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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Severely hyperlipidemic alloxan-diabetic cholesterol-fed rabbits were treated with different daily doses of insulin in order to study the effect of insulin on plasma lipids, lipoproteins and postheparin lipoprotein lipase activity. At plasma triglyceride levels of 15,000 mg/dl, untreated diabetic rabbits carried 73% (1950 mg/dl) of plasma total cholesterol in lipoproteins with a diameter larger than 75 nm (Sf greater than 400), 25% in smaller very low density lipoproteins (VLDL) and 1% in both low and high density lipoproteins (LDL, HDL). Insulin treatment greatly reduced plasma total cholesterol and triglyceride concentrations. The decrease of plasma total cholesterol concentration was paralleled by a decrease in the cholesterol of the largest lipoproteins (Sf greater than 400) and an increase in cholesterol of both smaller very low density lipoproteins and low density lipoproteins. At the same time, postheparin plasma lipoprotein lipase activity increased 2-8-fold. When plasma triglyceride levels were normalized by insulin treatment, the lipoprotein cholesterol distribution in diabetic cholesterol-fed rabbits was similar to that of normal cholesterol-fed rabbits. To study development of atherosclerosis, diabetic rabbits were cholesterol-fed and treated with insulin for eight weeks such that the triglyceride levels were normalized, but plasma glucose levels were still greatly elevated. Nondiabetic rabbits were cholesterol-fed simultaneously. Plasma cholesterol and triglyceride levels were similar in the two groups of rabbits, as well as cholesterol in Sf greater than 400 or smaller VLDL and cholesterol in HDL. However, LDL-cholesterol concentration in the insulin-treated diabetic rabbits was 1.5-2 times that in the nondiabetic rabbits. The two groups of rabbits developed similar degrees of atherosclerosis, as judged by aortic cholesterol content. Apparently, partially controlled diabetes in cholesterol-fed rabbits does not accelerate atherogenesis beyond that observed in nondiabetic cholesterol-fed rabbits.
Atherosclerosis 1988 Jul
PMID:Hyperglycemia in normotriglyceridemic, hypercholesterolemic insulin-treated diabetic rabbits does not accelerate atherogenesis. 306 65

In order to compare the effects of lovastatin and probucol on lipoprotein profiles, we treated 32 familial hypercholesterolemia (FH) heterozygotes and 26 patients with non-familial hypercholesterolemia for 14 weeks with either probucol (1 g/d) or lovastatin (40-80 mg/d) in a randomized double-blind study. Lovastatin at 80 mg/d reduced low density lipoprotein (LDL)-cholesterol and apo B by more than 40% in both familial and non-familial hypercholesterolemia (non-FH). Probucol reduced LDL-cholesterol by 10-17% while LDL-apo B levels were not influenced at all (FH) or fell by 13% (non-FH). Analysis of LDL composition demonstrated that the LDL-cholesterol lowering effect of probucol in FH was entirely due to reduction in the proportion of cholesterol in LDL with no reduction in LDL mass. Serum high density lipoprotein2 (HDL2)-cholesterol levels fell by 27-33% during probucol, whereas HDL2-cholesterol increased by 10-18% with lovastatin 80 mg/d. These changes in HDL2 were not mediated by lipoprotein lipase or hepatic lipase, both of which are known to participate in regulation of this lipoprotein.
Atherosclerosis 1988 Aug
PMID:Comparison of lovastatin and probucol in treatment of familial and non-familial hypercholesterolemia: different effects on lipoprotein profiles. 306 68

