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D B Zilversmit

Publications and source records attributed to D B Zilversmit.

136 records · Page 8Linked to original sources
PubMedDate not supplied

Postprandial lipemia and lipoprotein lipase in the rabbit are modified by olive and coconut oil.

Feeding a 14% coconut oil/0.5% cholesterol (CNO/chol) diet to rabbits resulted in plasma triglycerides that were, on average, 15 times higher than basal levels. Plasma triglycerides in rabbits fed a 14% olive oil/0.5% cholesterol (OO/chol) diet were significantly below baseline levels. Differences in postprandial triglyceride response and postheparin plasma lipoprotein lipase activity (LPL) in various feeding conditions were studied to determine the mechanism of the hypertriglyceridemia. Postprandial triglyceride responses after the first high fat/cholesterol meal were more prolonged in CNO/chol rabbits than in OO/chol rabbits; postprandial triglyceride responses after chronic CNO/chol feeding were significantly greater compared to OO/chol rabbits. When long-term CNO/chol rabbits were given one OO/chol or corn oil/chol meal, postprandial triglyceride peaks were greatly diminished, suggesting that these unsaturated fat meals may alter triglyceride clearance capacity. LPL activity was 400% higher than basal levels in chronically fed OO/chol rabbits but changed very little in chronically fed CNO/chol rabbits. Twenty-four hours after a single OO/chol meal was fed to chow-fed rabbits, LPL doubled; one CNO/chol meal was associated with only a 40% increase. Feeding a single OO/chol or corn oil/chol meal to chronically fed CNO/chol rabbits resulted in a 30% to 50% increase in LPL by 24 hours. Thus, the hypertriglyceridemia in CNO/chol rabbits may result in part from a decreased clearance capacity due to a lack of increase in LPL activity, while increased LPL may be partially responsible for the hypotriglyceridemia observed in OO/chol feeding. Aortic cholesterol was substantially higher in CNO/chol rabbits. Triglyceride was approximately eight times greater in livers from CNO/chol-fed rabbits than in those fed OO/chol, but liver cholesterol was only about one-third as much as that in OO/chol rabbits.

Animals↗
PubMedDate not supplied

Mechanisms of hypertriglyceridemia in the coconut oil/cholesterol-fed rabbit. Increased secretion and decreased catabolism of very low density lipoprotein.

Rabbits fed a 14% coconut oil/0.5% cholesterol (CNO/Chol) diet develop mild to severe hypertriglyceridemia compared with rabbits fed a 14% olive oil/0.5% cholesterol (OO/Chol) diet. Lipids and apolipoprotein (apo) B were significantly higher in the very low density lipoprotein (VLDL) and intermediate density lipoprotein fractions from CNO/Chol than from OO/Chol rabbits. Yet, the particle diameters of these lipoproteins were similar in both diet groups, indicating that CNO/Chol rabbits had a much larger number of VLDL and intermediate density lipoprotein particles in plasma. Although the composition of CNO/Chol VLDL differed from that of OO/Chol VLDL, the rates of triglyceride hydrolysis of CNO/Chol VLDL and OO/Chol VLDL by postheparin lipoprotein lipase in vitro were the same, suggesting that VLDLs from the two diet groups were equally good substrates for lipoprotein lipase. To determine the mechanisms of hypertriglyceridemia in the CNO/Chol rabbit, triglyceride and apo B of CNO/Chol VLDL and OO/Chol VLDL were labeled with tritium-containing triolein and iodine-131 and injected intravenously into CNO/Chol and OO/Chol rabbits. The fractional clearance rate for triglyceride in OO/Chol rabbits was twice that of CNO/Chol rabbits, which parallels the previously observed differences in postheparin lipoprotein lipase activity. Although the average fractional removal of apo B did not differ between diet groups, there was a significant inverse relation between plasma cholesterol and apo B fractional clearance rate. We conclude that the hypertriglyceridemia and the enhanced hypercholesterolemia in the CNO/Chol rabbit results primarily from increased hepatic secretion of VLDL and a modest decrease in VLDL triglyceride clearance capacity.

