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Jiayou Wang

  • Assistant Research Professor, Internal Medicine
Contact
  • (602) 827-2078
  • Biosciences Partnership Phx, Rm. E815L
  • Phoenix, AZ 85004
  • jwang11@arizona.edu
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  • Gopoju, R., Wang, J., Pan, X., Hu, S., Lin, L., Clark, A., Xu, Y., Yin, L., Wang, X., & Zhang, Y. (2024). Hepatic FOXA3 overexpression prevents Western diet-induced obesity and MASH through TGR5. Journal of lipid research, 65(4), 100527.
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    Forkhead transcription factor 3 (FOXA3) has been shown to regulate metabolism and development. Hepatic FOXA3 is reduced in obesity and fatty liver disease. However, the role of hepatic FOXA3 in regulating obesity or steatohepatitis remains to be investigated. In this work, C57BL/6 mice were i.v. injected with AAV8-ALB-FOXA3 or the control virus. The mice were then fed a chow or Western diet for 16 weeks. The role of hepatic FOXA3 in energy metabolism and steatohepatitis was investigated. Plasma bile acid composition and the role of Takeda G protein-coupled receptor 5 (TGR5) in mediating the metabolic effects of FOXA3 were determined. Overexpression of hepatic FOXA3 reduced hepatic steatosis in chow-fed mice and attenuated Western diet-induced obesity and steatohepatitis. FOXA3 induced lipolysis and inhibited hepatic genes involved in bile acid uptake, resulting in elevated plasma bile acids. The beneficial effects of hepatic FOXA3 overexpression on Western diet-induced obesity and steatohepatitis were abolished in Tgr5 mice. Our data demonstrate that overexpression of hepatic FOXA3 prevents Western diet-induced obesity and steatohepatitis via activation of TGR5.
  • Pan, X., Hu, S., Xu, Y., Gopoju, R., Zhu, Y., Cassim Bawa, F. N., Wang, H., Wang, J., Batayneh, Z., Clark, A., Zeng, Y., Lin, L., Wang, X., Yin, L., & Zhang, Y. (2024). Krüppel-like factor 10 protects against metabolic dysfunction-associated steatohepatitis by regulating HNF4α-mediated metabolic pathways. Metabolism: clinical and experimental, 155, 155909.
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    Krüppel-like factor 10 (KLF10), a zinc finger transcription factor, plays a pivotal role in modulating TGF-β-mediated cellular processes such as growth, apoptosis, and differentiation. Recent studies have implicated KLF10 in regulating lipid metabolism and glucose homeostasis. This study aimed to elucidate the precise role of hepatic KLF10 in developing metabolic dysfunction-associated steatohepatitis (MASH) in diet-induced obese mice.

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