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This review summarizes current evidence on microbial signatures and mechanistic pathways associated with pediatric obesity and evaluates microbiota-targeted strategies for prevention and intervention.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Data sources<\/jats:title>\n                    <jats:p>Relevant studies published between January 2000 and February 2026 were identified through searches of PubMed, Embase, and Web of Science using keywords related to pediatric obesity, gut microbiota, microbial metabolites, and microbiota-based interventions. Human studies and mechanistic animal models examining host\u2013microbe metabolic interactions were included.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Pediatric obesity is associated with shifts in gut microbial composition, although taxonomic findings are heterogeneous across studies and should not be interpreted as universal biomarkers. Relatively consistent patterns include reduced\n                      <jats:italic>Bifidobacterium<\/jats:italic>\n                      and\n                      <jats:italic>Akkermansia muciniphila<\/jats:italic>\n                      , whereas associations involving\n                      <jats:italic>Faecalibacterium<\/jats:italic>\n                      ,\n                      <jats:italic>Blautia<\/jats:italic>\n                      , and lactobacilli are context-, species-, and strain-dependent. Functional alterations include changes in short-chain fatty acid production, bile acid signaling, microbial branched-chain and aromatic amino acid metabolism, and endotoxin-related inflammatory pathways. The enrichment of Gram-negative taxa such as Enterobacteriaceae may contribute to impaired epithelial barrier integrity, lipopolysaccharide translocation, toll-like receptor 4 signaling, chronic low-grade inflammation, and insulin resistance. Early-life exposures, including cesarean delivery, formula feeding, and antibiotic use, are repeatedly associated with altered microbial succession and later obesity risk, although causality remains incompletely defined. Interventional studies indicate that dietary fiber enrichment and selected probiotic strains can improve microbial and metabolic outcomes in some settings, but efficacy remains strain-specific and clinically heterogeneous.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Microbial and metabolic signatures are associated with pediatric obesity, converging on pathways of energy harvest, epithelial barrier dysfunction, inflammation, and disrupted host\u2013microbe signaling. Integrative multi-omic and longitudinal studies are required to establish causality and guide the development of personalized, microbiota-based interventions for obesity prevention and treatment in children.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1007\/s12519-026-01094-7","type":"journal-article","created":{"date-parts":[[2026,10,3]],"date-time":"2026-10-03T18:37:57Z","timestamp":1791052677000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Microbiome signatures and mechanistic pathways in pediatric obesity: from early-life risk to precision interventions"],"prefix":"10.1007","author":[{"given":"Shan-Shan","family":"Xie","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jie","family":"Hu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wei","family":"Zhou","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiao-Long","family":"Ge","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"You-You","family":"Luo","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1363-6708","authenticated-orcid":false,"given":"Zhi-Gang","family":"Liu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2026,10,3]]},"reference":[{"key":"1094_CR1","doi-asserted-by":"publisher","first-page":"1027","DOI":"10.1016\/s0140-6736(23)02750-2","volume":"403","author":"NCD Risk Factor Collaboration (NCD-RisC)","year":"2024","unstructured":"NCD Risk Factor Collaboration (NCD-RisC). 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