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Biomedical subjects

A van Tol

Publications and source records attributed to A van Tol.

At least 91 records · Page 5Linked to original sources
PubMed1992

Apolipoprotein gene expression in analbuminemic rats and in rats with Heymann nephritis.

The nephrotic syndrome results from altered glomerular permselectivity, causing urinary protein loss, reduced albumin concentration, oncotic pressure (pi), and hyperlipidemia. Hepatic lipid and apolipoprotein synthesis increases and lipoprotein catabolism decreases. Decreased lipoprotein catabolism follows the onset of proteinuria but is not associated with hereditary analbuminemia [Nagase analbuminemic rat (NAR)] if proteinuria is absent. We measured plasma apolipoproteins (apo) AI, B, and E levels, their mRNA concentrations in liver, and the transcription rate of each mRNA in rats with Heymann nephritis (HN) or NAR to determine which alterations occurred in NAR alone without proteinuria. Plasma apo AI, B, and E were increased in both HN and NAR. Cholesterol and apo AI were inversely proportional to pi and independent of urinary protein loss or the presence of albumin in plasma. In contrast, triglycerides (TGs) were significantly greater in HN and were increased out of proportion to apo B. The concentration of apo AI mRNA increased in liver of both HN and NAR as did apo AI transcription. Apo E mRNA increased in neither HN nor NAR, whereas apo B mRNA increased only in HN. Transcription of neither apo B nor E increased. Plasma apo AI levels are likely to be regulated transcriptionally at the level of protein synthesis, whereas plasma apo B and E levels are regulated either posttranscriptionally, at the level of protein catabolism, or at both sites. Lipoproteins rich in TG and poor in apo B appear after the development of proteinuria but not as a consequence of analbuminemia alone. The accumulation of TG-rich apo B containing lipoproteins in rats with HN may result from impaired lipolysis occurring as a consequence of proteinuria.

Animals↗
PubMed1992

Fibrates influence the expression of genes involved in lipoprotein metabolism in a tissue-selective manner in the rat.

The influence of different fibrates on apolipoprotein metabolism was investigated. Administration of fenofibrate provoked a dose-dependent decrease in plasma cholesterol concentration that was already evident after 1 day. Intestinal apolipoprotein (apo) A-I and apo A-IV mRNA levels remained fairly constant. In contrast, liver apo A-I, apo A-II, and apo A-IV mRNA levels decreased in a dose-dependent fashion, which was associated with a lower transcription rate of the apo A-I but not the apo A-II gene. The decline in hepatic apo A-I, apo A-II, and apo A-IV mRNA had already started after 1 day and was associated with a drop in plasma apo A-I and apo A-IV concentrations. Plasma apo E had already decreased after 1 day of fenofibrate, whereas apo B initially remained constant and increased only after 14 days of fenofibrate at the highest dose. Hepatic and intestinal apo B mRNA contents and liver, heart, kidney, and testis apo E mRNA contents were only marginally affected after treatment with fenofibrate. Liver low density lipoprotein receptor mRNA levels rose slightly after a 3-day administration of the highest dose of fenofibrate. Both clofibrate and gemfibrozil had effects comparable to those of fenofibrate on liver and intestinal apolipoprotein mRNA levels except for liver apo A-II mRNA, which decreased only marginally. Compared with fenofibrate, clofibrate caused similar changes in plasma cholesterol, apo A-I, apo A-IV, and apo E concentrations, whereas gemfibrozil increased plasma cholesterol and apo E without changing apo A-I and apo A-IV concentrations.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Effect of phospholipid fatty acid composition of endothelial cells on cholesterol efflux rates.

Human endothelial cells (EA.hy 926 line) were loaded with cationized low density lipoprotein (LDL) and subsequently incubated with fatty acid/bovine serum albumin complexes. The fatty acids were palmitic, oleic, linoleic, arachidonic, and eicosapentaenoic acids. The preincubations resulted in extensively modified fatty acid profiles in cell membrane phospholipids and in cellular cholesteryl esters. The cholesterol efflux from these fatty acid-modified cells was measured using 0.2 mg high density lipoprotein3 (HDL3)/ml medium. The efflux was significantly higher for the palmitic acid-treated cells, compared to all other fatty acid treatments. These differences in efflux rates were not caused by changes in the binding of HDL3 to high affinity receptors on the EA.hy 926 cells. Efflux mediated by dimethyl suberimidate-treated HDL3, which does not interact with high affinity HDL receptors, was similar to efflux induced by native HDL3 after all fatty acid treatments. Our results indicate that high affinity HDL receptors are not important for HDL-mediated efflux of cell cholesterol. The fatty acid composition of the cell membrane phospholipids may be an important determinant.

