Effect and mechanism of waterborne prolonged Zn exposure influencing hepatic lipid metabolism in javelin goby Synechogobius hasta
Effect and mechanism of waterborne prolonged Zn exposure influencing hepatic lipid metabolism in javelin goby Synechogobius hasta
复制标题
水性长期暴露锌对标枪虾虎鱼肝脏脂质代谢的影响及机制
DOI：
10.1002/jat.3261
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发表时间：
2016-07-01
影响因子：
3.3
通讯作者：
Pan, Ya-Xiong
中科院分区：
文献类型：
--
作者：
Huang, Chao;Luo, Zhi;Pan, Ya-Xiong
本研究旨在探讨水中锌暴露对标枪虎鱼肝脏脂质沉积和代谢的影响及其机制。分别以0.005.18、0.36、0.5 5 mg −1、0.18、0.36、0.5 5 mg −1为对照，暴露于4种水生锌浓度下，共60 d。取样时间分别为第20、40、60天。锌暴露可增加锌含量，降低肝脂含量，降低脏体指数、肝体指数以及6-磷酸葡萄糖脱氢酶(6PGD)、葡萄糖-6-磷酸脱氢酶(G6PD)、苹果酸酶(ME)和脂肪酸合成酶(Fas)等成脂酶活性。在第20天和第60天，锌暴露降低了肝脏6PGD、G6PD、ME、Fas、乙酰辅酶A羧化酶α、乙酰辅酶Aβ、激素敏感脂肪酶a、激素敏感脂肪酶b、固醇调节元件结合蛋白-1、过氧化体增殖物激活受体α和过氧化体增殖物激活受体γ的表达水平。然而，CPT-1和脂肪甘油三酯脂肪酶的mRNA水平在锌暴露后升高。染锌后第40天，肝组织6PGD、G6PD、ME、Fas、Accα、Accβ、HSLA、HSLb、SREBP-1和PPARγ基因表达降低，而CPT1、脂肪甘油三酯脂肪酶和PPARα基因表达增加。总体而言，锌暴露通过抑制脂肪生成和促进脂肪分解来降低肝脏脂质含量。本研究首次提供了慢性锌暴露以时间依赖的方式不同地影响成脂和脂代谢相关基因和酶的mRNA表达和活性的证据，并为金属元素与脂代谢之间的关系提供了新的见解。版权所有©2015 John Wiley&Sons，Ltd.
The present study was conducted to determine the effect and mechanism of waterborne Zn exposure influencing hepatic lipid deposition and metabolism in javelin goby Synechogobius hasta. S. hasta were exposed to four waterborne Zn concentrations (Zn 0.005 [control], 0.18, 0.36 and 0.55 mg l−1, respectively) for 60 days. Sampling occurred at days 20, 40 and 60, respectively. Zn exposure increased Zn content, declined hepatic lipid content and reduced viscerosomatic and hepatosomatic indices and lipogenic enzyme activities, including 6‐phosphogluconate dehydrogenase (6PGD), glucose‐6‐phosphate dehydrogenase (G6PD), malic enzyme (ME) and fatty acid synthase (FAS). At days 20 and 60, Zn exposure decreased hepatic mRNA levels of 6PGD, G6PD, ME, FAS, acetyl‐CoA carboxylase (ACC)α, ACCβ, hormone‐sensitive lipase (HSL)a, HSLb, sterol‐regulator element‐binding protein (SREBP)‐1, peroxisome proliferators‐activated receptor (PPAR)α and PPARγ. However, the mRNA levels of CPT 1 and adipose triglyceride lipase increased following Zn exposure. On day 40, Zn exposure reduced hepatic mRNA expression of 6PGD, G6PD, ME, FAS, ACCα, ACCβ, HSLa, HSLb, SREBP‐1 and PPARγ but increased mRNA expression of CPT 1, adipose triglyceride lipase and PPARα. General speaking, Zn exposure reduced hepatic lipid content by inhibiting lipogenesis and stimulating lipolysis. For the first time, the present study provided evidence that chronic Zn exposure differentially influenced mRNA expression and activities of genes and enzymes involved in lipogenic and lipolytic metabolism in a duration‐dependent manner, and provided new insight into the relationship between metal elements and lipid metabolism. Copyright © 2015 John Wiley & Sons, Ltd.