Acesulfame potassium induces hepatic inflammation and fatty acids accumulation via disturbance of carnitine metabolism and gut microbiota

The controversy surrounding the impact of acesulfame potassium (Ace-K) on metabolic health has been growing. Here, male C57BL/6 mice were given Ace-K for 11 weeks (sterile water as the control group, 40 mg/kg body weight as the low dose group, 120 mg/kg as the high dose group), subsequently gut microbiome and targeted metabolomics were conducted to evaluate the effect of Ace-K on host health. Gut microbiota was perturbed by Ace-K, as evidenced by the down-regulation of beneficial bacteria and the increased abundance of Collinsella associated with inflammation. Fatty acids metabolism was altered by Ace-K, as evidenced by elevated long chain fatty acids (LCFAs) in liver and serum. Notably, the reduction of related genes and proteins correlated to carnitine metabolism and hepatic carnitine metabolites by Ace-K led to a reduction in the β-oxidation of LCFAs, ultimately causing the accumulation of LCFAs. These findings uncovered new perspectives on Ace-K-induced hepatic inflammation and fatty acids accumulation.