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试验旨在研究锌对黄颡鱼脂质沉积的机制。在黄颡鱼饲粮中添加不同浓度的锌,其浓度依次为锌19.82(适宜含量)、11.45(含量不足)和155.97(含量超标)mg·kg-1,试验共进行8周。测定了肝脏和肌肉中脂质和锌的含量、CPTI和LPL的活性以及与脂质代谢相关的12种基因的基因表达。与适宜含量的锌相比,饲喂过量的锌会降低肝脏和肌肉中的脂质含量,肌肉中的LPL活性也会降低,肝脏中的CPTI和LPL活性升高。锌含量缺乏则会增加组织中脂质含量和CPTI活性。饲料中过量的锌则会增加锌在肝脏、肌肉和整条鱼中的沉积,但缺锌则会降低肝脏和整条鱼中锌的沉积。在肝脏缺锌CPT1A、PPARα、Lep R、G6PD、6PGD和ACCb的转录水平显著下降,但FAS的转录水平会显著上升;锌过量会使CPT1A、PPARα、Lep、Lep R、SREBP-1、G6PD、6PGD、ACCb和LPL基因的转录水平会上升。但FAS、ACCa和PPARγ基因转录水平会降低。在肌肉中,缺锌会使f PPARα、Lep、SREBP-1、FAS和ACCa基因转录水平下降,升高6PGD和LPL基因表达。过量的锌会下调PPARγ、SREBP-1、G6PD、ACCa和LPL基因水平,上调CPT1A和Lep基因水平。这是首次可以表明饲粮中锌不足或过量对脂质沉积和代谢的不同影响,为锌的营养学和毒理学提供理论依据。
The purpose of the experiment was to investigate the mechanism of zinc deposition on lipid in yellow catfish. Different concentrations of zinc were added to yellow catfish diets in the order of zinc 19.82 (appropriate content), 11.45 (insufficient content) and 155.97 (excessive content) mg · kg-1 for 8 weeks. Lipid and zinc contents in liver and muscle, CPTI and LPL activity, and gene expression of 12 genes involved in lipid metabolism were determined. Excess zinc supplementation reduced lipid levels in the liver and muscle compared to appropriate levels of zinc, decreased LPL activity in muscle, and increased CPTI and LPL activity in the liver. The lack of zinc increases the lipid content and CPTI activity in the tissue. Excess zinc in the feed increases the deposition of zinc in the liver, muscle and whole fish, but zinc deficiency reduces the deposition of zinc in the liver and whole fish. The transcriptional level of FAS in the deficient zinc-deficient CPT1A, PPARα, Lep R, G6PD, 6PGD and ACCb decreased significantly, while the excess of zinc in CPT1A, PPARα, Lep, Lep R, SREBP-1, G6PD, 6PGD, ACCb and LPL gene transcription levels will rise. However, the transcriptional levels of FAS, ACCa and PPARγ genes are reduced. In muscle, zinc deficiency decreased the transcription of f PPARα, Lep, SREBP-1, FAS and ACCa genes, and increased the expression of 6PGD and LPL genes. Excessive zinc can down-regulate the gene levels of PPARγ, SREBP-1, G6PD, ACCa and LPL and up-regulate the levels of CPT1A and Lep genes. This is the first time that the different effects of dietary zinc deficiency or overdose on lipid deposition and metabolism can provide a theoretical basis for zinc nutrition and toxicology.