Environmental exposure to triclocarban (TCC), a common antibacterial agent widely used in thousands of personal care products, poses a potential risk for human health. Previous in vitro studies about biological effects of TCC have yielded a variety of inconsistent results and apparently not been verified in vivo. In the current study, dose-dependent effects of TCC exposure on lipid homeostasis in rats were investigated using a combination of untargeted 1H NMR metabolomics, targeted metabolite profiling (LC/GC-MS), histopathological assessments, and biological assays. Our results revealed that TCC dose-dependently activated aryl hydrocarbon receptor (AHR) and its transcriptional targets such as Cyp1a1 and Cyp1b1 in the liver of rats, suggesting that TCC may be a potent AHR agonist. Although TCC exhibited dose-dependent toxicity, oral exposure with relatively low dose TCC caused more significant hepatic lipogenesis of rats than relatively high and moderate doses of TCC. It was mainly manifested by histopathological observations and promotion of de novo fatty acid, phospholipid, and ceramide biosynthesis and gut microbiota fermentation. Our findings provide new insights into health effects of TCC exposure with different dosages in vivo, especially on the induction and progression of nonalcoholic fatty liver disease, and further our understanding in the pathogenesis of metabolic diseases induced by environmental pollutants.