The period from birth to two years is the phase of the fastest growth and development in children, as well as an important window for the development of intestinal microbiota. Dysbiosis of the gut microbiome can lead to various adverse conditions in children, including malabsorption and immune abnormalities, ultimately resulting in a series of negative events related to growth and development. Lysine acetylation, as a significant post-translational modification, plays a complex and crucial role in the regulation of gut microbiota. This study aims to investigate the mechanism by which ABX-induced lysine acetylation affects the abnormal physiological state simulating gut microbiota dysbiosis in children. In this study, we identified a total of 16,579 acetylation sites from 5,218 proteins. We found that antibiotic-induced dysbiosis in young mice (3 weeks) can cause extensive changes in the lysine acetylation and proteomic profiles of cecal tissue. Differentially acetylated proteins are involved in various metabolic pathways, including the citrate cycle (TCA) cycle, butanoate metabolism, pyruvate metabolism, glycolysis/gluconeogenesis, and fatty acid biosynthesis. These differential acetylation sites are distributed across the cytoplasm, nucleus, and mitochondria, suggesting that multiple cellular functions are involved in regulation. Our findings suggest that early-life gut microbiota dysbiosis may lead to a series of metabolic disorders by regulating lysine acetylation in cecal tissue, resulting in delayed growth and development. This study aims to provide valuable insights into the molecular mechanisms underlying a series of pathophysiological processes caused by early-life gut microbiota dysbiosis. It contributes to a deeper understanding of the consequences of acetylation changes associated with early-life gut microbiota dysbiosis and its potential role in metabolic disorders.