Formyl peptide receptor 2 determines sex-specific differences in the progression of nonalcoholic fatty liver disease and steatohepatitis

Chanbin Lee, Jieun Kim, Jinsol Han, Dayoung Oh, Minju Kim, Hayeong Jeong, Tae-Jin Kim, Sang-Woo Kim, Jeong Nam Kim, Young-Su Seo, Ayako Suzuki, Jae Ho Kim and Youngmi Jung ()
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Chanbin Lee: Pusan National University
Jieun Kim: Pusan National University
Jinsol Han: Pusan National University
Dayoung Oh: Pusan National University
Minju Kim: Pusan National University
Hayeong Jeong: Pusan National University
Tae-Jin Kim: Pusan National University
Sang-Woo Kim: Pusan National University
Jeong Nam Kim: Pusan National University
Young-Su Seo: Pusan National University
Ayako Suzuki: Duke University
Jae Ho Kim: Pusan National University
Youngmi Jung: Pusan National University

Nature Communications, 2022, vol. 13, issue 1, 1-17

Abstract: Abstract Nonalcoholic fatty liver disease (NAFLD) is an important health concern worldwide and progresses into nonalcoholic steatohepatitis (NASH). Although prevalence and severity of NAFLD/NASH are higher in men than premenopausal women, it remains unclear how sex affects NAFLD/NASH pathophysiology. Formyl peptide receptor 2 (FPR2) modulates inflammatory responses in several organs; however, its role in the liver is unknown. Here we show that FPR2 mediates sex-specific responses to diet-induced NAFLD/NASH. NASH-like liver injury was induced in both sexes during choline-deficient, L-amino acid-defined, high-fat diet (CDAHFD) feeding, but compared with females, male mice had more severe hepatic damage. Fpr2 was more highly expressed in hepatocytes and healthy livers from females than males, and FPR2 deletion exacerbated liver damage in CDAHFD-fed female mice. Estradiol induced Fpr2 expression, which protected hepatocytes and the liver from damage. In conclusion, our results demonstrate that FPR2 mediates sex-specific responses to diet-induced NAFLD/NASH, suggesting a novel therapeutic target for NAFLD/NASH.

Date: 2022
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DOI: 10.1038/s41467-022-28138-6

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