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

• Published in: World journal of gastroenterology : WJG 2006-11, Vol.12 (42), p.6828-6834
• Main Authors: Aller, Maria-Angeles, Vara, Elena, García, Cruz, Nava, Maria-Paz, Angulo, Alejandra, Sánchez-Patán, Fernando, Calderón, Ana, Vergara, Patri, Arias, Jaime
• Format: Article
• Language: English
• Subjects: Animals; Basic Research; Blood Pressure - physiology; Body Weight - physiology; Cholesterol - metabolism; Fatty Acids, Nonesterified - metabolism; Hypertension, Portal - metabolism; Hypertension, Portal - physiopathology; Lipid Metabolism - physiology; Liver - blood supply; Liver - metabolism; Liver - pathology; Liver Circulation - physiology; Male; Organ Size - physiology; Phospholipids - metabolism; Portal Vein - physiopathology; Rats; Rats, Wistar; Time Factors; Triglycerides - metabolism; 代谢状态; 甘油三酸酯; 肝疾病; 高血压
• ISSN: 1007-9327; 2219-2840
• DOI: 10.3748/wjg.v12.i42.6828

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.