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短期和长期肝前性门静脉高压大鼠的肝脏脂质代谢变化

Hepatic lipid metabolism changes in short- and long-term prehepatic portal hypertensive rats.

作者信息

Aller Maria-Angeles, Vara Elena, García Cruz, Nava Maria-Paz, Angulo Alejandra, Sánchez-Patán Fernando, Calderón Ana, Vergara Patri, Arias Jaime

机构信息

Surgery I Department, School of Medicine, Complutense University of Madrid, Spain.

出版信息

World J Gastroenterol. 2006 Nov 14;12(42):6828-34. doi: 10.3748/wjg.v12.i42.6828.

Abstract

AIM

To verify the impairment of the hepatic lipid metabolism in prehepatic portal hypertension.

METHODS

The concentrations of free fatty acids, diacylglycerol, triglycerides, and phospholipids were assayed by using D-[U-14C] glucose incorporation in the different lipid fractions and thin-layer chromatography and cholesterol was measured by spectrophotometry, in liver samples of Wistar rats with partial portal vein ligation at short- (1 mo) and long-term (1 year) (i.e. portal hypertensive rats) and the control rats.

RESULTS

In the portal hypertensive rats, liver phospholipid synthesis significantly decreased (7.42 +/- 0.50 vs 4.70 +/- 0.44 nCi/g protein; P < 0.01) and was associated with an increased synthesis of free fatty acids (2.08 +/- 0.14 vs 3.36 +/- 0.33 nCi/g protein; P < 0.05), diacylglycerol (1.93 +/- 0.2 vs 2.26 +/- 0.28 nCi/g protein), triglycerides (2.40 +/- 0.30 vs 4.49 +/- 0.15 nCi/g protein) and cholesterol (24.28 +/- 2.12 vs 57.66 +/- 3.26 mg/g protein; P < 0.01).

CONCLUSION

Prehepatic portal hypertension in rats impairs the liver lipid metabolism. This impairment consists in an increase in lipid deposits (triglycerides, diacylglycerol and cholesterol) in the liver, accompanied by a decrease in phospholipid synthesis.

摘要

目的

验证肝前性门静脉高压时肝脏脂质代谢的损伤情况。

方法

采用D-[U-14C]葡萄糖掺入不同脂质组分并结合薄层色谱法测定Wistar大鼠部分门静脉结扎短期(1个月)和长期(1年)(即门静脉高压大鼠)及对照大鼠肝脏样本中游离脂肪酸、二酰甘油、甘油三酯和磷脂的浓度,采用分光光度法测定胆固醇浓度。

结果

门静脉高压大鼠肝脏磷脂合成显著降低(7.42±0.50对4.70±0.44 nCi/g蛋白;P<0.01),并伴有游离脂肪酸(2.08±0.14对3.36±0.33 nCi/g蛋白;P<0.05)、二酰甘油(1.93±0.2对2.26±0.28 nCi/g蛋白)、甘油三酯(2.40±0.30对4.49±0.15 nCi/g蛋白)和胆固醇(24.28±2.12对57.66±3.26 mg/g蛋白;P<0.01)合成增加。

结论

大鼠肝前性门静脉高压损害肝脏脂质代谢。这种损害表现为肝脏脂质沉积(甘油三酯、二酰甘油和胆固醇)增加,同时磷脂合成减少。

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