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Peer-reviewedCC BY-NC-ND 4.0ACS Omega

Cadmium Exposure Aggravates SREBP-1c-Mediated Hepatic Steatosis and Liver Injury in High-Fat Diet-Fed Mice

  • Shuying Wu1
  • Yaqian Li1
  • Yuru Zong2
  • Qibin Mai1
  • Ruirui Qiu1
  • Huidong Song1
  • Hanqing Chen2
  1. 1Guangzhou Medical University , , ,
  2. 2Capital Medical University , , ,
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Abstract

Cadmium (Cd) is a persistent environmental heavy metal that bioaccumulates and is associated with diverse toxicities. Metabolic dysfunction-associated steatotic liver disease (MASLD) is highly prevalent, and steatotic metabolic stress may increase vulnerability to toxicological insults. In this study, we used a free fatty acid (FFA)-treated hepatocyte model and high-fat diet (HFD)-fed steatotic mice to characterize hepatic responses to a short-term CdCl2 toxicological challenge under lipid overload conditions. In FFA-treated QSG-7701 cells, CdCl2 exposure was associated with increased lipid droplet accumulation, elevated oxidative stress, and increased apoptosis. In HFD-fed steatotic mice, short-term CdCl2 administration was associated with worsened liver injury and greater hepatic lipid accumulation compared with parallel steatotic controls. These phenotypic changes were accompanied by increased expression of lipogenesis-related markers, including SREBP-1c and SCD1, consistent with enhanced lipogenic signaling under steatotic stress. CdCl2 exposure was also associated with increased α-SMA and TGF-β, consistent with early fibrogenic activation in this short-term model rather than staged fibrosis. Rapamycin-treated mice exhibited attenuation of multiple injury- and lipid-related readouts compared with parallel CdCl2-treated groups, supporting its use as a pharmacological probe in this acute setting. Collectively, these observations support a model in which short-term CdCl2 challenge aggravates steatotic liver injury under lipid overload.

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Cite

BibTeXRIS
BibTeX
@article{wu2026cadmium,
  title = {{Cadmium Exposure Aggravates SREBP-1c-Mediated Hepatic Steatosis and Liver Injury in High-Fat Diet-Fed Mice}},
  author = {Shuying Wu and Yaqian Li and Yuru Zong and Qibin Mai and Ruirui Qiu and Huidong Song and Hanqing Chen},
  journal = {ACS Omega},
  year = {2026},
  month = oct,
  doi = {10.1021/acsomega.5c11799},
  url = {https://pubs.acs.org/acsodf/article/11/42/64359/5449448/Cadmium-Exposure-Aggravates-SREBP-1c-Mediated},
  note = {CC BY-NC-ND 4.0},
}
RIS
TY  - JOUR
TI  - Cadmium Exposure Aggravates SREBP-1c-Mediated Hepatic Steatosis and Liver Injury in High-Fat Diet-Fed Mice
AU  - Shuying Wu
AU  - Yaqian Li
AU  - Yuru Zong
AU  - Qibin Mai
AU  - Ruirui Qiu
AU  - Huidong Song
AU  - Hanqing Chen
PY  - 2026
DA  - 2026/10/13
JO  - ACS Omega
DO  - 10.1021/acsomega.5c11799
UR  - https://pubs.acs.org/acsodf/article/11/42/64359/5449448/Cadmium-Exposure-Aggravates-SREBP-1c-Mediated
AB  - Cadmium (Cd) is a persistent environmental heavy metal that bioaccumulates and is associated with diverse toxicities. Metabolic dysfunction-associated steatotic liver disease (MASLD) is highly prevalent, and steatotic metabolic stress may increase vulnerability to toxicological insults. In this study, we used a free fatty acid (FFA)-treated hepatocyte model and high-fat diet (HFD)-fed steatotic mice to characterize hepatic responses to a short-term CdCl2 toxicological challenge under lipid overload conditions. In FFA-treated QSG-7701 cells, CdCl2 exposure was associated with increased lipid droplet accumulation, elevated oxidative stress, and increased apoptosis. In HFD-fed steatotic mice, short-term CdCl2 administration was associated with worsened liver injury and greater hepatic lipid accumulation compared with parallel steatotic controls. These phenotypic changes were accompanied by increased expression of lipogenesis-related markers, including SREBP-1c and SCD1, consistent with enhanced lipogenic signaling under steatotic stress. CdCl2 exposure was also associated with increased α-SMA and TGF-β, consistent with early fibrogenic activation in this short-term model rather than staged fibrosis. Rapamycin-treated mice exhibited attenuation of multiple injury- and lipid-related readouts compared with parallel CdCl2-treated groups, supporting its use as a pharmacological probe in this acute setting. Collectively, these observations support a model in which short-term CdCl2 challenge aggravates steatotic liver injury under lipid overload.
SN  - 2470-1343
ER  -