MECHANISTIC INSIGHTS INTO THE EFFECTS OF PROBIOTIC SUPPLEMENTATION ON GUT-DERIVED FECAL SHORT-CHAIN FATTY ACIDS AND CENTRAL OBESITY IN OVERWEIGHT AND OBESE ADOLESCENTS: A NARRATIVE REVIEW

Abstract

Central fat distribution, rather than total body mass, drives most of the cardiometabolic risk associated with adolescent obesity. Yet, the interventions that might modulate it via the gut microbiota remain poorly characterized. Gut-derived short-chain fatty acids (SCFAs) are candidate mediators, and probiotics are candidate modulators, but the evidence in adolescence is sparse and inconsistent. The objective of the review is to synthesize the mechanistic and clinical evidence linking probiotic supplementation, fecal SCFAs, and central obesity, indexed by the waist-to-height ratio (WHtR), in overweight and obese adolescents, and to define the study-design features needed to test that link. A narrative review was conducted using PubMed, Scopus, Web of Science, and ScienceDirect as primary databases (records to July 2026), with Google Scholar as a supplementary source; every finding was verified against the primary article. Eligible records addressed gut microbiota or SCFAs, probiotic supplementation, or central adiposity/WHtR; evidence from children, adults, animal models, and in vitro work was used only to support mechanistic explanations. Fecal SCFA concentration reflects only the small unabsorbed remainder of colonic production in the distal gut and is shaped by production, absorption, transit, and stool water content; it therefore indexes luminal microbial activity, not microbial synthesis or systemic exposure. SCFAs act on adiposity through GPR41/GPR43 signaling, gut-hormone secretion, hepatic and adipocyte lipid handling, and histone deacetylase inhibition, but these effects are context-dependent rather than uniformly beneficial. Adolescent probiotic trials are few and heterogeneous; based on our search, no probiotic-only trial has reduced WHtR, none have paired probiotic supplementation with fecal SCFA or metabolomic profiling alongside WHtR, and strain, dose, duration, baseline microbiota, diet, and pubertal stage all modify efficacy. The probiotic–SCFA–central obesity axis is biologically plausible but not yet validated in adolescents; its clinical benefit and causal direction remain unproven. WHtR, paired with untargeted fecal metabolomics, is proposed as the readout most likely to capture microbiota-mediated change.