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Query: UMLS:C0042373 (vascular disease)
17,070 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Variation of HDL cholesterol levels in man shows a strong inverse relationship to the incidence of atherosclerotic vascular disease. Thus the regulation of HDL cholesterol levels has been the subject of intense investigation. Human genetic differences in cholesteryl ester transfer protein and hepatic lipase illustrate the importance of these factors in the normal catabolism of HDL, while metabolic and population studies show that lipoprotein lipase activity plays a central role in the transfer of lipids and apoproteins into HDL. Metabolic turnover studies in humans suggest that variations in the fractional catabolism of the HDL structural proteins, apoA-I and apoA-II, account for much of the variation of HDL levels in human populations. Although the catabolism of these apolipoproteins is poorly understood, changes in the core lipid composition of HDL may lead to changes in catabolism of the HDL proteins. The core lipid composition of HDL appears to be determined by lipid transfer processes, and the activities of lipoprotein and hepatic lipase. Thus many genetic and environmental factors that influence HDL levels appear to operate by changing the activities of the lipases or the lipid transfer process.
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PMID:Metabolic and genetic control of HDL cholesterol levels. 161 89

Lipase activities were measured at pH 4 and pH 8 in the placentas of rats made diabetic by streptozotocin treatment and also in the placentas of women classified as having 1) impaired glucose tolerance or type 2 diabetes, 2) type 1 diabetes with no associated vascular complication, and 3) type 1 diabetes with associated vascular disease. In both sets of experiments, the placentas were compared with normal control groups. The placental lipase activity measured at pH 8 was not significantly different in either streptozotocin-treated rats or impaired glucose tolerance/diabetic women as compared with controls, whereas the lipase activity measured at pH 4 increased significantly as compared with controls in both species. Furthermore, in the women there was a significant correlation between placental lipase activity at pH 4 and birth weight in impaired glucose tolerance/type 2 diabetes. It is suggested that the increased placental lipase activity may contribute to the increased fetal weight in human diabetic pregnancy, by contributing to the increased fat transfer across the placenta from mother to fetus.
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PMID:The effects of diabetes on placental lipase activity in the rat and human. 180 50

A turbidimetric kinetic fixed-time method for the rapid determination of serum low density lipoprotein (LDL) has been developed. It is based on specifically precipitating this lipoprotein with the use of a combination of heparin, Ca2+, EDTA and lipase. The method has been adapted to the Eppendorf spectrum line photometer and to the ENI Gemsaec centrifugal analyzer. It yielded satisfactory results with regard to linearity and precision. The values agreed closely to those obtained by conventional procedures for LDL-cholesterol and LDL-apolipoprotein B. The predictive value of this new method for the assessment of the individual risk of vascular disease remains to be proven by clinical and epidemiological studies.
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PMID:Turbidimetric kinetic method for serum low density lipoprotein quantitation. 640

Changes in circulating lipoproteins, which may be related to the risk for atherosclerotic vascular disease, were studied in a control group and in two groups of 24 or 26 women using different preparations of low-dose oral contraceptives for 3 months. One preparation contained 150 micrograms levo-norgestrel and 30 micrograms ethinylestradiol (Stediril-d 150/30); the other contained 750 micrograms lynestrenol and 37.5 micrograms ethinylestradiol (Ministat). No significant changes were found with either of the preparations in serum cholesterol or high density lipoprotein cholesterol (HDL-C) levels. Apolipoprotein A-II levels increased during Ministat treatment from 50.4 to 61.4 mg/dL and during Stediril-d 150/30 treatment from 52.7 to 58.9 mg/dL (both P less than 0.001). These changes differed significantly from each other (P less than 0.01). Apolipoprotein A-I levels increased significantly during use of Ministat only. Apolipoprotein B in low density lipoprotein increased by about 20% (P less than 0.001) in both groups. Post-heparin lipoprotein lipase activity did not change, but hepatic lipase activity decreased to the same extent in both groups (P less than 0.001). Reductions in post-heparin lipase activity were not correlated with increases in HLD-C.
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PMID:Effect of low-dose oral contraceptives on lipoproteins and lipolytic enzymes: differences between two commonly used preparations. 649 47