Apolipoproteins E↗
PubMed1992

Lecithin:cholesterol acyltransferase gene expression is regulated in a tissue-selective manner by fibrates.

Plasma lipoprotein metabolism is influenced by several factors that may act by regulating the expression of proteins involved in lipoprotein metabolism, such as lecithin:cholesterol acyltransferase (LCAT). We determined the influence of several hormones and hypolipidemic drugs on hepatic LCAT gene expression and plasma LCAT activity. Liver LCAT mRNA levels were resistant to regulation by the hormones ethinylestradiol, L-thyroxine, hydrocortisone, or by the hypolipidemic drugs probucol, simvastatin, and nicotinic acid. In contrast, hepatic LCAT mRNA levels decreased to 67%, 64%, and 46% of the control levels after treatment with the fibric acid derivatives clofibrate, gemfibrozil, and fenofibrate, respectively. Fenofibrate lowered liver LCAT mRNA levels in a dose-dependent manner, which was paralleled by a decrease in plasma LCAT activity to 54% of the controls at a dose of 0.5% (w/w) in rat chow. The decrease in liver LCAT mRNA levels was maximal after 1 day, whereas the fall in plasma LCAT activity trailed by 2 days. Cessation of treatment with fenofibrate restored liver LCAT mRNA levels to control levels within 1 week. The transcription rate of the LCAT gene decreased by 25% in nuclei isolated from fenofibrate-treated rat liver, thereby indicating that hepatic LCAT gene expression is, at least partly, regulated at a transcriptional level. In contrast to the liver, brain and testis LCAT mRNA levels remained constant after treatment with fenofibrate, indicating that fibrates regulate LCAT gene expression in a tissue-selective manner.

Analysis of Variance↗
PubMed1991

The effects of probucol on lipoprotein metabolism in the rat.

The effects of probucol on liver and intestinal apolipoprotein, LDL-receptor and hepatic lipase gene expression, as well as plasma lipid and apolipoprotein levels and liver lipase activity were evaluated in male rats. Administration of probucol decreased plasma triacylglycerols, without affecting plasma cholesterol. Plasma apo E and apo B concentrations increased after probucol. Since liver and intestinal apo B and apo E mRNA levels remained unchanged, this increase could be attributed to a delayed clearance by the LDL-receptor, whose mRNA levels dropped by 50% in the liver. For the HDL-apolipoproteins, only liver apo A-IV mRNA levels decreased after probucol, which was reflected by a fall of plasma apo A-IV. Neither hepatic lipase activity nor mRNA levels were significantly influenced by probucol.

Animals↗
PubMed1991

Diet-induced alteration in the activity of plasma lipid transfer protein in normolipidemic human subjects.

Studies were performed to investigate the effect of diets rich in oleic or linoleic acids on the activity of plasma cholesteryl ester transfer protein (CETP) in normolipidemic subjects. Previous to the test diets, all subjects consumed a baseline diet rich in saturated fatty acids ("sat-diet") for 17 days. The test diets, rich in either monounsaturated fatty acids ("mono-diet") or rich in polyunsaturated fatty acids ("poly-diet"), were given for 5 weeks to 52 normolipidemic healthy volunteers. The activity of CETP was measured, using a method independent of endogenous plasma lipoproteins, as the rate of exchange of radioactive cholesteryl oleate between labelled LDL and unlabelled HDL. The "mono-diet" induced a statistically significant decrease in CETP activity (from 115 +/- 20 to 102 +/- 19 units/ml plasma, P less than 0.01), while the small decrease on the "poly-diet" (from 111 +/- 23 to 107 +/- 22 units/ml plasma) did not reach significancy. The percentual decrease in CETP activity induced by the "mono-diet" was higher than that induced by the "poly-diet" as was also found for the decrease in LDL cholesterol. In both diet groups a positive correlation was found between changes in CETP activity and changes in plasma total or (VLDL + LDL) cholesterol. The results suggest that high levels of dietary monounsaturated fatty acids may result in decreased plasma CETP activity, as well as LDL cholesterol levels. The mechanisms of these effects, and their possible interrelations, remain to be established.

