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Biomedical subjects

A van Tol

Publications and source records attributed to A van Tol.

125 records · Page 7Linked to original sources

In vivo uptake of human and rat low density and high density lipoprotein by parenchymal and nonparenchymal cells from rat liver.

The relative contribution of the parenchymal and nonparenchymal rat liver cells to the hepatic uptake of human and rat high density lipoprotein (HDL) and low density lipoprotein (LDL) was determined in vivo. Nonparenchymal cells, isolated 6 h after intravenous injection of iodinated human HDL and LDL, contained respectively 4.2 and 6.3 times the amount of trichloroacetic acid-precipitable radioactivity per mg cell protein as compared to parenchymal cells. For rat iodinated HDL and LDL these factors were 3.4 and 4.1, respectively. These results indicate that nonparenchymal liver cells play a substantial role in the hepatic uptake of human and rat HDL and LDL in vivo.

Animals↗

Moderate alcohol consumption and changes in postprandial lipoproteins of premenopausal and postmenopausal women: a diet-controlled, randomized intervention study.

Moderate alcohol consumption is associated with a reduced risk of coronary heart disease. Earlier studies in men have shown that moderate alcohol consumption affects lipoprotein metabolism and hemostasis. In this diet-controlled, randomized, crossover trial, we investigated the effect on lipoprotein metabolism of moderate consumption of red wine or red grape juice with evening dinner for 3 weeks in premenopausal women using oral contraceptives and in postmenopausal women. After 3 weeks, blood samples were collected 1 hour before dinner up to 19 hours after starting dinner at 2-hour or 4-hour intervals. Plasma triglyceride concentrations and very low density lipoprotein (VLDL) triglyceride levels peaked 3 hours after dinner with wine in both premenopausal and postmenopausal women. After wine consumption, the overall high-density lipoprotein (HDL) cholesterol level was increased in postmenopausal women (mean increase 0.17 mmol/L, or 12%, p = 0.03), and the plasma low-density lipoprotein (LDL) cholesterol level was reduced in premenopausal women (mean reduction 0.35 mmol/L, or 12%, p = 0.01) as compared with grape juice consumption. The findings suggest that postprandial lipoprotein metabolism after moderate alcohol consumption differs between oral contraceptive-using premenopausal women and postmenopausal women. The response of postmenopausal women to alcohol resembled the response found in earlier studies in men.

Adult↗

Moderate doses of alcoholic beverages with dinner and postprandial high density lipoprotein composition.

Moderate alcohol consumption is associated with a reduced risk of coronary heart disease. In this study, postprandial changes in plasma lipids, high-density lipoprotein (HDL) composition and cholesteryl ester transfer protein (CETP) and lecithin: cholesterol acyltransferase (LCAT) activity levels were investigated in response to moderate alcohol consumption. A dose of 40 g of alcohol was consumed as beer, wine or spirits by eight healthy middle-aged men before and during dinner thus simulating social drinking. Lipid parameters were studied before, and at 1, 3, 5, 9, and 13 h after dinner. An alcohol-induced elevation of plasma triglycerides was observed at 3 and 5 h after dinner, but total plasma cholesterol and apolipoprotein B were hardly affected. HDL lipids changed during the postprandial phase after alcohol consumption, HDL triglycerides were elevated at 5 and 9 h, HDL phospholipids were elevated at 9 and 13 h, and HDL cholesterol was elevated at 13 h. A 6% increase in the concentration of apolipoprotein A-II was observed at 13 h. Plasma LCAT activity was slightly increased 9 h after dinner, but CETP activity levels were not affected. The LCAT changes appeared similar for all three alcoholic beverages. It is concluded that moderate alcohol consumption with dinner affects plasma triglyceride concentration as well as HDL composition.

Alcohol Drinking↗

Postprandial lipoprotein metabolism in normolipidemic men with and without coronary artery disease.

A delayed clearance of postprandial lipoproteins from the plasma may play a role in the etiology of premature coronary atherosclerosis. To address this hypothesis, we studied chylomicron (remnant) metabolism in two groups of 20 selected normolipidemic men aged 35-65 years, a group of coronary artery disease (CAD) patients, and a matched control group with documented minimal coronary atherosclerosis. Subjects received an oral fat load supplemented with cholesterol and retinyl palmitate. Plasma samples obtained during the next 24-hour period were analyzed for total as well as d less than 1.019 g/ml and d greater than 1.019 g/ml triacylglycerol, cholesterol, and retinyl ester concentrations. Although both groups of patients responded identically in terms of the appearance of gut-derived lipids in the plasma, CAD patients showed a marked delay in the clearance of retinyl esters as well as in the normalization of plasma triacylglycerol concentrations. Postheparin plasma hepatic lipase activity was significantly lower in the CAD group. Apolipoprotein E phenotype measurements did not reveal marked differences in frequency between both groups. The frequency distribution was not unusual in comparison with the normal Dutch population. The magnitude of the postprandial responses of triacylglycerol and retinyl esters was correlated positively with the fasting levels of plasma triacylglycerol and negatively with high density lipoprotein subfraction 2 cholesterol concentrations. These data indicate that the clearance of postprandial lipoproteins in normolipidemic CAD patients as selected in the present study is delayed as compared with that of controls without coronary atherosclerosis and suggest that postprandial lipoproteins may play a role in the etiology of their disease.

Adult↗

Variable effects of different corticosteroids on plasma lipids, apolipoproteins, and hepatic apolipoprotein mRNA levels in rats.

Treatment of male rats with hydrocortisone provoked a dose- and time-dependent decrease in plasma cholesterol concentration without a change in plasma triglyceride levels. In contrast, administration of triamcinolone and dexamethasone at equipotent glucocorticoid doses increased plasma cholesterol and triglyceride levels, respectively. Small effects on apolipoprotein E (apo E) and apo B mRNA levels were observed, but all corticosteroids increased apo A-I and apo A-IV mRNA and decreased apo A-II mRNA levels in the liver. Triamcinolone and dexamethasone, however, were three times more potent in stimulating hepatic apo A-IV gene expression than was hydrocortisone, whereas liver apo A-I and apo A-II mRNA levels were altered to a similar extent by all corticosteroids. Plasma apo A-I and apo B concentrations always varied in a similar fashion with their respective liver mRNA levels after administration of the distinct corticoids. For apo A-IV and apo E, discrepancies between plasma and liver mRNA levels after administration of the different steroids, however, point to additional regulatory effects on plasma apolipoprotein levels. We conclude that 1) in contrast to plasma apo A-I and apo B, alterations in plasma lipid, apo A-IV, and apo E levels depend on the type of corticosteroid used; and 2) glucocorticoids have a differential effect on hepatic mRNA levels of apo A-I and apo A-IV on the one hand and apo A-II on the other hand, an effect that may be of consequence in the process of reverse cholesterol transport.

Adrenal Cortex Hormones↗