiposity independently of food intake.

P. faecium accelerated gut transit and improved serum lipid clearance, thereby limiting adiposity independently of food intake.

• Gut transit was accelerated in P. faecium-treated DIO mice.
• Serum lipid clearance was enhanced following P. faecium administration.
• These effects contributed to limiting adiposity through mechanisms independent of the anorexigenic (food intake reduction) effect.
• These findings were identified in the context of a diet-induced obesity mouse model.

P. faecium administration modified gut microbiota composition in diet-induced obese mice.

• Changes in gut microbiota composition were observed following daily P. faecium treatment.
• The dose used was 2 × 10⁹ cells/mouse per day.
• Gut microbiota modification was described as one of the effects alongside increased intestinal BCAA levels and PYY stimulation.

P. faecium, a human intestinal bacterium previously linked to obesity protection, was investigated for its mode of action via enteroendocrine pathways in a diet-induced obesity mouse model.

• P. faecium is described as a human intestinal bacterium recently linked to obesity protection.
• The study aimed to determine whether it could prevent obesity via enteroendocrine pathways.
• The experimental model was diet-induced obesity (DIO) in mice.
• Daily administration at 2 × 10⁹ cells/mouse was used throughout the study.