Adult↗
PubMed1991

Different locations of cholesteryl ester transfer protein and phospholipid transfer protein activities in plasma.

Activities of cholesteryl ester transfer protein (CETP) and phospholipid transfer protein (PLTP) were measured in plasma of four vertebrate species: man, rabbit, pig, and rat. The activities were measured in the absence and presence of antibodies raised against purified human CETP. PLTP activities were present in all four species with highest values in pig (11.7 +/- 1.2 U/ml) and human plasma (9.2 +/- 1.6 U/ml). Considerable lower activities were found in rabbit (3.5 +/- 0.6 U/ml) and rat plasma (1.6 +/- 0.7 U/ml). These activities were not affected significantly by antibody against human CETP. CETP activities could be measured in human (0.23 +/- 0.05 U/ml) and in rabbit plasma (0.19 +/- 0.03 U/ml). CETP activity in human plasma was inhibited over 97% by antibody against human CETP. Plasma was chromatographed on a Superose 6 gel filtration column. Average HDL particle sizes in the four species differed notably and decreased in the order: rat HDL greater than rabbit HDL greater than human HDL greater than pig HDL. A separation of the two lipid transfer activities was evident after gel filtration chromatography. The peak of the PLTP activity coeluted with a fraction of HDL particles with the size of human HDL2 (particle weights 300-375 kDa). CETP activity in human and rabbit plasma coeluted largely with relatively small HDL particles (particle weights 140-180 kDa). These results show that CETP and PLTP activities are located in different macromolecular complexes.

Animals↗
PubMed1991

Hyperlipoproteinemia in one-year-old analbuminemic rats.

Plasma lipoprotein distribution and apolipoprotein concentrations, as well as kidney function and histopathology of heart, aorta, liver and kidney were investigated in 1-year-old Nagase analbuminemic rats (NAR) and control Sprague-Dawley rats (SDR). The NAR, particularly the females, were found to be severely hyperlipidemic. Plasma total cholesterol in non-fasted animals was 6.1 +/- 0.3 mM in the female NAR vs. 2.5 +/- 0.2 mM in the female SDR (P less than 0.01). Most of the cholesterol was located in the LDL (1.019-1.063 g/ml) and HDL2 (1.063-1.125 g/ml) density range. Plasma triglycerides were 6.1 +/- 0.6 mM in the female NAR vs. 1.3 +/- 0.3 mM (P less than 0.01) in the female SDR. Plasma phospholipids were raised up to 5.4 +/- 0.3 mM vs. 2.4 +/- 0.1 mM (P less than 0.01). NAR have increased concentrations of plasma apolipoproteins A-I (about 3-4-fold) and B (about 2-fold), but the levels of apolipoproteins A-IV and E are not increased. There was less proteinuria in the male NAR than in the male SDR (P less than 0.01). Relevant histopathological findings in the NAR included hepatocytic lipofuscinosis and hemosiderosis in Kupffer cells. Tubular lesions were more common in kidneys from NAR than from SDR, and included protein casts, cortical lipofuscinosis, proximal tubular hyperplasia and proliferative interstitial nephritis. Glomerular changes were similar in both strains. Calcinosis of the aortic media and the corticomedullary region of the kidney was characteristically present in the female SDR but absent in the female NAR. Atherosclerotic lesions were not observed. In summary, 1-year-old NAR maintained on standard rat chow, are hyperlipoproteinemic. The increased levels of plasma LDL and HDL cholesterol are not associated with an increase in the incidence or severity of atherosclerotic or glomerular lesions.

Animals↗
PubMed1991

Cholesterol efflux from cells to immunopurified subfractions of human high density lipoprotein: LP-AI and LP-AI/AII.