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PubMedDate not supplied

Comparison of cholesteryl ester transfer from chylomicrons and other plasma lipoproteins to aortic intima media of cholesterol-fed rabbits.

Lymph chylomicrons labeled with 14C-cholesterol and plasma very low and intermediate density lipoproteins (d less than 1.019) labeled with 3H-cholesterol were injected simultaneously into recipient cholesterol-fed rabbits. The cholesteryl ester of chylomicron origin (14C) found in the tissues 1 to 4 hours after the injection is the sum of both direct and indirect uptake of chylomicron cholesteryl ester. The direct uptake of chylomicron cholesteryl ester is defined as occurring in situ during the interaction between chylomicrons and lipoprotein lipase in endothelial cells. The indirect uptake of chylomicron cholesteryl ester results from the uptake of chylomicron remnants and of other plasma lipoproteins which become labeled during the degradation of the injected chylomicrons by net lipid transfer or by exchange. The indirect contribution of chylomicron cholesteryl ester to tissues was calculated from tissue 3H-cholesteryl ester derived from injected plasma d less than 1.019 lipoproteins. In rabbits fed 0.5 g cholesterol daily for 40-60 days, with plasma cholesterol concentrations between 20 and 30 mM (800-1200 mg/dl), less than 1% of the cholesteryl ester influx into aortic intima media and less than 10% in liver was derived from the direct uptake of chylomicron cholesteryl ester.

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PubMedDate not supplied

Influx, efflux, and hydrolysis of cholesteryl ester in atheromatous lesions of cholesterol-fed rabbits.

Total plasma lipoproteins were labeled with radioactive cholesteryl ester or cholesteryl ether by transfer of these lipids from phosphatidylcholine vesicles in the presence of plasma lipid transfer activity. Intravenous injection of these preparations into hypercholesterolemic rabbits showed disappearance curves identical to those of in vivo labeled lipoproteins. Disappearance of cholesteryl ester and ether were similar during the first 24 hours, but they diverged at later time intervals, indicating recirculation of labeled cholesteryl ester. Lipoproteins labeled with cholesteryl ether were injected at 25 days, 7 days and 1 day before sacrifice of the rabbits. The maximal loss of labeled ether from the aortas during a 24-hour period ranged from 1.6% to 8.9% of the labeled ether taken up from plasma. Hydrolysis of cholesteryl ester by the artery during 24 hours averaged 35% of the calculated cholesteryl ester influx. After hydrolysis, cholesteryl ester fatty acid appeared to be esterified more rapidly than the cholesterol moiety of the cholesteryl ester.

Adrenal Glands↗
PubMedDate not supplied

Effect of 17 beta estradiol on aortic cholesterol content and metabolism in cholesterol-fed rabbits.

Administration of estrogen to cholesterol-fed rabbits dramatically retarded arterial lesion development despite its lack of effect on plasma cholesterol concentration and on lipoprotein patterns. Cholesteryl ester influx into the aortic wall was also much lower in the estrogen-treated animals and paralleled the aortic cholesterol content in treated and untreated animals; the fraction of aortic cholesteryl ester lost by efflux was the same in treated and untreated animals. The fraction of newly entered cholesteryl ester hydrolyzed by aorta was significantly reduced in the estrogen-treated animals. Low cholesteryl ester influx and relatively less hydrolysis of cholesteryl ester by the aorta may be indicative of reduced internalization of plasma cholesteryl ester by aortic cells, which may in turn account for the reduced atherogenesis in the estrogen-treated rabbits.

Adrenal Glands↗
PubMedDate not supplied

Enhanced accumulation and turnover of esterified cholesterol in injured rabbit aorta.

