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JCR:LA肥胖大鼠肝细胞中极低密度脂蛋白(VLDL)分泌过多,而非高密度脂蛋白(HDL)。

Hypersecretion of VLDL, but not HDL, by hepatocytes from the JCR:LA-corpulent rat.

作者信息

Vance J E, Russell J C

机构信息

Lipid and Lipoprotein Group, University of Alberta, Edmonton, Canada.

出版信息

J Lipid Res. 1990 Aug;31(8):1491-501.

PMID:2280189
Abstract

The JCR:LA-corpulent male rat, when homozygous for the cp gene (cp/cp) is hyperlipidemic and prone to atherosclerosis. Both male and female cp/cp rats have markedly elevated serum levels of triacylglycerols and phospholipids [Dolphin, P.J. et al. 1987. Biochim. Biophys. Acta. 919: 140-148]. In the present study, monolayer cultures of hepatocytes were prepared from male and female, corpulent and lean, rats. There was a marked hypersecretion of all very low density lipoprotein (VLDL) lipid and apoprotein components from corpulent-derived cells. The increased secretion most likely accounts for the increased levels of VLDL lipids and apoproteins previously observed in serum. In contrast, there was no difference between the corpulent and lean hepatocytes in their secretion of high density lipoprotein (HDL) lipids and apoproteins. The difference in triacylglycerol secretion between the lean and corpulent cells was sustained even when the cells were cultured for 24, 48, and 72 h prior to the experiment, by which time the hormonal differences between the corpulent and lean animals would have been largely eliminated. The magnitude of the difference in triacyglycerol secretion did not diminish with increasing time in culture. The biochemical basis responsible for the hypersecretion of VLDL has not yet been established. However, preliminary results suggest that there is an inherent difference in glycerolipid metabolism in the two types of hepatocytes.

摘要

JCR

LA肥胖雄性大鼠在纯合cp基因(cp/cp)时会出现高脂血症并易患动脉粥样硬化。雄性和雌性cp/cp大鼠的血清甘油三酯和磷脂水平均显著升高[多尔芬,P.J.等人,1987年。生物化学与生物物理学报。919:140 - 148]。在本研究中,从雄性和雌性、肥胖和瘦的大鼠中制备了肝细胞单层培养物。肥胖来源的细胞中所有极低密度脂蛋白(VLDL)脂质和载脂蛋白成分均有明显的高分泌。分泌增加很可能是先前在血清中观察到的VLDL脂质和载脂蛋白水平升高的原因。相比之下,肥胖和瘦的肝细胞在高密度脂蛋白(HDL)脂质和载脂蛋白的分泌方面没有差异。即使在实验前将细胞培养24、48和72小时,肥胖和瘦细胞之间甘油三酯分泌的差异仍然存在,此时肥胖和瘦动物之间的激素差异已基本消除。甘油三酯分泌差异的幅度不会随着培养时间的增加而减小。导致VLDL高分泌的生化基础尚未确定。然而,初步结果表明,两种类型的肝细胞在甘油脂质代谢方面存在内在差异。

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Hypersecretion of VLDL, but not HDL, by hepatocytes from the JCR:LA-corpulent rat.JCR:LA肥胖大鼠肝细胞中极低密度脂蛋白(VLDL)分泌过多,而非高密度脂蛋白(HDL)。
J Lipid Res. 1990 Aug;31(8):1491-501.
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Exposure to a northern contaminant mixture (NCM) alters hepatic energy and lipid metabolism exacerbating hepatic steatosis in obese JCR rats.暴露于北方污染物混合物(NCM)会改变肥胖JCR大鼠的肝脏能量和脂质代谢,加剧肝脏脂肪变性。
PLoS One. 2014 Sep 15;9(9):e106832. doi: 10.1371/journal.pone.0106832. eCollection 2014.
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Irbesartan-mediated reduction of renal and cardiac damage in insulin resistant JCR : LA-cp rats.厄贝沙坦对胰岛素抵抗 JCR:LA-cp 大鼠肾脏和心脏损伤的减轻作用。
Br J Pharmacol. 2009 Nov;158(6):1588-96. doi: 10.1111/j.1476-5381.2009.00417.x. Epub 2009 Oct 8.
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Increased insulin sensitivity and reduced micro and macro vascular disease induced by 2-deoxy-D-glucose during metabolic syndrome in obese JCR: LA-cp rats.
在肥胖的JCR:LA-cp大鼠代谢综合征期间,2-脱氧-D-葡萄糖诱导胰岛素敏感性增加以及微血管和大血管疾病减少。
Br J Pharmacol. 2007 May;151(2):216-25. doi: 10.1038/sj.bjp.0707226. Epub 2007 Mar 20.
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A novel complex of arginine-silicate improves micro- and macrovascular function and inhibits glomerular sclerosis in insulin-resistant JCR:LA-cp rats.一种新型精氨酸-硅酸盐复合物可改善胰岛素抵抗的JCR:LA-cp大鼠的微血管和大血管功能,并抑制肾小球硬化。
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Improvement of vascular dysfunction and blood lipids of insulin-resistant rats by a marine oil-based phytosterol compound.一种基于海洋油的植物甾醇化合物对胰岛素抵抗大鼠血管功能障碍和血脂的改善作用。
Lipids. 2002 Feb;37(2):147-52. doi: 10.1007/s11745-002-0874-6.
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Cardiovascular disease in the JCR:LA-cp rat.JCR:LA-cp大鼠的心血管疾病
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Insulin promotes the biosynthesis and secretion of apolipoprotein B-48 by altering apolipoprotein B mRNA editing.胰岛素通过改变载脂蛋白B信使核糖核酸编辑来促进载脂蛋白B-48的生物合成和分泌。
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