ArticleMicroorganisms2026
Lactational Enrofloxacin Exposure Promotes Offspring Lipid Metabolic Disorder and Adiposity Involving Gut Microbiota-Derived LPS and PPARγ Signaling.
Article in Microorganisms, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Early-life antibiotic exposure is a critical environmental trigger for developmental metabolic disorders and long-term obesity risk. Lactational enrofloxacin exposure exerts potential metabolic programming toxicity, but its long-term effects and underlying mechanisms remain poorly defined. This study aimed to investigate the persistent influences of lactational enrofloxacin exposure on postnatal growth, lipid metabolism and adipogenesis in mouse offspring and explore the potential gut microbiota-associated regulatory mechanism. A combined in vivo and in vitro approach was utilized. In vivo mouse models with lactational enrofloxacin exposure were established to assess growth phenotypes, serum lipid profiles, adipose morphology, and gut microbial composition via high-throughput sequencing. Antibiotic cocktail treatment was performed to deplete gut microbiota. In vitro 3T3-L1 cell models and pharmacological inhibition assays were used to investigate the downstream signaling pathway. Lactational enrofloxacin exposure was associated with disrupted postnatal growth, persistent weight gain, fat accumulation and progressive dyslipidemia in offspring. Adipose expansion was mainly attributed to adipocyte hyperplasia. It triggered sustained gut dysbiosis, increased Gram-negative
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