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Physiological and molecular changes in large yellow croaker ( P seudosciaena crocea R .) with high‐fat diet‐induced fatty liver disease
Author(s) -
Wang Xinxia,
Li Yongjin,
Hou Chonglin,
Gao Yang,
Wang Yizhen
Publication year - 2015
Publication title -
aquaculture research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.646
H-Index - 89
eISSN - 1365-2109
pISSN - 1355-557X
DOI - 10.1111/are.12176
Subject(s) - biology , fatty liver , triglyceride , endocrinology , medicine , nefa , fatty acid synthase , fatty acid , lipoprotein lipase , steatosis , high density lipoprotein , hepatic lipase , cholesterol , lipoprotein , lipid metabolism , biochemistry , adipose tissue , disease
Abstract Fatty liver disease is regularly observed in cultured large yellow croaker, and the disease leads to lower growth rates and reduced harvest yields. The goal of this study was to achieve a more detailed understanding of the physiological and molecular changes in response to high‐fat diet‐induced fatty liver in large yellow croaker. Large yellow croaker fed a high‐fat diet ( HFD ) for 9 weeks developed hepatic steatosis characterized by histological observation and significantly increased plasma triglyceride levels and serum alanine aminotransferase ( ALT ) activities. However, no significant differences in serum total protein, glucose, cholesterol, non‐esterified free fatty acids ( NEFA ), aspartate aminotransferase, high‐density lipoprotein and low‐density lipoprotein were observed between the normal diet and the high‐fat diet ( HFD ) group. The fatty acid composition of tissue lipids was not affected significantly by dietary lipid levels. Gene expression analysis demonstrated that the HFD decreased fatty acid synthase expression and increased PPAR γ expression, but had no effect on lipoprotein lipase and PPAR α expression. These results suggest that the HFD ‐induced physiological changes and fatty liver may be due to the alteration of related gene expression. As such, further investigations of the metabolic pathways and differentially expressed genes are of particular significance in the mechanistic study and understanding of HFD ‐induced fatty liver disease.