5-HIAA alleviates lipid accumulation in rat liver caused by atrazine by promoting the activation of the AMPK/p38 signaling pathway.

Authors

Honghao Qian, Haoyan Ma, Jiaxin Zhang, Ziyu Wang, Xijun Zhang, Xiaoyu Jia, Xinyi Wang, Rui Zhao, Yinlong Zhao, Yuezhu Zhang

Published in

Molecular and cellular endocrinology. Pages 112906. Sep 05, 2026. Epub Sep 05, 2026.

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
Bibliographic data and abstract were imported from PubMed on 06 Sep 2026.

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