Using immunoaffinity chromatography, we separated human high density lipoprotein (HDL) into two subfractions: LP-AI, in which all particles contain apolipoprotein A-I (apoA-I) but no apoA-II, and LP-AI/AII, in which all particles contain both apoA-I and apoA-II. To compare LP-AI and LP-AI/AII as acceptors of cell cholesterol, the isolated subfractions were diluted to 50 micrograms phospholipid/ml, and then incubated with monolayer cultures of cells in which whole-cell and lysosomal cholesterol has been labeled with 14C and 3H, respectively. We used three cell types (Fu5AH rat hepatoma cells, normal human skin fibroblasts, and rabbit aortic smooth muscle cells). When these cells were prepared to contain normal physiological quantities of cholesterol (20-35 micrograms/mg protein), LP-AI and LP-AI/AII were nearly equally efficient in promoting efflux of both whole-cell and lysosomal cholesterol. For whole-cell cholesterol, the rate constants for efflux to LP-AI and LP-AI/AII were: 0.050/h and 0.053/h, respectively, with Fu5AH cells; 0.0063/h and 0.0074/h with GM3468 human skin fibroblasts; and 0.0076/h and 0.0079/h with rabbit aortic smooth muscle cells. When cholesterol in hepatoma cells or fibroblasts was elevated two- to threefold above normal, there was still not difference in efflux of whole-cell cholesterol to LP-AI and LP-AI/AII. In longterm incubations, the net depletion of cholesterol mass from cholesterol-enriched cells was either identical with the two HDL subfractions, or somewhat greater with LP-AI/AII.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Changes in plasma lipoproteins after cardiac rehabilitation in patients not on lipid-lowering drugs.

The extent to which a conventional cardiac rehabilitation programme can influence plasma lipoproteins was investigated in a prospective study. The relationship between changes in plasma lipoproteins and baseline characteristics, as well as variables related to the physical training and to dietary habits were assessed in 77 cardiac patients. All patients participated in a physical training programme, including general dietary advice. Patients who received lipid-lowering drugs were excluded from this study. Total plasma cholesterol decreased from 7.1 +/- 1.6 to 6.8 +/- 1.2 mmol l-1 (P less than 0.05), but it remained high in many patients, 61% having a level above 6.5 mmol l-1. The high- and low-density lipoprotein fractions (HDL- and LDL-cholesterol), and the ratio of total cholesterol to HDL-cholesterol, did not change significantly. The change in total plasma cholesterol was greatest (P less than 0.05) in patients who changed their diet in the recommended direction, and was poorly related to the change in maximal workload. It is concluded that a combination of general dietary advice and moderate physical exercise training is followed by a small reduction in total plasma cholesterol levels without changing HDL-cholesterol, and that cardiac rehabilitation should include strict programmes for the reduction of elevated plasma cholesterol.

Cholesterol↗
PubMed1990

Apolipoprotein A-IV messenger ribonucleic acid abundance is regulated in a tissue-specific manner.

The influence of development and estrogen, thyroid hormone, corticosteroid, and fibrate administration on apolipoprotein (apo) A-IV mRNA levels in the liver and intestine and on serum or plasma concentrations of apo A-IV was studied in the rat. Treatment of ovariectomized rats with ethinyl estradiol provoked a dose-dependent decrease in liver apo A-IV mRNA levels, whereas intestinal apo A-IV mRNA did not change. The serum apo A-IV concentration decreased in a dose-dependent manner. Administration of L-T4 increased liver apo A-IV mRNA levels more than 2-fold, while n-propylthiouracil (PTU) decreased these levels more than 4-fold. Intestinal apo A-IV mRNA levels remained constant upon L-T4 treatment, but increased after PTU. Change in thyroid hormone levels caused no significant alteration of plasma apo A-IV levels. Hydrocorticsone increased liver and intestinal apo A-IV mRNA levels 2- and 1.5-fold, respectively, without changing plasma apo A-IV. Liver and intestinal apo A-IV mRNA underwent opposite changes during development. Intestinal apo A-IV mRNA decreased gradually during the period of weaning, while liver apo A-IV mRNA was undetectable before day 20 of life and rose to adult levels thereafter. Both L-T4 and hydrocortisone were able to increase liver apo A-IV mRNA prematurely when rat pups were treated from day 9 on. Hypothyroidism induced by PTU, on the other hand, was able to delay the developmental rise in liver apo A-IV mRNA. The hypolipidemic drug clofibrate reduced liver apo A-IV mRNA more than 10-fold without changing the intestinal levels. Plasma apo A-IV decreased by one third. Ethinyl estradiol, thyroid hormones, and clofibrate regulate apo A-IV mRNA abundance in a tissue-specific manner. Only liver, not intestinal, apo A-IV mRNA levels respond to treatment. Furthermore, opposing changes in liver and intestinal apo A-IV mRNA levels occur during development, and thyroid hormones and glucocorticoids are able to accelerate the developmental changes in liver apo A-IV mRNA.