The following conclusions and speculations can be tentatively drawn from the changes in lipoprotein composition and metabolism: (1) The presence of apo B-48 in serum VLDL and the high serum apo A-IV concentrations indicate a greater than normal contribution of alimentary remnant particles to the hypertriglyceridemia of uremic patients, (2) The presence of apo E and C in triglyceride-enriched serum LDL, together with the triglyceride enrichment of all lipoproteins, probably stems from a deficiency of lipoprotein lipase (LPL) and hepatic lipase (HL) activity, (3) The decreased ratio of serum apo C-II/C-III in VLDL is at least in part responsible for the depressed activity of LPL, (4) The accumulation of lipoprotein particles with distorted apoprotein and lipid patterns (particularly beta-VLDL with enrichment in cholesterol) could be associated with an increased atherogenesis because a recent study has demonstrated a strong association between raised serum IDL and VLDL concentrations and the degree of coronary atherosclerosis, (5) The increased apo E content of VLDL and HDL in uremic patients could particularly point to a disturbed cholesterol metabolism because such lipoproteins could interact with LDL at apo B, E receptors, (6) The decrease in serum HDL-cholesterol has been shown to be strongly associated with atheromatous vascular disease, and this could also hold for uremic patients; however, it is probable that low serum HDL-cholesterol together with a diminished capacity to form cholesterol-rich, apo E containing HDL represents a decrease in the antiatherogenic defense of the organism rather than an increased atherogenic potential [21].
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PMID:Recent advances in factors that alter lipid metabolism in chronic renal failure. 658 43

A new lipoprotein lipase-like gene has been cloned from endothelial cells through a subtraction methodology aimed at characterizing genes that are expressed with in vitro differentiation of this cell type. The conceptual endothelial cell-derived lipase protein contains 500 amino acids, including an 18-amino acid hydrophobic signal sequence, and is 44% identical to lipoprotein lipase and 41% identical to hepatic lipase. Comparison of primary sequence to that of lipoprotein and hepatic lipase reveals conservation of the serine, aspartic acid, and histidine catalytic residues as well as the 10 cysteine residues involved in disulfide bond formation. Expression was identified in cultured human umbilical vein endothelial cells, human coronary artery endothelial cells, and murine endothelial-like yolk sac cells by Northern blot. In addition, Northern blot and in situ hybridization analysis revealed expression of the endothelial-derived lipase in placenta, liver, lung, ovary, thyroid gland, and testis. A c-Myc-tagged protein secreted from transfected COS7 cells had phospholipase A1 activity but no triglyceride lipase activity. Its tissue-restricted pattern of expression and its ability to be expressed by endothelial cells, suggests that endothelial cell-derived lipase may have unique functions in lipoprotein metabolism and in vascular disease.
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PMID:Cloning of a unique lipase from endothelial cells extends the lipase gene family. 1031 35

Type 2 diabetic patients are at increased risk to develop atherosclerotic vascular disease. These patients are often treated with sulphonylurea derivatives, and it has been suggested that this treatment might contribute to the increased atherosclerotic process. The aim of the present study was therefore to investigate whether tolbutamide influences lipid metabolism in such a way that the atherosclerotic process may be promoted. Addition of tolbutamide (5-500 mg/l) to isolated rat fat adipocytes inhibited the lipoprotein lipase (LPL) activity in a dose-dependent manner to levels about 50% of those registered in the absence of tolbutamide. This effect was due to inhibition of the activation of the enzyme in the tissue and not to interference with the interaction of enzyme with its substrate. Addition of tolbutamide (500 mg/l) also inhibited noradrenaline (100 nM) and isoprenaline (40 nM)-induced lipolysis by 48.1 +/- 7.4% (mean +/- S.E.M.) and 47.3 +/- 5.5%, respectively. The decreased lipolysis in tolbutamide preincubated adipocytes was shown to be the result of an inhibition of the phosphorylation of hormone sensitive lipase (HSL). Three months of tolbutamide treatment (0.5 g t.i.d.) in diet treated type 2 diabetic patients did not influence the plasma concentrations of cholesterol, triglycerides, LDL cholesterol, HDL cholesterol as well as HDL triglycerides and HDL phospholipids, and there were no differences compared to placebo treated patients. There was a tendency towards a decrement in the elimination rate of exogenous triglycerides in the tolbutamide group (P = 0.0801). No differences between the groups and no treatment effects were seen on LPL and hepatic lipase activities. In conclusion, our in vitro data show that tolbutamide has dual effects on lipid transport, with impairment of the LPL system, which would tend to decrease plasma lipoproteins by reducing hepatic production of lipoproteins. In vivo, these two effects seem to balance each other and plasma lipoprotein levels remain unaffected.
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PMID:The effects of tolbutamide on lipoproteins, lipoprotein lipase and hormone-sensitive lipase. 1072 87

