IMPACT OF THE GUT MICROBIOTA ON INSULIN RESISTANCE AND OBESITY

Abstract

The rising prevalence of obesity and insulin resistance (IR) represents a global health challenge, driving the search for new etiological factors. This systematic review aimed to critically analyze recent mechanisms (2020–2025) through which altered gut microbiota, or dysbiosis, influences the progression of these metabolic conditions. The methodology employed a rigorous search across databases like PubMed and Scopus, using keywords such as "Gut Microbiota," "Insulin Resistance," and "Obesity," following PRISMA guidelines. The results consolidated that dysbiosis is an active causal factor, characterized by a loss of microbial diversity and functional changes that promote pathogenesis. The primary linking mechanism is low-grade metabolic inflammation, triggered by endotoxemia resulting from increased intestinal permeability and the translocation of Lipopolysaccharide (LPS) into systemic circulation. LPS activates inflammatory pathways that disrupt insulin signaling in key tissues. Additionally, dysbiosis regulates host metabolism through the modulation of microbial metabolites. While an excess of Short-Chain Fatty Acids (SCFAs) can contribute to lipogenesis and weight gain, the alteration in the Bile Acids (BAs) pool affects glucose homeostasis via endocrine receptors. In conclusion, microbiota modulation, primarily through dietary intervention, and the development of precision therapies (next-generation probiotics and postbiotics) are promising strategies. However, it is essential that future research focuses on functional metagenomics to validate causality and optimize targeted interventions in the gut-host axis for the effective treatment of obesity and IR.