Twelve subjects (6 women, 6 men) were given 120 g fat orally for 2 h to study its effect on serum high density lipoproteins (HDL), HDL subfractions and apoproteins A-I and A-II. In addition, we measured the fasting activity of adipose tissue lipoprotein lipase (LPL). The HDL2 mass concentration increased significantly in women (216 +/- 10 vs 232 +/- 12 mg/dl, P less than 0.01) but not in men (114 +/- 10 vs 119 +/- 11 mg/dl, NS). The changes of the HDL2 mass in women were due to significant increases of phospholipids, and both apoproteins A-I and A-II. In men, only HDL2 phospholipids rose slightly. The HDL2 cholesterol remained unchanged postprandially. Both fasting and maximal postprandial concentrations of HDL2 correlated positively with adipose tissue LPL activity (r = +0.63, P less than 0.05 and r = +0.61, P less than 0.05). The concentration of HDL3 remained unchanged postprandially but compositional changes were observed. Thus, the HDL3 phospholipids increased slightly in both sexes whereas the HDL3 cholesteryl esters fell significantly. The postprandial changes of HDL2 and HDL3 phospholipids were evident in both zonal ultracentrifugation and equilibrium ultracentrifugation. In addition, 5 women received intragastric fat infusions with or without extra soya phospholipids, lecithin. The HDL2 mass concentration increased after both infusions. In 4 of the 5 subjects the overall increment of the HDL2 phospholipids was larger after the phospholipid-rich emulsion than after phospholipid-poor one. This difference was obvious in zonal profile of HDL subfractions which revealed also a slight increase of HDL3 phospholipids after both infusions. In conclusion, the response of HDL2 to fat meal is more pronounced in women than in men and it seems to be dependent on fasting LPL activity which is higher in women than in men. Further, the alterations in postprandial composition of HDL subfractions can be modified by the composition of fat meal.
Atherosclerosis 1986 Feb
PMID:High density lipoproteins in postprandial lipemia. Relation to sex and lipoprotein lipase activity. 308 30

The chemical composition and biologic properties of a fraction (f) of Sulodexide, a heparin-like GAG, were studied and compared with those of two sulfated GAG preparations and heparin from intestinal mucosa. f-Sulodexide and the sulfated GAG preparations were fractionated on a Dowex-1Cl- column and subsequently on an antithrombin III affinity column. Low affinity and high affinity fractions had similar chemical composition and lipoprotein lipase releasing ability, but they varied in anticoagulant activity. Low affinity fractions from f-Sulodexide had negligible anticoagulant activity while high affinity fractions had one-half the activity of mucosal heparin. When compared to heparin, both fractions had one third amount of lipoprotein lipase releasing activity. The low anticoagulant activity of f-Sulodexide suggests a suitability for long-term use as an antiatherogenic agent.
Atherosclerosis 1986 May
PMID:Studies of chemical and biologic properties of a fraction of sulodexide, a heparin-like glycosaminoglycan. 308 74

Apoproteins A-I and A-II, and the activities of lipoprotein lipase (LPL) and hepatic lipase (HL), were studied in 16 patients 3-12 years after ileal bypass operation and in 13 controls, all heterozygous for familial hypercholesterolemia, to investigate why the operated subjects had a higher HDL cholesterol level than the unoperated controls. HDL- and HDL2-cholesterol and apoprotein A-I were higher, HDL3-cholesterol was similar and apoprotein A-II tended to be lower in the operated than the control subjects. The activities of LPL and HL were similar in the 2 groups. HL was negatively correlated with HDL2-cholesterol, whereas LPL was not associated with any of the HDL components. The controls had gained in weight during the follow-up, but the HDL components were not correlated with relative body weight. It is concluded that in familial hypercholesterolemia ileal bypass results in higher HDL- and HDL2-cholesterol and apoprotein A-I level than conservative treatment and that postheparin plasma lipolytic enzymes do not explain the higher level of these HDL components in the operated subjects.
Atherosclerosis 1987 Feb
PMID:High density lipoprotein, apoproteins A-I and A-II and postheparin plasma lipolytic enzymes after ileal bypass. 310 35

