Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019204 (hepatocellular carcinoma)
 71,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Serum lipoproteins were measured by ultracentrifugal means in rats bearing hepatomas of different degrees of malignancy (Morris hepatomas 16, 5123TC and 7777) to determine the effect of these hepatomas on serum lipoprotein levels. Serum lipoprotein patterns were altered, especially in rats bearing hepatomas 16 and 7777, which had elevated high-density lipoproteins. (They were not elevated in serum of rats bearing hepatoma 5123TC). This increase in high-density lipoproteins seems to be specific for chemically induced hepatomas since HDL2 is usually decreased in humans and animals with types of cancer not involving the liver. It appears that hepatomas can synthesize lipoproteins, and the serum levels of the host rats are altered depending on the hepatoma. Different biochemistries appear to be associated with each hepatoma. Cholesterol and fatty acid levels of unfractionated serum and of isolated lipoproteins also indicate abnormal lipid/lipoprotein metabolism associated with these hepatomas.
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PMID:Serum lipoproteins in rats bearing Morris hepatomas of different degrees of differentiation. 23 1

The metabolism of cholesterol has been investigated in tumour cells, ascitic fluid and blood serum during the growth of an ascites hepatoma (Yoshida AH-130) in the rat. High rates of cholesterol synthesis and elevated free and esterified cholesterol content were observed in tumour cells. During tumour growth, the host animals progressively developed marked changes in the level and distribution of serum cholesterol consisting in an increase of total cholesterol and of a marked reduction of HDL cholesterol (HDL2 subfraction in particular). In agreement with previous observations, these findings indicate that a consistent pattern of altered cholesterol homeostasis develops in relation to normal or neoplastic tissue growth. High synthetic rates and intracellular accumulation of cholesterol are observed in the proliferating cells. Moreover, blood serum cholesterol decreases in the HDL fraction while it increases in LDLs, suggesting that during proliferative processes cholesterol fluxes between tissues and serum lipoproteins are markedly perturbed.
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PMID:Cholesterol metabolism during the growth of a rat ascites hepatoma (Yoshida AH-130). 141 21

HDL-subfraction was studied in blood serum of drinkers after alcohol intake and control group of men-nondrinkers. Blood serum incubation with fibroblasts culture did not indicate principal differences between drinkers and nondrinkers both with normolipemia and hyperalphacholesterolemia. Increase of HDL2 and decrease of HDL3-subfraction were observed. Incubation of the same species with hepatoma cells culture (Hep G-2) demonstrated significant differences between normolipemia and hyperalphacholesterolemia. The reduction of HDL2 subfraction level and increase of HDL3 have been found in nondrinkers with normolipemia. The raise of HDL2 was demonstrated in hyperalphacholesterolemia (due to HDL2b and HDL2a in drinkers and HDL2a in nondrinkers). Besides, in several samples of normolipidemic blood serum taken after alcohol abuse the changes of HDL-subfractions were identical to those receiving in hyperalphacholesterolemia. It is postulated that one of the mechanisms of the alcoholic hyperalphacholesterolemia development is the decline of the transfer rate of cholesterol ethers to the liver and accumulation of HDL2 particles in total HDL pool.
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PMID:[Effects of recent alcohol intake on high density lipoprotein accepting properties and their interactions with liver cells]. 196 13

Subfractional alterations of high density lipoproteins (HDL) were studied after incubation of blood serum from patients with normal lipid spectrum and with four types of dyslipidemia (hypercholesterolemia, hypertriglyceridemia, hypo- and hyper-alpha-cholesterolemia) in mixtures containing human skin fibroblasts and G-2 hepatoma cells used as typical populations of peripheric and liver cells. Incubation of normolipidemic blood sera with fibroblasts overloaded with cholesterol led to conversion of small HDL3 particles into large HDL2 subfractions arising due to the lipoprotein acception of cholesterol. At the same time, incubation of these blood sera with the hepatoma cells resulted in a decrease of the large particles ratio in total pool of HDL because of their absorption by the cells. No distinct differences were detected in formation of large particles from small subfractions when cholesterol was accepted from fibroblasts under conditions of hypercholesterolemia, hypertriglyceridemia and hyper-alpha-cholesterolemia, while formation of the largest particles HDL2b was impaired in hypo-alpha-cholesterolemia. These HDL2b particles interacted less effectively with hepatoma cells, thus suggesting the decreased cholesterol transport function of HDL in hypo-alpha-cholesterolemia. Content of HDL2b in total pool of HDL was unaltered if blood serum from patients with hyper-alpha-cholesterolemia was incubated together with the hepatoma cells. Antiatherogenic effect of hyper-alpha-cholesterolemia was caused mainly by active transfer of cholesterol from low density lipoproteins to HDL and a decrease in the LDL concentration but not by increased absorption of HDL particles by liver cells.
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PMID:[Changes in high density lipoprotein subfractions during interaction with fibroblasts and hepatoma G-2 in various dyslipidemias]. 217 87

