Article

Dietary fenofibrate attenuated high-fat-diet-induced lipid accumulation and inflammation response partly through regulation of pparα and sirt1 in juvenile black seabream (Acanthopagrus schlegelii)

Citation

Jin M, Zhu T, Tocher D, Luo J, Shen Y, Li X, Pan T, Yuan Y, Betancor M, Jiao L, Sun P & Zhou Q (2020) Dietary fenofibrate attenuated high-fat-diet-induced lipid accumulation and inflammation response partly through regulation of pparα and sirt1 in juvenile black seabream (Acanthopagrus schlegelii). Developmental and Comparative Immunology, 109, Art. No.: 103691. https://doi.org/10.1016/j.dci.2020.103691

Abstract
An 8-week feeding trail was conducted in Acanthopagrus schlegelii with an initial body weight of 8.34±0.01g. Three isonitrogenous diets were formulated, (1) Control: medium-fat diet (12%); (2) HFD: high-fat diet (18%); (3) HFD+FF: high-fat diet with fenofibrate (0.15%). Liver histological analysis revealed that, compared to HFD, vacuolar fat drops were smaller and fewer in fish fed fenofibrate. Expression of lipid catabolism regulator peroxisome proliferator-activated receptor alpha (pparα) was up-regulated by fenofibrate compared with HFD. In addition, fenofibrate significantly increased the expression level of silent information regulator 1 (sirt1). Meanwhil e, the expression level of anti-inflammatory cytokine interleukin 10 (il-10) in intestine was up-regulated, while pro-inflammatory cytokine interleukin 1β (il-1β) in liver and intestine were down-regulated by dietary fenofibrate supplementation. Overall, the present study indicated that fenofibrate reduced fat deposition and attenuated inflammation response caused by HFD partly through a pathway involving regulation of pparα and sirt1.

Keywords
fenofibrate; high-fat diet; inflammation response; pparα; sirt1

Journal
Developmental and Comparative Immunology: Volume 109

StatusPublished
Publication date31/08/2020
Publication date online03/04/2020
Date accepted by journal25/03/2020
URLhttp://hdl.handle.net/1893/30911
ISSN0145-305X
eISSN1879-0089