Open Access

Atorvastatin promotes AMPK signaling to protect against high fat diet‑induced non‑alcoholic fatty liver in golden hamsters

  • Authors:
    • Bin Zhang
    • Chenyang Zhang
    • Xuelian Zhang
    • Nannan Li
    • Zhengqi Dong
    • Guibo Sun
    • Xiaobo Sun
  • View Affiliations

  • Published online on: January 22, 2020     https://doi.org/10.3892/etm.2020.8465
  • Pages: 2133-2142
  • Copyright: © Zhang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Non‑alcoholic fatty liver disease (NAFLD) is characterized by diffuse fatty acid degeneration and excess fat accumulation in the liver. Notably, the currently available medications used to treat NAFLD remain limited. The aim of the present study was to investigate the protective role of atorvastatin (Ato) against NAFLD in golden hamsters fed a high fat diet (HFD) and in HepG2 cells treated with palmitate, and identify the underlying molecular mechanism. Ato (3 mg/kg) was administered orally every day for 8 weeks to the hamsters during HFD administration. Hamsters in the model group developed hepatic steatosis with high serum levels of triglyceride, cholesterol, insulin and C‑reactive protein, which were effectively reduced by treatment with Ato. Additionally, the relative liver weight of hamsters treated with Ato was markedly lower compared with that of the model group. Hematoxylin and eosin, and oil red O staining indicated that the livers of the animals in the model group exhibited large and numerous lipid droplets, which were markedly decreased after Ato treatment. Western blot analysis indicated that Ato inhibited fat accumulation in the liver through the AMP‑activated protein kinase (AMPK)‑dependent activation of peroxisome proliferator activated receptor α (PPARα), peroxisome proliferator‑activated receptor‑γ coactivator 1 α and their target genes. Furthermore, in vitro, Ato inhibited PA‑induced lipid accumulation in HepG2 cells. This inhibitory effect was attenuated following Compound C treatment, indicating that AMPK may be a potential target of Ato. In conclusion, the increase in AMPK‑mediated PPARα and its target genes may represent a novel molecular mechanism by which Ato prevents NAFLD.
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March 2020
Volume 19 Issue 3

Print ISSN: 1792-0981
Online ISSN:1792-1015

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APA
Zhang, B., Zhang, C., Zhang, X., Li, N., Dong, Z., Sun, G., & Sun, X. (2020). Atorvastatin promotes AMPK signaling to protect against high fat diet‑induced non‑alcoholic fatty liver in golden hamsters. Experimental and Therapeutic Medicine, 19, 2133-2142. https://doi.org/10.3892/etm.2020.8465
MLA
Zhang, B., Zhang, C., Zhang, X., Li, N., Dong, Z., Sun, G., Sun, X."Atorvastatin promotes AMPK signaling to protect against high fat diet‑induced non‑alcoholic fatty liver in golden hamsters". Experimental and Therapeutic Medicine 19.3 (2020): 2133-2142.
Chicago
Zhang, B., Zhang, C., Zhang, X., Li, N., Dong, Z., Sun, G., Sun, X."Atorvastatin promotes AMPK signaling to protect against high fat diet‑induced non‑alcoholic fatty liver in golden hamsters". Experimental and Therapeutic Medicine 19, no. 3 (2020): 2133-2142. https://doi.org/10.3892/etm.2020.8465