Journal
FRONTIERS IN MARINE SCIENCE
Volume 7, Issue -, Pages -Publisher
FRONTIERS MEDIA SA
DOI: 10.3389/fmars.2020.00363
Keywords
steatosis; endoplasmic reticulum (ER) stress; autophagy; high-fat diet; Oreochromis niloticus
Funding
- Jiangsu Provincial Natural Science Foundation of China [BK20170218]
- National Natural Science Foundation of China [31702318]
- Central Public-interest Scientific Institution Basal Research Fund, Freshwater Fisheries Research Center, CAFS [2019JBFM10, 2019JBFM11]
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Hepatic steatosis is the most common phenomenon of lipid metabolism disorder in farmed fish, but its molecular mechanism is poorly understood. Therefore, the present study was aimed to investigate hepatic steatosis induced by high-fat diet (HFD) and explore underlying mechanism in tilapia. The fish were fed on control diet or HFD for 90 days. The blood and liver tissues were collected to determine biochemical parameter, gene expression and protein level after 30, 60, and 90 days, and analyzed lipid accumulation, endoplasmic reticulum (ER) stress and autophagy. After 30 days of feeding, the plasmatic and hepatic lipid content (TG, TCH, LDL-C, and HDL-C) and fatty acid (FA) transportation (fabp1 and CD36) were enhanced significantly in HFD-fed tilapia. After 60 days, HFD feeding increased TG synthesis and free CH formation, and decreased FAs beta-oxidation and biosynthesis in liver of tilapia. Further, with increasing lipid accumulation, ER stress was induced, which worsened hepatic steatosis via activating IRE1 signaling pathway in liver of HFD group after 90 days. Meanwhile, HFD feeding suppressed autophagy via impairing AMPK and TFEB pathways in tilapia liver after 90 days. Our results demonstrated that HFD feeding induced extensive lipid deposition, promoted ER stress, suppressed autophagy in tilapia liver. Interestingly, these pathological features were positively correlated with the duration of HFD feeding.
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