Intestinal Microbiome Dysbiosis and Its Role in Obesity and Metabolic Syndrome: Mechanistic Pathways and Therapeutic Perspectives

Abstract

Background: Intestinal microbiota dysbiosis is increasingly recognized as a central factor in the pathogenesis of metabolic disorders, driving low-grade systemic inflammation and insulin resistance.

Methods: This study included patients with metabolic syndrome and varying degrees of obesity, alongside healthy controls. High-throughput 16S rRNA gene sequencing was used for microbiome profiling, gas chromatography for short-chain fatty acid quantification, and serum assays for bacterial lipopolysaccharide, pro-inflammatory cytokines, and bile acid metabolites.

Results: Patients with metabolic syndrome exhibited reduced microbiota alpha-diversity, an elevated Firmicutes/Bacteroidetes ratio, and depletion of butyrate-producing taxa (Faecalibacterium prausnitzii, Akkermansia muciniphila). Impaired intestinal barrier integrity promoted metabolic endotoxemia, inducing chronic inflammation in adipose tissue and the liver via TLR4 signaling.

Conclusion: Gut microbiota dysbiosis contributes significantly to the development of obesity and metabolic syndrome. Microbiome-targeted therapies—including personalized dietary protocols, pre- and probiotic supplementation, and fecal microbiota transplantation—represent promising strategies to restore metabolic homeostasis.