BACKGROUND/AIMS: The liver plays a central role in the production and metabolism of lipoproteins, regulating their synthesis and degradation. The protein content of the lipoproteins are the so-called apolipoproteins. Some of the apolipoproteins serve as cofactors for enzymatic reactions, as ligands for interaction with specific receptors, and as structural proteins. Apolipoprotein B (apoB) is the primary structural component of the atherogenic low density lipoprotein (LDL) particles and has a specific binding region for interacting with the LDL-receptor. In contrast, apolipoprotein A-I (apoA-I) represents the primary protein content of the high density lipoprotein (HDL) particles, which interacts with the putative HDL-receptor, and stimulates the enzymatic reaction of lecithin-cholesterol acyltransferase (LCAT) resulting in esterified cholesterol, which is the essential step in the process of reverse cholesterol transport. METHODOLOGY: We studied lipid parameters in arterial and hepatic venous serum samples from 52 patients with cirrhosis and from 16 patients in the clinically stable long-term course after liver transplantation. Splanchnic blood flow was measured (indocyanine-green steady-state infusion) and hepatic extraction/production rates were calculated. To assess the influence of the clinical stage of established cirrhosis, the quantitated parameters were statistically analyzed. RESULTS: In cirrhosis, apolipoprotein A-I levels are decreased depending on the clinical stage (p<0.01). This parameter showed excellent correlations to liver function tests. Triglycerides (TG) (p<0.05) and cholesterol (Chol) (p<0.05) were reduced as well, whereas apolipoprotein B levels did not change. In cirrhosis, hepatic production of both cholesterol and triglycerides were decreased (p<0.05 each), as well as hepatic extraction of free fatty acids (FFA) (p<0.01). Except for cholestatic liver disease with raised serum cholesterol (p<0.05) and apolipoprotein B levels (p<0.001), the etiology of cirrhosis had no impact on the observed serum lipid alterations. CONCLUSIONS: The serum concentrations of the determined lipid parameters depend primarily on liver function. Decreased liver function was associated with reduced extraction of free fatty acids and reduced cholesterol and triglyceride synthesis. Liver transplantation restored the lipid abnormalities to normal. Finally, apolipoprotein A-I served as an excellent parameter for predicting liver function in the studied patients.
BACKGROUND/AIMS: The liver plays a central role in the production and metabolism of lipoproteins, regulating their synthesis and degradation. The protein content of the lipoproteins are the so-called apolipoproteins. Some of the apolipoproteins serve as cofactors for enzymatic reactions, as ligands for interaction with specific receptors, and as structural proteins. Apolipoprotein B (apoB) is the primary structural component of the atherogenic low density lipoprotein (LDL) particles and has a specific binding region for interacting with the LDL-receptor. In contrast, apolipoprotein A-I (apoA-I) represents the primary protein content of the high density lipoprotein (HDL) particles, which interacts with the putative HDL-receptor, and stimulates the enzymatic reaction of lecithin-cholesterol acyltransferase (LCAT) resulting in esterified cholesterol, which is the essential step in the process of reverse cholesterol transport. METHODOLOGY: We studied lipid parameters in arterial and hepatic venous serum samples from 52 patients with cirrhosis and from 16 patients in the clinically stable long-term course after liver transplantation. Splanchnic blood flow was measured (indocyanine-green steady-state infusion) and hepatic extraction/production rates were calculated. To assess the influence of the clinical stage of established cirrhosis, the quantitated parameters were statistically analyzed. RESULTS: In cirrhosis, apolipoprotein A-I levels are decreased depending on the clinical stage (p<0.01). This parameter showed excellent correlations to liver function tests. Triglycerides (TG) (p<0.05) and cholesterol (Chol) (p<0.05) were reduced as well, whereas apolipoprotein B levels did not change. In cirrhosis, hepatic production of both cholesterol and triglycerides were decreased (p<0.05 each), as well as hepatic extraction of free fatty acids (FFA) (p<0.01). Except for cholestatic liver disease with raised serum cholesterol (p<0.05) and apolipoprotein B levels (p<0.001), the etiology of cirrhosis had no impact on the observed serum lipid alterations. CONCLUSIONS: The serum concentrations of the determined lipid parameters depend primarily on liver function. Decreased liver function was associated with reduced extraction of free fatty acids and reduced cholesterol and triglyceride synthesis. Liver transplantation restored the lipid abnormalities to normal. Finally, apolipoprotein A-I served as an excellent parameter for predicting liver function in the studied patients.
Authors: Maria Pleguezuelo; Laura M Lopez-Sanchez; Antonio Rodriguez-Ariza; Jose L Montero; Javier Briceno; Ruben Ciria; Jordi Muntane; Manuel de la Mata Journal: World J Hepatol Date: 2010-03-27
Authors: Kamlesh K Bhopale; Samir M Amer; Lata Kaphalia; Kizhake V Soman; John E Wiktorowicz; Ghulam A Shakeel Ansari; Bhupendra S Kaphalia Journal: Alcohol Clin Exp Res Date: 2017-09-08 Impact factor: 3.455
Authors: Valeria R Mas; Daniel G Maluf; Kellie J Archer; Kenneth Yanek; Karen Bornstein; Robert A Fisher Journal: Transplantation Date: 2009-01-15 Impact factor: 4.939