Using gradient gel electrophoresis, the dynamics of subfractional spectrum of high density lipoproteins (HDL) according to the particle size was studied during HDL interaction with hepatoma Hep-G2 cells and human skin fibroblasts. It was found that incubation of sera obtained from normolipidemic donors with cholesterol-loaded fibroblasts results in a decrease of the proportion of all small-sized particles of the HDL3 subclass, i.e., HDL3a, HDL3b and HDL3c as well as in an increase in the proportion of large-sized particles of the HDL2 subclass (HDL2a and HDL2b) due to cholesterol acceptance by HDL. In contrast, incubation of the same sera with hepatoma Hep-G2 cells causes a decrease in the proportion of HDL2b and a release of smaller cholesterol-deficient HDL3a particles. The dynamics of subfractional spectrum of HDL in hypoalphacholesterolemic sera is somewhat different, i.e., incubation with fibroblasts results in a decrease of the proportion of HDL3b and HDL3c; that of HDL2a is increased. The HDL2b fraction is unchanged. After incubation of the same sera with hepatoma Hep-G2 cells, the proportion of HDL2b does not fall as in the case of normolipidemic sera, but shows a marked increase. It is concluded that hypoalphacholesterolemia is characterized not only by a low HDL level in the plasma, but also by the formation of HDL2b-deficient particles which less effectively interact with liver cells.
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PMID:[Hypoalphacholesterolemia: dynamics of the subfractional spectrum of high density lipoproteins during their interaction with fibroblasts and hepatoma Hep-G2 cell line]. 275 63

Alterations in plasma lipoprotein lipid and apoprotein accompanying the hyperlipidemia of rats bearing Morris hepatoma 7288C were characterized. In tumor-bearing animals all plasma lipid classes except cholesterol ester (CE) were elevated, particularly free cholesterol (FC) and triglyceride (TG), which increased by 57 and 63%, respectively. Fasting only partially reduced the tumor-induced hyperlipidemia and had no effect on the ratios of FC/CE and TG/CE. Analysis of plasma lipoproteins revealed an elevation of VLDL, IDL, and LDL in host rats, with more than a 2-fold increase in both lipid and protein of VLDL. In contrast, the three high density fractions, HDL2, HDL3, and d greater than 1.21 g/ml, were reduced. The inverse changes in concentration of host lipoproteins of lower versus higher density indicate a defective catabolism of TG-rich lipoprotein. This possibility is supported by the analysis of apolipoprotein. The percentage of total apoprotein contributed by apo C-I and C-II was reduced in all host fractions except HDL2, while the C-IIIs remained unchanged except for a small decrease in C-III-3 of host VLDL and a slight increase in the combined C-IIIs of HDL2. These changes were reflected in the decreased C-I+C-II/C-III ratios of all host lipoprotein fractions. Apo E levels remained similar to control values except for a significant decrease in HDL2. Host VLDL showed increased apo A-IV and A-I content, while A-IV was decreased in HDL2. Changes in apo B profiles were also observed.
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PMID:Characterization of alterations in plasma lipoprotein lipid and apoprotein profiles accompanying hepatoma-induced hyperlipidemia in rats. 394 72

Serum apoprotein A-I and A-II levels were determined by electroimmunoassay in patients with liver diseases and cholestasis. Significant decreases in apoprotein A-I and A-II levels were observed in such patients. The decreases were especially pronounced in the early phase of acute hepatitis and cholestasis. The decreases in A-II levels were more prominent than the decreases in A-I in severe hepatic dysfunction or cholestasis. Accordingly, the A-I/A-II ratio showed no change in the convalescent phase of acute hepatitis or chronic hepatitis but increased significantly in the early phase of acute hepatitis, cirrhosis of the liver, hepatoma, and cholestasis. The results suggested the existence of a high density lipoprotein with an abnormal apoprotein composition or a more profound decrease of HDL3 than of HDL2 in severe hepatocellular dysfunction of cholestasis.
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PMID:Serum apoprotein A-I and A-II levels in liver diseases and cholestasis. 627 23