Arterial injury exacerbates experimental atherogenesis. This report evaluates cholesteryl ester influx and loss during the first 5 days after arterial injury. Selected areas of aortas from rabbits made hypercholesterolemic by 12 to 16 days of cholesterol feeding were injured with a balloon catheter. This allowed measurements and a relatively precise comparison of cholesterol and cholesteryl ester influx into the uninjured and injured arterial wall within the same animal. The animals received oral doses of 3H- or 14C-cholesterol either just before injury or 1 day later. Most animals were given the other isotope of cholesterol 1 day before sacrifice, which took place 2 to 5 days after injury. Measurement of accumulated labelled esterified cholesterol within the same animal during two different time periods allowed the estimation of total influx and fractional loss of entered esterified cholesterol within the artery. Between 2 and 5 days after injury, total influx into areas of injured artery averaged 30 to 60 times the total influx into the adjacent uninjured areas. By the fifth day after injury, the esterified cholesterol content was about 10 times greater in injured areas than in adjacent, uninjured areas. The nonesterified cholesterol content of injured areas was about 70% greater than that of adjacent noninjured areas. Total influx and fractional loss of arterial cholesteryl ester calculated from radioactivity data could account for 117 +/- 6 (mean +/- SEM) percent of the cholesteryl ester mass that accumulated during the interval from injury to sacrifice. The total influx rates and daily increments in cholesteryl ester content of injured areas were positively related.

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PubMedDate not supplied

Comparison of arterial intimal clearances of LDL from diabetic and nondiabetic cholesterol-fed rabbits. Differences in intimal clearance explained by size differences.

Arterial intimal clearances of low density lipoproteins (LDL) from diabetic cholesterol-fed rabbits (D-LDL) and LDL from nondiabetic cholesterol-fed rabbits (N-LDL) were compared. In six experiments, D-LDL and N-LDL were isolated from a diabetic and a nondiabetic rabbit, were iodinated with 125I and 131I, respectively, were mixed, and were reinjected into the same two rabbits as well as into a normal rabbit. Fractional catabolic rates for D-LDL and N-LDL in normal rabbits were 0.065 and 0.074 h-1 (p less than 0.05), respectively. For five of the six pairs of LDL, the D-LDL was smaller than N-LDL as determined by gel filtration. The arterial permeability to N-LDL, when normalized for differences in arterial cholesterol content, did not appear to differ between diabetic and nondiabetic rabbits. The relative arterial intimal clearance (D-LDL/N-LDL) in arteries from diabetic and nondiabetic rabbits was inversely related to the relative molecular weight (D-LDL/N-LDL). For example, when the molecular weight of D-LDL was as low as 60% of that of N-LDL (i.e., the diameter of D-LDL was reduced 16%), the intimal clearance of D-LDL was 40% larger than that of N-LDL. When, on the other hand, molecular weights and diameters of the two LDL were similar, the intimal clearance was also quite similar. These results suggest that arterial intimal clearance of LDL from diabetic and nondiabetic cholesterol-fed rabbits is comparable unless the two types of LDL have a different size.

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PubMedDate not supplied

Increased lipid transfer activities in hyperlipidemic rabbit plasma.

Three models of hypercholesterolemia in rabbits were positively associated with plasma cholesteryl ester and triglyceride transfer activities. In cholesterol-fed rabbits, the transfer activities increased two- to three-fold when plasma cholesterol concentration reached about 1500 mg/dl. In hypercholesterolemia induced by feeding a cholesterol-free semisynthetic casein-sucrose diet, plasma cholesterol increased up to three-fold and the increase in cholesteryl ester and triglyceride transfer activities per unit of plasma cholesterol increment was similar to that in cholesterol-fed rabbits. Watanabe heritable hyperlipidemic rabbits, in which hypercholesterolemia is induced by a genetic defect of the LDL receptor, had significantly higher transfer activities than normolipidemic rabbits. However, fasting, which also induced hypercholesterolemia, lowered transfer activities, whereas refeeding returned them to prefasting levels. In rats, hypercholesterolemia induced by a high cholesterol diet did not increase cholesteryl ester and triglyceride transfer activities. Although hypercholesterolemia in rabbits may not be the primary cause of increased lipid transfer activities, some mechanism related to hypercholesterolemia appears to be associated with increased cholesteryl ester and triglyceride transfer activities.

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