Small Intestinal Bacterial Overgrowth and Pediatric Obesity-A Systematic Review

Abstract

Background/Objectives: Childhood obesity is a growing global concern linked to metabolic disorders such as nonalcoholic fatty liver disease (NAFLD). Small intestinal bacterial overgrowth (SIBO) may exacerbate these conditions by promoting systemic inflammation and metabolic dysfunction. This review evaluates the prevalence of SIBO in obese children, its association with inflammatory and metabolic markers, and the efficacy of diagnostic and therapeutic strategies. Methods: A systematic search of PubMed, Scopus, and Web of Science (2010-present) was conducted using Boolean operators: ('small intestinal bacterial overgrowth' OR 'SIBO') AND 'prevalence' AND ('low-grade inflammatory markers' OR 'metabolic status') AND 'gut microbiome' AND 'dysbiosis' AND 'obese children'. Results: The data show that SIBO is frequently observed in obese pediatric populations and is associated with gut dysbiosis, impaired nutrient absorption, and reduced production of short-chain fatty acids. These changes contribute to increased intestinal permeability, endotoxemia, and chronic low-grade inflammation. Several microbial taxa have been proposed as biomarkers and therapeutic targets. Diagnostic inconsistencies persist, but treatments such as probiotics, prebiotics, dietary interventions, and selective antibiotics show potential, pending further validation. Conclusions: Early identification and treatment of SIBO with tailored strategies may help reduce metabolic complications and improve outcomes in children with obesity.

Keywords: gut microbiota; metabolic dysfunction; pediatric obesity; small intestinal bacterial overgrowth (SIBO); systemic inflammation.

Figure 1

PRISMA flowchart for assessment of eligible studies.

Figure 2

Interplay between SIBO, inflammation, NAFLD and pediatric obesity. (created with https://app.biorender.com/). Legend: Pediatric obesity and proton pump inhibitor use promote the development of SIBO in children. The subsequent promotion of cytokine release, including TLR4 and TNF-α, stimulates the development of NAFLD, together with the production of ethanol by bacterial overgrowth, which stimulates the release of ROS by the mitochondrion. Nevertheless, SIBO determines a decrease in insulin production through impairment of pancreatic beta cell function. NAFLD—nonalcoholic fatty liver disease; SIBO—small intestinal bacterial overgrowth; TLR4—toll-like receptor 4; TNF-α—tumor necrosis factor-alpha.