期刊
AQUACULTURE RESEARCH
卷 48, 期 9, 页码 4874-4885出版社
WILEY
DOI: 10.1111/are.13307
关键词
short-term starvation; silver pomfret; lipid mobilization; lipid utilization
类别
资金
- Zhejiang Natural Science Foundation, China [LY15C190004]
- Project of Ministry of Education, China [20133305130001]
- Ningbo Science and Technology Research Projects, China [2014C10005]
- Ningbo Marine Algae Biotechnology Team, China [2011B81007]
- K. C. Wong Magna Fund in Ningbo University
To investigate the effects of short-term starvation on lipid metabolism, juvenile silver pomfret (Pampus argenteus) with an initial weight of 18.1 +/- 1.53g were starved for 6days. Fish were sampled on days 0, 2, 4 and 6 of starvation (S0, S2, S4 and S6, respectively) and then analysed. The results showed that short-term starvation induced a significant decrease in visceral index, hepatosomatic index. The crude lipid content was also significantly decreased by 42.22% and 82.96% on S2 and S6 respectively. In addition, short-term starvation significantly decreased the plasma triacylglycerol, non-esterified fatty acid and low-density lipoprotein cholesterol. Moreover, short-term starvation significantly increased the expressions of hormone-sensitive lipase (HSL) and adipose triglyceride lipase (ATGL) at the mRNA and protein levels in the muscle and the ATGL expression at the protein level in the liver. The expressions of fatty acid translocase (CD36) and plasma membrane fatty acid-binding protein (FABPpm) at the protein level in the muscle were significantly increased by short-term starvation, while the expressions of fatty acid transport protein 1 (FATP1), FABPpm and lipoprotein lipase (LPL) at the protein level in the liver were significantly increased by short-term starvation. Furthermore, the expressions of peroxisome proliferator activated receptor (PPAR) and PPAR at the mRNA and protein levels in the muscle were significantly elevated by short-term starvation. These findings suggested that short-term starvation increased lipid mobilization and utilization possibly through activation of lipolysis-related genes (HSL and ATGL), lipid uptake-related genes (LPL, CD36, FATP1 and FABPpm) and PPARs.
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