In order to investigate the in vivo function of hepatic lipase, cats were injected with anti-cat hepatic lipase antibodies which produced a complete and specific inhibition of heparin-releasable hepatic lipase. The cat was chosen as an animal model because it displays, like man, a relative deficiency of lipoprotein lipase compared to hepatic lipase and because the possession of two subfractions of high density lipoproteins, HDL2 and HDL3. In fasted cats no changes were observed in plasma triglycerides or phospholipids. In fed animals triglycerides increased considerably, indicating that hepatic lipase may have a function in the postprandial phase. In fat-loaded cats (6 g of fat/kg) triglycerides in the d less than 1.019 g/ml fraction increased from 4 h after the blockade due to accumulation of lipoproteins with pre-beta-mobility containing the apoproteins, apo B-100, apo E and apo A-I. Apo B-48 did not accumulate consistently. Phospholipids in the HDL2-fraction and those in the HDL3-fraction of the fat-loaded cats tended to increase and decrease from 6 and 9 h after the blockade, respectively. The absolute change in HDL2 phospholipids approximated that of HDL3-phospholipids. Overall, the density of HDL particles decreased, apparently secondary to the accumulation of apo A-I in the d less than 1.019 g/ml fraction. Our findings suggest that hepatic lipase is involved in the hydrolysis of a special class of apo A-I containing triglyceride-rich lipoproteins synthesised in the postprandial phase.
Atherosclerosis 1988 Feb
PMID:Studies on the function of hepatic lipase in the cat after immunological blockade of the enzyme in vivo. 312 48

We studied the effects of testosterone substitution on serum concentrations of lipids, lipoproteins, apoproteins and on the activity of hepatic lipase (HL) and lipoprotein lipase (LPL) in postheparin plasma and on the activity of LPL in adipose tissue (AT-LPL) in 13 male hypopituitary patients. The activities of LPL and HL in postheparin plasma were markedly increased by 1 week after a testosterone enanthate injection (P less than 0.001). The HL activity remained elevated (P less than 0.05) after 1 month's treatment, but the LPL activity declined to presubstitution levels. The prolonged substitution decreased serum apoproteins A-I and A-II (P less than 0.05). The changes of apo A-I and A-II correlated inversely with those of the free testosterone index (FTI) (r = -0.74, r = -0.67, P less than 0.05). Serum HDL-cholesterol level decreased slightly by 1 week and it correlated inversely with the increase in testosterone and the FTI (r = -0.67, r = -0.85, P less than 0.05). The results suggest that testosterone increases the activity of both lipolytic enzymes in postheparin plasma. The effect on HL appears to be more persistent than that on LPL. The data support a role for androgens in the regulation of serum lipoprotein and HDL-cholesterol levels.
Atherosclerosis 1988 Feb
PMID:Testosterone substitution increases the activity of lipoprotein lipase and hepatic lipase in hypogonadal males. 312 49

With the advent of nocturnal intragastric feeding which protects against acute metabolic complications and promotes growth, patients with glycogen storage disease type I are attracting less attention. However, several biochemical alterations persist and suggest that the long-term risk of atherosclerotic heart disease remains high. Persisting hypertriglyceridemia and hypercholesterolemia were found in seven glycogen storage disease type I subjects, six of them following 5-6 yr of nocturnal intragastric feeding. When compared to ten age-matched controls, the patients showed significantly (P less than 0.001) higher low density lipoprotein cholesterol (LDL-C) (247.7 +/- 46.8 vs. 115.3 +/- 5.0 mg/dl) and lower high density lipoprotein cholesterol (HDL-C) (26.4 +/- 3.4 vs. 55.8 +/- 2.9 mg/dl). Triglyceride (TG) enrichment with cholesteryl ester depletion characterized the lipoprotein classes. The diameters of very low density lipoproteins (VLDL) and LDL were larger, while that of HDL was smaller and consistent with the predominance of the HDL3 subclass and a lower apoA-I/apoA-II ratio. The raised levels of TG appeared attributable not only to the well-described lipogenesis, but also to impaired catabolism of fat, as evidenced by the significantly (P less than 0.001) decreased activity of both peripheral lipoprotein lipase (3.17 +/- 0.43 vs. 14.15 +/- 0.50 mumol FFA.ml-1.hr-1) and hepatic lipase (1.88 +/- 0.30 vs. 4.83 +/- 0.90). This may well explain the high concentration of intermediate density lipoprotein (IDL) and the impaired conversion of HDL3 to HDL2. Low apoC-II/apoC-III1 could be related to defective lipoprotein lipase activity. These data suggest that glycogen storage disease type I patients on nocturnal intragastric feeding remain at risk for atherosclerosis and its complications.
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PMID:Circulating lipids and lipoproteins in glycogen storage disease type I with nocturnal intragastric feeding. 313 Apr 54

