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961.
Increased plasma lipoprotein(a)-Lp(a)-levels are linked to a high risk of cardiovascular disease unrelated to other lipoproteins. It seems that Lp(a) values in childhood remain unaltered up to adulthood. In a randomly chosen population of 1970 children, aged from 4 to 18 years and living in a Spanish community, the following serum parameters were studied: total cholesterol, total triglycerides, Lp(a), high-density lipoprotein cholesterol and low-density lipoprotein cholesterol. Mean Lp(a) serum values were 15.0 ± 14.7mg dl-1. No differences were seen between either sex in the first years of childhood. Of the studied children, 15.1% presented Lp(a) concentrations above 30 mg dl-1. A correlation between Lp(a) and total cholesterol concentrations, which disappeared when low-density lipoprotein cholesterol concentrations were corrected according to cholesterol present in Lp(a), was observed.  相似文献   
962.
Patientswithchronicrenalfailureoftenhavehypertriglyceridemiaanddecreasedhigh-densitylipoproteincholesterol(HDL-C)concentrations[l'2].Whilecardiovasculardiseaseisamajorcauseofhighmorbidityandmortalityamongthesepatients['].Somestudiessuggestedthatabnormallipoproteinmetabolismwasoneofthecauses.InChina,fewreportswereavailableonlipids,lipoproteins,especiallyapolipoproteinsmetabolisminpatientsundergoingdialysis.Thepurposeofthisstudyistoobservethelipids,lipoproteinsandapolipoproteins(Apo)levelsinp…  相似文献   
963.
探讨不同浓度胆固醇对低密度脂蛋白(LDL)细胞受体结合的影响。方法:用超离心法从人体血清中提取LDL,测糖化值并予以酶标,用酶联免疫受体法测定不同浓度胆固醇(0、5.0、10.0、25.0、50.0、100.0mm。l/L。)对正常组(HbA1c为4.76士0.25%,n=10)及糖尿病Ⅰ组(HbA1c为6.80士0.43%,n=1O)和Ⅱ组(HbA1c为11.57士1.83%,n=1O)的LDL细胞特异受体结合。结果:正常组、Ⅰ及Ⅱ组LDL糖化值分别为18.45士2.15、31.30士4.56、69.10士6.32Glycogroups/LDL,LDL受体结合在无胆固醇时最大,最高浓度胆固醇时最小。结论:胆固醇增高可引起糖尿病患者LDL受体结合的下降。  相似文献   
964.
王海燕  戴振华 《江苏医药》1996,22(4):224-225
采用临床病例对照研究,分析56例心肌梗塞(MI)患者血清脂蛋白(a)(LP(a))水平和纤港功能。结果显示;MI组Lp(a)水平明显高于对照组(227mg/L与136mg/L,P<0.001),多因素分析控制年龄、体重指数、腰臀比、血压、烟酒史、血脂质、纤维蛋白原、血糖和胰岛素后,MI组Lp(a)仍呈非常显著意义(P=0.0037。MI组纤溶酶原活化物的抑制物(PAI-1)为11.23AU/ml,高于对照组(9.57AU/ml,P<0.05),同样用多因素分析控制上述因素后,MI组PAI-1仍有显著意义。Lp(a)与PAI-1之间无明显相关性。多元逐步回归分析发现胰岛素与Lp(a)有关,体重指数和年龄与PAI-1有关。  相似文献   
965.
The application of methods to create transgenic mice in which a gene of interest is either overexpressed or genetically inactivated has provided us with an ever-growing number of animal models to study complex physiological processes in vivo. Analysis of these mouse models has increased our knowledge about basic mechanisms that control biological systems and the pathological processes in human genetic disorders. This review focuses on the analysis of mouse models in which individual components of the hepatic clearance pathway for plasma lipoproteins have been inactivated. These studies have demonstrated that two hepatic lipoprotein receptors, the low-density lipoprotein receptor and the low-density lipoprotein receptor-related protein operate jointly in the uptake of dietary lipoproteins from the circulation. These findings have important implications for our understanding of pathophysiological processes resulting in hyperlipoproteinemia and atherosclerosis in patients.Abbreviations apo Apolipoprotein - ER Endoplasmic reticulum - FPLC Fast performance liquid chromatography - FH Familial hypercholesterolemia - HDL High-density lipoproteins - IDL Intermediate density lipoproteins - LDL Low-density lipoproteins - LDLR LDL Receptor - LRP LDLR-related protein - RAP Receptor-associated protein - VLDL Very low density lipoproteins  相似文献   
966.
