INFLUENCE OF EROTIC ACID AND ESTROGEN ON HEPATIC LIPID STORAGE AND SECRETION IN THE GOOSE SUSCEPTIBLE TO LIVER STEATOSIS
INFLUENCE OF EROTIC ACID AND ESTROGEN ON HEPATIC LIPID STORAGE AND SECRETION IN THE GOOSE SUSCEPTIBLE TO LIVER STEATOSIS
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DOI：
10.1016/0005-2760(94)90143-0
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发表时间：
1994-02-10
期刊：
影响因子：
--
通讯作者：
SELLIER, N
中科院分区：
文献类型：
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作者：
HERMIER, D;ROUSSELOTPAILLEY, D;SELLIER, N
鹅的脂肪肝是由于过度饲养引起的肝脏脂肪生成增加，以及作为极低密度脂蛋白（VLDL）的三酰甘油分泌不足。乳清酸和雌激素，这两个改变肝脏中的脂质代谢，在雄性鹅作为工具，以了解肝脏脂肪变性诱导过程中肝脏脂质和血浆脂蛋白的变化。溶剂提取后分析肝脏脂质，密度梯度超离心分离后分析血浆脂蛋白。与大鼠中已知的相反，色情酸（食物中1%，持续2周）未能诱导肝脏脂肪变性。在强制喂养的鹅，肝脏重量增加约100克至约800克，在2周内，作为一个特定的积累的三酰甘油的结果;在这两组中，极低密度脂蛋白含有较少的三酰甘油（35%）比正常。这种解偶联的三酰甘油的合成和分泌，其确切的原因仍然是未知的，可能会促进他们的积累时，强制喂养增加肝脏脂肪生成。与强制喂食一样，雌激素促进了三酰甘油的合成，但它们作为VLDL的分泌非常有效，几乎完全防止了肝脏脂肪变性。由于HDL浓度大大降低雌激素，极低密度脂蛋白是主要的脂蛋白种类，与48克/升和62%的三酰甘油。在雌激素处理的鹅强迫喂食伴随，VLDL浓度甚至更高（62克/升），但三酰甘油分泌不能防止肝脏脂肪变性（肝重640克）。数据进行了讨论，在体外研究表明，三酰甘油对分泌的VLDL或肝存储通道取决于他们的停留时间在不同的细胞内隔室。
Fatty liver in the goose results from an increased hepatic lipogenesis in response to overfeeding, together with a deficient secretion of triacylglycerol as very-low-density lipoproteins (VLDL). Orotic acid and estrogen, which both modify lipid metabolism in the liver, were used in male geese as tools to understand the alterations of liver lipids and plasma lipoproteins during the induction of liver steatosis. Liver lipids were analyzed after solvent extraction and plasma lipoproteins after separation by density gradient ultracentrifugation. Contrary to what is known in the rat, erotic acid (1% in food for 2 weeks) failed to induce liver steatosis. In force-fed geese, liver weight increased from approximate to 100 g to approximate to 800 g in 2 weeks, as a consequence of a specific accumulation of triacylglycerol; In both groups, VLDL contained less triacylglycerol (35%) than normal. Such an uncoupling of triacylglycerol synthesis and secretion, of which the precise reason is still unknown, may facilitate their accumulation when force-feeding increases hepatic lipogenesis. As with force-feeding, triacylglycerol synthesis was enhanced by estrogen, but their secretion as VLDL was very efficient and prevented liver steatosis almost completely. Since HDL concentrations were considerably decreased by estrogen, VLDL were the main lipoprotein species, with 48 g/l and 62% triacylglycerol. Where estrogen-treated geese were force-fed concomitantly, VLDL concentration was even higher (62 g/l), but triacylglycerol secretion could not prevent liver steatosis (liver weight 640 g). The data are discussed in relation to in vitro studies showing that channelling of triacylglycerol towards secretion as VLDL or hepatic storage depends on their residence time in the different intracellular compartments.