Animals↗
PubMed1990

[Role of hepatic lipases, cholesterol ester transfer proteins and LCAT in the postprandial phase].

Hepatic, heparin-releaseable lipase is a multifunctional enzyme that may act on all lipoprotein classes present in plasma from fasted subjects. Recent evidence suggests that the enzyme also plays a role in the metabolism of chylomicronremnants. Its activity is impaired in normolipidemic patients with coronary heart disease, which also have a delayed removal of chylomicronremnants from plasma. Therefore hepatic lipase, in addition to lipoprotein lipase, plays an important role in postprandial lipoprotein metabolism. The activity levels of lecithin: cholesterol acyltransferase (LCAT) and cholesterylester transfer protein (CETP) are virtually unchanged after the ingestion of an oral fat load by normolipidemic subjects. However, the net mass transfer of cholesterylesters out of HDL into apo B-containing lipoproteins (chylomicronremnants, VLDL/IDL/LDL) is strongly increased. All triglyceride-rich lipoprotein fractions accumulate postprandially and, as a result of CETP action, become enriched in cholesterylesters. Defects in hepatic remnant removal may result in influx of remnants into the arterial wall. In patients with hyperlipidemia (and increased risk for atherosclerosis) the CETP-mediated formation of cholesterylester-rich remnants may operate, not only during the postprandial phase, but continuously.

Carrier Proteins↗
PubMed1990

Development, food intake, and ethinylestradiol influence hepatic triglyceride lipase and LDL-receptor mRNA levels in rats.

The influence of development and ethinylestradiol on low density lipoprotein (LDL)-receptor mRNA and hepatic triglyceride lipase (HTGL) activity and mRNA levels was studied in rat liver and intestine. Intestinal LDL-receptor mRNA levels are maximal in the perinatal period, whereas liver LDL-receptor and HTGL mRNA levels are highest after weaning in adult life. All mRNA levels reach a maximum between day 15 and 20 when rats still consume a lipid-rich diet, and increase twofold during weaning. Liver and intestinal LDL-receptor mRNA levels are not influenced by ovariectomy, but increase after ethinylestradiol treatment. Liver LDL-receptor mRNA shows a dose-dependent increase after ethinylestradiol and a sevenfold rise in liver LDL-receptor mRNA is attained with a dose of 2000 micrograms/day. Intestinal LDL-receptor mRNA increases slightly more than twofold after ethinylestradiol and this increase is not dose-dependent. Changes in LDL-receptor mRNA are independent of changes in food intake induced by ethinylestradiol treatment, since they are still observed after pair-feeding. The ethinylestradiol-induced increases in LDL-receptor mRNA levels are reflected by decreased serum apoB levels. HTGL mRNA levels increase after ovariectomy and show a dose-dependent decrease after ethinylestradiol. Pair-feeding abolishes the increase seen after ovariectomy, while the estrogen-mediated decrease is attenuated. These alterations in HTGL mRNA are reflected by similar changes in liver HTGL activity.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Effect of lipid transfer protein on plasma lipids, apolipoproteins and metabolism of high-density lipoprotein cholesteryl ester in the rat.

