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首页> 外文期刊>Journal of applied toxicology >Effect and mechanism of waterborne prolonged Zn exposure influencing hepatic lipid metabolism in javelin goby Synechogobius hasta
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Effect and mechanism of waterborne prolonged Zn exposure influencing hepatic lipid metabolism in javelin goby Synechogobius hasta

机译：水延长锌暴露对标枪鱼Synechogobius hasta肝脂质代谢的影响及其机制

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摘要

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)alpha, ACC beta, hormone-sensitive lipase (HSL)a, HSLb, sterol-regulator element-binding protein (SREBP)-1, peroxisome proliferators-activated receptor (PPAR)alpha and PPAR gamma. 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, ACC alpha, ACC beta, HSLa, HSLb, SREBP-1 and PPAR gamma but increased mRNA expression of CPT 1, adipose triglyceride lipase and PPAR alpha. 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 (C) 2015 John Wiley & Sons, Ltd.
机译：本研究旨在确定水锌暴露对标枪虾虎鱼Synechogobius hasta中肝脂质沉积和代谢的影响及其机理。哈萨克链霉菌暴露于四种水性锌浓度下（锌分别为0.005 [对照]，0.18、0.36和0.55 mg l（-1））60天。分别在第20、40和60天进行采样。锌暴露增加了锌含量，降低了肝脂质含量，降低了内脏和肝体指数以及脂肪酶的活性，包括6-磷酸葡萄糖酸脱氢酶（6PGD），葡萄糖-6-磷酸脱氢酶（G6PD），苹果酸酶（ME）和脂肪酸合酶（ FAS）。在第20天和第60天，锌暴露降低了6PGD，G6PD，ME，FAS，乙酰辅酶A羧化酶（ACC）alpha，ACC beta，激素敏感性脂肪酶（HSL）a，HSLb，固醇调节因子结合的肝mRNA水平蛋白（SREBP）-1，过氧化物酶体增殖物激活受体（PPAR）alpha和PPARγ。然而，CPT 1和脂肪甘油三酸酯脂肪酶的mRNA水平在锌暴露后增加。在第40天，锌暴露降低了6PGD，G6PD，ME，FAS，ACCα，ACC beta，HSLa，HSLb，SREBP-1和PPARγ的肝mRNA表达，但增加了CPT 1，脂肪甘油三酯脂肪酶和PPARα的mRNA表达。一般而言，锌暴露通过抑制脂肪生成和刺激脂肪分解而降低了肝脂质含量。本研究首次提供证据，表明长期锌暴露以持续时间依赖性方式不同地影响参与脂肪和脂解代谢的基因和酶的mRNA表达和活性，并提供了对金属元素与脂质代谢之间关系的新见解。 。版权所有（C）2015 John Wiley＆Sons，Ltd.

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