The impact of antibiotic exposure on obesity and metabolic phenotypes via the gut microbiota

Antibiotics are among the most commonly used anti-infective agents in modern medicine. However, their long-term effects on the gut microbiome have attracted increasing attention. Epidemiological studies and animal experiments in recent years suggest that antibiotic exposure can disrupt the structure and function of the gut microbiota, thereby affecting host energy metabolism, fat deposition, and immune homeostasis. Such disruptions may contribute to the development of obesity and related metabolic phenotypes. Different classes of antibiotics exert markedly distinct effects on the gut microbiota. Broad-spectrum antibiotics such as macrolides, lincosamides, and fluoroquinolones often induce more pronounced and prolonged microbial alterations, whereas the effects of certain β-lactam antibiotics appear relatively transient. Antibiotic-induced gut dysbiosis can influence host metabolism through multiple mechanisms, including reduced short-chain fatty acid production, disrupted bile acid metabolism, impaired intestinal barrier function, and chronic low-grade inflammation. These alterations may promote fat accumulation, insulin resistance, and disruption of immune homeostasis. Early-life antibiotic exposure occurs during a critical developmental window for gut microbiota maturation and may exert more profound effects on long-term metabolic health. Recent advances in multi-omics technologies have further illuminated the complex interaction network among antibiotics, the microbiome, and host metabolism. Microecological intervention strategies, such as probiotics and synbiotics, show potential for improving metabolic abnormalities associated with antibiotic-induced dysbiosis. However, their efficacy is strain-specific, and the overall effect size remains limited. This review summarizes current research progress on how antibiotic exposure influences obesity and metabolic phenotypes through the gut microbiota, outlines the underlying mechanisms, and discusses potential applications of microbiological intervention strategies. It also provides insights into antibiotic-related metabolic risks and future precision intervention approaches.