The role of human plasma lipid transfer protein (LTP) in lipoprotein metabolism was studied in the rat, a species without endogenous cholesteryl ester and triacylglycerol transfer activity. Partially purified human LTP was injected intravenously into rats. The plasma activity was between 1.5- and 4-fold that of human plasma during the experiments. 6 h after the injection of LTP, a significant increase in serum apoB, and no significant changes in serum total cholesterol, free cholesterol, triacylglycerols, apoA-I, apoE, or apoA-IV were noted. Cholesterol was increased in very-low density and low-density lipoproteins (VLDL and LDL) and decreased in large-sized apoE-rich HDL. ApoA-I-containing particles with a size smaller than in normal rats were present in serum of LTP-treated rats. The mean diameter of HDL particles decreased and apoE, normally present on large-sized HDL, was present on smaller sized particles. The metabolic fate of cholesteryl ester, originally associated with HDL, was studied by injection of [3H]cholesteryl linoleyl ether-labelled apoA-I-rich HDL in the absence and in the presence of LTP. The disappearance of [3H]cholesteryl linoleyl ether, injected as part of apoA-I-rich HDL, from serum was increased in the LTP-treated rats; the t1/2 changed from 3.9 to 2.2 h, resulting in an increased accumulation of [3H]cholesteryl linoleyl ether in the liver. This can be explained by the redistribution of HDL [3H]cholesteryl linoleyl ether to VLDL and LDL in the presence of LTP, leading to the combined contribution of VLDL, LDL and HDL to the hepatic uptake. The present findings show profound effects of LTP on the chemical composition of HDL subspecies, the size of HDL and on the plasma turnover and hepatic uptake of cholesteryl esters originally present in apo A-I-rich HDL.

Animals↗
PubMed1989

Binding characteristics of high density lipoprotein subclasses to porcine liver, adrenal and skeletal muscle plasma membranes.

1. We compared binding characteristics of 125I-labeled high density lipoprotein (HDL) subclasses to porcine liver, adrenal and skeletal muscle plasma membranes. 2. HDL subclasses were discriminated by their buoyant densities (HDL2 and HDL3) or by their apolipoprotein (apo) content (Lp-AI (particles containing apoA-I but no apoA-II) and LpA-I/A-II (particles containing both apoA-I and apoA-II)). 3. HDL2 and HDL3 showed saturable binding to the three types of membrane preparations. 4. No differences were found in the Kds within one HDL subclass. 5. Kds and maximal binding of HDL2 were lower than these of HDL3. Unlabeled HDL2 and HDL3, but not LDL, effectively displaced 125I-HDL2 and 125I-HDL3. 6. Binding of HDL was independent of the concentration of NaCl and did not require calcium. 7. These results suggest a process mediated by a single specific receptor in porcine liver, adrenal and skeletal muscle plasma membranes. 8. We also studied binding characteristics of HDL subclasses Lp-AI and LpA-I/A-II to porcine liver membranes. LpA-I showed the highest Kd and maximal binding. 9. All types of HDL subclasses studied (i.e. HDL2, HDL3, LpA-I and LpA-I/A-II) effectively competed for binding of both Lp-AI and LpA-I/A-II, suggesting that the HDL subclasses studied bind to the same receptor by their apoA-I moiety.

Adrenal Glands↗
PubMed1989

Influence of development, estrogens, and food intake on apolipoprotein A-I, A-II, and E mRNA in rat liver and intestine.

UNLABELLED: The influence of development and ethinylestradiol (EE) on apolipoprotein (apo) A-I, A-II, and E mRNA in rat liver and intestine was studied by dot blot hybridization and Northern blot analysis. ApoA-I mRNA levels were maximal in the perinatal period and declined after day 15. An opposite trend was noted for the apoA-II mRNA levels, whereas apoE mRNA remained fairly constant. Liver apoA-I mRNA levels increased after ovariectomy (OVX). A further rise was observed when EE was given at 2000 micrograms/day. When the influence of OVX and EE was controlled for food intake by pair-feeding, OVX still increased hepatic apoA-I mRNA. The rise in liver apoA-I mRNA after EE, however, was no longer significant. Under the same conditions OVX slightly increased intestinal apoA-I mRNA. EE (2000 micrograms/day) decreased intestinal apoA-I mRNA to 80% of the pair-fed controls. Liver apoA-II mRNA levels did not change after OVX when the animals were fed ad libitum, but decreased slightly when the rats were pair-fed. EE caused a dose-dependent decrease in liver apoA-II mRNA, irrespective of food intake. None of these treatments caused any change in liver apoE mRNA levels. Serum apoA-I levels increased upon OVX, while serum apoE did not change. EE provoked a dose-dependent decrease of both apolipoproteins in serum. IN CONCLUSION: 1) Changes in food intake play an important role in the in vivo effects of estrogens on apolipoprotein mRNA levels. 2) The stimulatory effect of OVX on hepatic apoA-I mRNA as well as the inhibitory effect of EE on hepatic apoA-II mRNA are independent of food intake.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