- Atrazine exposure suppresses the AMPK/p38 signalling pathway, inhibiting fatty acid oxidation and causing hepatic lipid accumulation in rat liver.
- 5-HIAA promotes activation of the AMPK/p38 pathway, restores fatty acid oxidation and alleviates atrazine-induced hepatic lipid accumulation.
- Transcriptomic and metabolomic analyses reveal enrichment in non-alcoholic fatty liver disease pathways and the tryptophan metabolic pathway.
Mol Cell Endocrinol. 2026 Sep 5:112906. doi: 10.1016/j.mce.2026.112906. Online ahead of print.
ABSTRACT
Atrazine (ATR) is one of the most widely used herbicides in global agricultural production, it enters the body mainly through drinking water and diet. Liver is the main organ of ATR metabolism. As the end product of tryptophan metabolism, 5-HIAA can regulate liver metabolism. To investigate the hepatotoxic mechanism of ATR and the rescue effect of 5-HIAA against ATR-induced hepatic lipid accumulation, Wistar rats were treated with ATR for 90 days, L02 cells were treated with ATR for 24 hours. Transcriptomic and metabolomic analyses revealed that differentially expressed genes and metabolites were enriched in non-alcoholic fatty liver disease and the tryptophan metabolic pathway, respectively. In this study, ATR suppressed the AMPK/p38 signaling pathway, inhibiting FAO and leading to hepatic lipid accumulation. Conversely, 5-HIAA indirectly modulated the activation of the AMPK/p38 signaling pathway to alleviate ATR-induced lipid accumulation and restore reduced FAO in the liver.
PMID:42700948 | DOI:10.1016/j.mce.2026.112906
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