A lipoprotein lipase-like gene was recently cloned from endothelial cells. In vitro functional experiments have suggested that this endothelial-derived lipase (EDL) has phospholipase activity, and preliminary in vivo studies have suggested a role in the regulation of high-density lipoprotein metabolism. To investigate local control of lipase activity and lipid metabolism in the blood vessel wall, we have examined the regulation of EDL expression in cultured human umbilical vein and coronary artery endothelial cells. EDL mRNA levels were upregulated in both cell types by inflammatory cytokines implicated in vascular disease etiology, including TNF-alpha and IL-1beta. In addition, both fluid shear stress and cyclic stretch were found to increase the EDL mRNA levels in these cultured cells. This highly regulated expression of EDL in vascular endothelial cells suggests that this recently identified lipase is intricately involved in modulating vessel wall lipid metabolism and may play a role in vascular diseases such as atherosclerosis.
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PMID:Regulated expression of endothelial cell-derived lipase. 1087 8

Impaired insulin action has been associated with diabetes, dyslipidemia and atherosclerotic vascular disease. The expression of insulin resistance results from the interaction of environmental and genetic factors. Human hepatic lipase (HL) is a lipolytic enzyme that plays a role in the metabolism of several lipoproteins, while insulin up-regulates the activity of HL via insulin-responsive elements in the HL promoter. We have examined the influence of -514 C/T polymorphism in the hepatic lipase gene promoter on insulin sensitivity in 59 healthy young subjects (30 males and 29 females). The volunteers were subjected to three dietary periods, each lasting four weeks. During the first period all subjects consumed a saturated fat (SFA)-enriched diet with 38% as fat (20% SFA, 12% monounsaturated fatty acids (MUFA) and 6% polyunsaturated fatty acids (PUFA)). In the second and third dietary periods, a randomized crossover design was used, consisting of a low fat, high carbohydrate diet (CHO diet) (< 10% SFA, 12% MUFA and 6% PUFA) and a high-MUFA, or Mediterranean diet, with < 10% SFA, 22% MUFA and 6% PUFA. We determined the in vivo insulin resistance using the insulin suppression test with somatostatin. Steady-state plasma glucose (SSPG) concentrations (a measure of insulin sensitivity) were significantly higher in men carriers of the -514T allele after the consumption of the SFA diet than after the CHO diet and the Mediterranean diet. This effect was not observed in women. Moreover, there were no significant differences in insulin sensitivity after the three diets in men and women with the CC genotype. In summary, our results show an improvement in insulin sensitivity in men with the -514T allele of the HL promoter polymorphism, when MUFA and carbohydrates are consumed instead of SFA fat.
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PMID:The -514 C/T polymorphism in the hepatic lipase gene promoter is associated with insulin sensitivity in a healthy young population. 1582 Nov

The role of homocysteine role in inflammation and malignancy has been studied experimentally. Some researchers suggest that a relationship exists between pancreatitis and homocystinuria, possibly being secondary to occlusive vascular disease of the pancreas. To date, plasma homocysteine levels in pancreatic disease have not been studied. We aimed to analyze the homocysteine status in patients with acute pancreatitis, and the changes of the plasma homocysteine level at the acute phase of the disease and six months after hospital discharge. Fourteen acute pancreatitis patients and 14 healthy subjects were studied. Plasma homocysteine, vitamin B12, folate, amylase, lipase, C-reactive protein, total, HDL and LDL cholesterol, triglycerides, blood urea nitrogen, white blood cells, and creatinine were measured in the two groups of subjects. Plasma levels of homocysteine were significantly higher in patients with acute pancreatitis as were serum creatinine, blood urea nitrogen, WBC counts, amylase, lipase, and C-reactive protein. An impaired creatinine clearance was also found in these patients but this did not reach statistical significance. Serum total, HDL, and LDL cholesterol concentrations were not significantly different between the two groups of subjects. Our data suggest that homocysteine may play a role in inflammatory diseases of the pancreas. Increased plasma homocysteine levels in acute pancreatitis may be a reason, or a marker, for the diagnosis of acute pancreatitis. In conclusion, this is the first report showing that patients with acute pancreatitis have higher plasma homocysteine levels than healthy subjects.
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PMID:Changes in plasma levels of homocysteine in patients with acute pancreatitis. 1846 55


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