2. Academic Validation
  3. Ellagitannins-Derived Intestinal Microbial Metabolite Urolithin A Ameliorates Fructose-Driven Hepatosteatosis by Suppressing Hepatic Lipid Metabolic Reprogramming and Inducing Lipophagy

Ellagitannins-Derived Intestinal Microbial Metabolite Urolithin A Ameliorates Fructose-Driven Hepatosteatosis by Suppressing Hepatic Lipid Metabolic Reprogramming and Inducing Lipophagy

  • J Agric Food Chem. 2023 Feb 24. doi: 10.1021/acs.jafc.2c05776.
Cong Zhang 1,  Yingying Song 1,  Ming Yuan 1,  Liang Chen 1,  Qianyu Zhang 1,  Junjie Hu 1,  Yan Meng 1,  Shan Li 2 3,  Guohua Zheng 4,  Zhenpeng Qiu 1 5
Affiliations

Affiliations

  • 1 College of Pharmacy, Hubei University of Chinese Medicine, Wuhan 430065, People's Republic of China.
  • 2 Hubei Key Laboratory of Wudang Local Chinese Medicine Research, Hubei University of Medicine, Shiyan 442000, People's Republic of China.
  • 3 Department of Biochemistry, Institute of Basic Medical Sciences, Hubei University of Medicine, Shiyan 442000, People's Republic of China.
  • 4 Key Laboratory of Chinese Medicine Resource and Compound Prescription, Ministry of Education, Hubei University of Chinese Medicine, Wuhan 430065, People's Republic of China.
  • 5 Hubei Key Laboratory of Resources and Chemistry of Chinese Medicine, Hubei University of Chinese Medicine, Wuhan 430065, People's Republic of China.
PMID: 36825491 DOI: 10.1021/acs.jafc.2c05776
Abstract

Excessive fructose consumption exacerbates the progression of nonalcoholic fatty liver disease (NAFLD) by disrupting hepatic lipid homeostasis. This study sought to evaluate the efficacy of urolithin A (UroA) in a fructose-induced NAFLD mouse model. UroA was administered in the high-fructose-fed mice to investigate the antisteatotic effects in vivo. Fructose-stimulated HepG2 cells and primary hepatocytes were established for in vitro mechanistic assessment. The results suggested that UroA ameliorated fructose-induced hepatic steatosis in mice. Mechanistically, UroA impaired lipogenesis and enhanced β-oxidation in the livers of fructose-fed mice. Notably, UroA facilitated hepatic lipophagy through the AMPK/ULK1 pathway both in vivo and in vitro, degrading lipid droplets for fueling β-oxidation. This study indicates that UroA alleviates excessive lipid accumulation and restores lipid homeostasis in the livers of fructose-fed mice by suppressing lipid metabolic reprogramming and triggering lipophagy. Therefore, dietary supplementation of UroA or ellagitannins-rich foods may be beneficial for NAFLD individuals with high fructose intake.

Keywords

fructose; lipogenesis; lipophagy; nonalcoholic fatty liver disease; urolithin A.

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