The localization of platelet factor 4 (PF4) in the megakaryocyte has been determined by indirect immunofluorescent studies using monospecific rabbit antibody to human PF4. Also, specific staining has demonstrated that platelets in peripheral blood contain PF4 antigen. Absorption studies established that the staining was specific for PF4. Using this technique, it has been demonstrated that PF4 is also localized in the megakaryocytes in bone marrow. The existence of PF4 antigen in the megakaryocytes suggests that PF4 may be synthesized in the megakaryocytes.  相似文献   
967.
Previous studies have indicated that quantitative as well as qualitative abnormalities of bile acid metabolism frequently occur in hypercholesterolaemia. In order to determine if this is a feature of familial hypercholesterolaemia, bile acid kinetics and biliary lipid composition were determined in 15 affected (heterozygous) and six unaffected siblings of four kindreds with familial hypercholesterolaemia. Furthermore, serum levels of cholic acid, chenodeoxycholic acid and deoxycholic acid were measured with a mass fragmentographic technique in 15 members of two of the kindreds, and secretion rates of biliary lipids were measured in six members of two kindreds. No differences with regard to these parameters between affected and unaffected siblings could be detected. There was a close resemblance between relatives of a given kindred concerning bile acid pool size and serum bile acid levels. No evidence for a defective bile acid metabolism in familial hypercholesterolaemia could be gained from the present study. It is concluded that the deficient receptor-mediated elimination of low density lipoprotein cholesterol in this disorder does not influence the maintenance of normal bile acid metabolism.  相似文献   
968.
Summary Diabetes was induced in Wistar male rats by streptozotocin given peritoneally. The control rats received the rame volume of buffer. Twelve days after injection of streptozotocin, the levels of plasma triglyceride, total cholesterol and free fatty acid increased significantly as compared with those of the control rats. The plasma very low density lipoprotejn-choleslerol (VLDL-C) of the diabetic rats was twice as much as that of the control rats. No difference in low density lipoprotein-cholesterol (LDL-C) and high density lipoproteincholesterol (HDL-C) was found between the two groups. However, the HDL3 in diabetic rats increased significantly. These results indicated that the degradation of VLDL was reduced in diabetic rats and concurrently the conversion of HDL3 to HDL2 was impaired. Therefore, we are led to assume that the accumulation of VLDL remnants and the impairment of reverse transport of tissue cholesterol may facilitate the development of atherosclerosis in diabetes mellitus.  相似文献   
969.
Non-insulin-dependent diabetes mellitus is frequently associated with premature atherosclerosis. Abnormalities in lipid and lipoprotein metabolism contribute to the increased risk of coronary heart disease. One of the most common lipid abnormalities in non-insulin-dependent diabetes mellitus is hypertriglyceridaemia. In the present paper, the authors review the metabolism of triglyceride-rich lipoproteins, with special emphasis on the post-prandial state. Several studies have demonstrated that levels of atherogenic post-prandial lipoproteins are increased in patients with non-insulin-dependent diabetes mellitus. An increased supply of glucose and free fatty acids contributes to overproduction of very low-density lipoproteins, increasing the burden of triglyceride-rich lipoproteins on the common lipolytic pathway at the level of lipoprotein lipase. Low lipoprotein lipase activity and increased amounts of lipolysis-inhibiting free fatty acids further impair lipolysis of post-prandial lipoproteins. The clearance of atherogenic remnants is also delayed in non-insulin-dependent diabetes mellitus. There is evidence that a relative hepatic removal defect exists, secondary to impaired remnant-receptor interaction and increased competition with very low density lipoprotein remnants. Correction of the increased post-prandial lipaemia in non-insulin-dependent diabetes mellitus is advisable, as it may contribute to attenuation of the risk on premature atherosclerosis. When dietary measures and hypoglycaemic agents have failed to achieve acceptable lipid levels, lipid-lowering drugs should be advised. Fibric acids and hydroxymethylglutaryl coenzyme A (HMG CoA) reductase inhibitors are the drugs of choice.  相似文献   
970.
《Nutrition reviews》1985,43(9):263-265
Feeding three to six eggs per-day increases plasma LDL and HDL cholesterol levels in about 50 percent of normocholesterolemic subjects. This effect is blunted by increasing the dietary P/S to 1.0.  相似文献   
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