Abstract Introduction: Prader–Willi syndrome (PWS) is a genetic neuroendocrine disorder with developmental transitions from infant feeding difficulty to hyperphagia, altered body composition, and heterogeneous metabolic risk. The contribution of intestinal microbial activity to these features remains uncertain. Aim of the study: To critically appraise evidence for microbiota–endocrine–brain interactions in PWS and identify testable mechanisms that may distinguish PWS from common obesity.