Lipids are transported in the blood in four major classes of lipoproteins. The triacylglycerol-rich lipoproteins are chylomicrons and very-low-density lipoproteins (VLDL) which are produced by the small intestine and liver, respectively. These lipoproteins mainly carry fatty acids to adipose tissue and muscle where the triacylglycerol is hydrolysed by lipoprotein lipase. The resulting particles that remain in the blood are chylomicron remnants and low-density lipoprotein (LDL), respectively. The remnant is taken up by the liver via endocytosis which is mediated by a specific receptor for apolipoprotein E (apoE). LDL, which are rich in cholesterol, can also be taken up by the liver or extrahepatic tissues by a receptor-mediated endocytosis that specifically recognises apoB or apoE. 'Nascent' high-density lipoprotein (HDL) particles are secreted by the liver and intestine and then undergo modification to become HDL3 and then HDL2 as they acquire cholesterol ester. They facilitate the reverse transport of cholesterol back to the liver. Little is known of the hormonal regulation of lipoprotein uptake by the liver. Recently, we have shown that insulin and tri-iodothyronine (T3) increase the specific binding of LDL to cultured hepatocytes whereas dexamethasone (a synthetic glucocorticoid) has the opposite effect. The changes in binding produced by insulin and dexamethasone are paralleled by alterations in the rate of degradation of apoB. These findings may in part explain the hypercholesterolaemia and increased risk of premature atherosclerosis that can be associated with poorly controlled diabetes or hypothyroidism.
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PMID:The biochemistry of lipoproteins. 314 85

Thirty postmenopausal women were randomly treated with desogestrel (DG) or levonorgestrel (LN) 125 micrograms/day for 3 weeks. Desogestrel reduced the serum total and free (non-protein bound) testosterone concentrations. It caused a small decrease in the sex hormone binding globulin capacity (SHBG) but did not influence the free testosterone index (testosterone/SHBG ratio). Levonorgestrel, on the other hand, did not influence the free testosterone concentration, but caused a significant increase in the free testosterone index. Levonorgestrel reduced the HDL and particularly the HDL2 cholesterol concentrations (mean change from 1.75 to 1.45 mmol/l for HDL and from 0.73 to 0.50 mmol/l for HDL2, P less than 0.001). It also caused a reduction in the VLDL triglyceride (P less than 0.05) but not the total serum triglyceride concentration. Desogestrel did not cause any significant changes in HDL or HDL2 cholesterol concentrations, but it reduced the VLDL triglyceride (P less than 0.01) and total serum (P less than 0.05) triglyceride concentrations. Neither of the two progestins influenced the postheparin plasma lipoprotein lipase (LPL) activity or the serum cholesterol esterification rate by lecithin:cholesterol acyltransferase (LCAT). It is therefore possible that both steroids decreased the hepatic output of triglycerides, which may be clinically important since both progestins are used in combination with ethinylestradiol (EE) which increases the hepatic TG synthesis. The failure of desogestrel to change HDL levels is consistent with earlier data on the lack of effects on HDL by non-androgenic progestins. Levonorgestrel increased the mean activity of postheparin plasma hepatic lipase (HL) from 23.3 to 28.0 mumol X h-1 X ml-1 (P less than 0.05). In contrast, this activity was not influenced by desogestrel. The magnitude of the changes in postheparin plasma HL activity and the free testosterone index (testosterone/SHBG ratio) showed significant positive correlation (+ 0.41, P less than 0.05). On the other hand, the changes in the HDL2 cholesterol and the postheparin plasma HL activity were inversely interrelated (r = 0.52, P less than 0.01). These relationships are consistent with the idea that the effects of different progestins on the HDL cholesterol are mediated by the sex steroid sensitive hepatic endothelial lipase.
Atherosclerosis 1985 Mar
PMID:Effects of two progestins with different androgenic properties on hepatic endothelial lipase and high density lipoprotein2. 315 21


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