Hepatocytes express on their surfaces more than one class of receptors capable of mediating the internalization of lipoproteins. However, relatively little is known about the binding characteristics of hepatic receptors for various lipoproteins, about the regulation of the receptors, and about the consequences for intracellular lipid metabolism of uptake of lipoproteins via different classes of receptors. The aim of the present studies was to characterize the binding and degradation of various lipoproteins and their mutual competition for cellular processing. Since these kinds of studies may be more easily carried out in continuous established hepatoma cell lines than in nondividing primary hepatocyte cultures, we examined the lipoprotein receptor functions of a well differentiated rat hepatoma (H-35). Cells were grown to confluence in Eagle's minimal essential medium in 15% newborn calf serum. Medium then was changed to 15% lipoprotein-deficient serum for 44 hr before experiments. External binding of 125I-labeled rat plasma and intestinal lymph lipoproteins was assessed at 4 degrees C. Cellular uptake and degradation were assessed at 37 degrees C. Lipoproteins were isolated by fixed angle or zonal ultracentrifugation or by heparin affinity column chromatography and characterized as to their lipid and apoprotein compositions. Labeled low density (LDL), high density (HDL2), non-apoE-HDL, very low density lipoproteins (VLDL), and chylomicron remnants (CM-R) each manifested specific and saturable binding and degradation by the hepatoma cells. Competition experiments indicated that separate receptors were present for LDL, HDL2, and CM-R. Most of HDL2 appeared to be bound to the non-apoE-HDL receptor.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Receptors for homologous plasma lipoproteins on a rat hepatoma cell line. 632 20

Lipids of HDL (high density lipoproteins) and their subfractions (HDL2 and HDL3), and LCAT activity (lecithin: cholesterol acyltransferase) were determined in hepatobiliary diseases without severe hyperbilirubinemia (less than 10 mg/dl). The decrease in major lipid constituents (cholesterol and phospholipids) of HDL was mainly attributable to the decrease in those of HDL3, except in some liver diseases of acute or severe stage (acute hepatitis in an acute stage and hepatoma) which were accompanied with a simultaneous moderate decrease in those of HDL2 and in fatty liver which showed a preferential decrease in those of HDL2. The LCAT activity also decreased in several diseases. Some of the hepatobiliary diseases, on the contrary, showed an increase in HDL-triglycerides (mostly in HDL3 and in some diseases also in HDL2) which might participate to some extent in secondary hyperlipidemia in the liver parenchymal diseases, although they were the minor lipid constituents of HDL. From results that HDL3- but not HDL2-cholesterol levels significantly correlated with serum total protein, albumin and choline esterase, it was suggested that the decrease in large constituents of HDL, particularly of HDL3, is caused by hepatocellular dysfunction which causes inhibition of protein and lipid syntheses in the liver in most of the hepatobiliary diseases except for fatty liver which has a preferential decrease in HDL2 lipids.
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PMID:Changes in high density lipoproteins in patients with hepatobiliary diseases. Levels and lipid composition of HDL2 and HDL3 and LCAT reaction. 685 43

We have previously described the lipoprotein abnormalities in cholestatic children with paucity of interlobular bile ducts (PILBD), and we have shown that two different profiles emerged among these patients, depending on the level of lecithin:cholesterol acyltransferase (LCAT) activity. Reduced LCAT activity was associated with hypo-alpha-lipoproteinemia (group I) whereas normal LCAT activity was associated with hyper-alpha-lipoproteinemia (group II). In both groups, high density lipoproteins (HDL) were enriched with phospholipids and LpA-I particles were predominant. Here, we have investigated the ability of serum and of isolated HDL, obtained from PILBD and control subjects, to promote cellular cholesterol efflux, from Fu5AH rat hepatoma cells. The mean fractional efflux to 5% serum in each group was, on average, following the differences in HDL concentrations (control: 30.1 +/- 4.2%; group I: 23.7 +/- 7.9%, ns; group II: 44.2 +/- 6.5%, P < 0.001). The variations in efflux values in group II were positively correlated to the variations in HDL-PL concentrations (P < 0.0001) and in HDL-PL to serum apo-AI ratio (P < 0.003). By contrast, the variation in efflux in group I was only positively related to the large range of HDL-PL to free cholesterol (FC) ratio values (P < 0.0004). Fractional efflux to isolated HDL, measured at a constant HDL-PL amount, confirmed this relationship (P < 0.0001). Two-dimensional gel electrophoresis of the HDL size and apo A-I distribution in serum, revealed that small size HDL(3) and pre-beta HDL were predominant in the serum of patients from group I, especially those exhibiting low HDL-PL to FC ratio, whereas in the serum of patients from group II, both small HDL(3) and large HDL2 were present. These results suggest that a combination of an imbalance between phospholipids and free cholesterol in the HDL particles and a deficit in large acceptors of cholesterol will be responsible for an impairment of cellular cholesterol efflux in PILBD patients with reduced lecithin:cholesterol acyltransferase activity.-Davit-Spraul, A., V. Atger, M. L. Pourci, M. Hadchouel, A. Legrand, and N. Moatti. Cholesterol efflux from Fu5AH cells in the serum of patients with Alagille syndrome: importance of the HDL-phospholipids/free cholesterol ratio and of the HDL size distribution.
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PMID:Cholesterol efflux from Fu5AH cells to the serum of patients with Alagille syndrome. Importance of the hdl-phospholipids/free cholesterol ratio and of the hdl size distribution. 992 63


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