Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Many of hypertensive individuals have glucose intolerance and dyslipidemia, and insulin resistance is common disorder on the basis of these diseases. It is important to take care of these metabolic disease for not only the control of hypertension, blood glucose and hyperlipidemia, but also the prevention of atherosclerosis. We reviewed the effects of angiotensin II receptor antagonists on insulin resistant syndrome.
 ...
PMID:[The effects of angiotensin II receptor antagonists on insulin resistance]. 1036 53

Renal disease is accompanied by characteristic alterations of lipoprotein metabolism, which appear as a consequence of nephrotic syndrome or renal insufficiency and are primarily reflected in an altered apolipoprotein profile rather than elevated plasma lipid levels. Their full characterization requires identification of discrete lipoprotein particles. While nephrotic syndrome results in increased concentrations of both cholesterol- and triglyceride-rich apoB-containing lipoproteins, renal insufficiency is characterized by an accumulation of intact or partially metabolised triglyceride-rich apoB-containing lipoproteins. The dyslipidemia has been discussed as a contributory factor for the progression of renal insufficiency through development of glomerulosclerosis and tubulointerstitial lesions together with accelerated atherosclerosis. Several experimental studies have shown that hyperlipidemia accelerates renal damage. Lipid-lowering treatment can reduce renal lesions and preserve renal function. The documentation in human nondiabetic progressive renal insufficiency is more limited. We have found that increased concentrations of triglyceride-rich, but not cholesterol-rich, apoB-containing lipoproteins are, associated with a more rapid loss of renal function. The underlying pathophysiological mechanisms for the relation between triglyceride-rich apoB-containing lipoproteins and progression of renal insufficiency are not fully understood. Treatment with hypolipemic drugs may attenuate the renal dyslipidemia, but thus far there have been no reports about controlled clinical trials testing the possible effect of such treatment on the progression of renal insufficiency. In summary, there is evidence to suggest that some specific lipoprotein abnormalities are a risk factor for the progression of renal dysfunction, but the final test of such assumptions still rests on the results of urgently needed controlled intervention studies.
 ...
PMID:Lipoprotein abnormalities as a risk factor for progressive nondiabetic renal disease. 1041 28

Low density lipoprotein (LDL) with low sialic acid content has been shown to cause intracellular lipid accumulation and therefore is suggested to be atherogenic. We investigated the sialic acid content of total LDL and its subfractions, and their relations to lipoprotein kinetics in 22 subjects with primary moderate hypercholesterolemia (IIa) and in 21 subjects with combined hyperlipidemia (IIb) matched for age, sex, BMI and the frequency of coronary artery disease. Sialic acid to protein ratio decreased gradually from VLDL and IDL to light and dense LDL and HDL, but was high in very dense LDL probably due to presence of Lp(a). Sialic acid to apo B ratio was significantly lower in dense and very dense subfractions of IIb than IIa. The sialic acid/apo B ratios of dense and very dense LDL subfractions were interrelated and were negatively associated with their cholesterol and triglyceride concentrations, and with the transport rate (TR) for dense LDL apo B. The only metabolic variable differing between the groups was the TR for dense LDL apo B, which was significantly higher in IIb vs. IIa. In addition, the TR for dense LDL apo B was positively associated with the esterification percentage of LDL cholesterol. In conclusion, low sialic acid content in dense and very dense LDL subfractions was associated with enhanced TR for LDL apo B and type IIb dyslipidemia.
 ...
PMID:Sialic acid content of LDL and lipoprotein metabolism in combined hyperlipidemia and primary moderate hypercholesterolemia. 1048 24

Combined hyperlipidaemia, associating hypercholesterolaemia and hypertriglyceridaemia, is a common metabolic disorder with a prevalence of about 1/500. It has a genetic background, but its phenotype is triggered by various predisposing factors such as obesity, type 2 diabetes and alcohol consumption. Combined hyperlipidaemia is undoubtedly associated with an increased cardiovascular risk and thus deserves specific management. After diet failure, the first drug choice remains controversial. Indeed, fibrates are more active on hypertriglyceridaemia while statins are more active on hypercholesterolaemia (LDL subfraction). Both pharmacological classes have their advantages and disadvantages, and there is no prospective study comparing the cardiovascular protective efficacy of these two treatments in patients with such dyslipidemia. Furthermore, monotherapy is generally incapable of normalizing the lipid profile in the presence of severe combined hyperlipidaemia. Ideally, a statin-fibrate combination would be most appropriate in order to act on the two components of such hyperlipidaemia and to benefit of the complementary and additive action of the two pharmacological classes. Such association is still contra-indicated because of the description of some cases of rhabdomyolysis is high risk patients; however, it now deserves much interest and is currently being tested in large prospective studies, especially in the population with type 2 diabetes.
 ...
PMID:[Treatment of combined hyperlipidemia: fibrate and/or statin?]. 1049 79

Coronary hypersensitivity to serotonin promotes platelet aggregation and, therefore, the progression of the atherosclerotic process. This abnormality occurs in the early stages of coronary atherosclerosis when the responses to bradykinin are still preserved. To determine whether such changes also occur early after cardiac transplantation, intracoronary injections of bradykinin and serotonin were performed in 7 control patients, in 19 patients with dyslipidemia, and in 15 cardiac transplant recipients (1 year after operation). Coronary angiography was normal in the 3 groups. In the segments where serotonin effects were the most pronounced, the diameter changes were measured by quantitative angiography. Bradykinin (60, 200, and 600 ng) increased in the same way as the coronary diameters in the 3 groups; in contrast, serotonin elicited vasodilation only in the control group (7+/-3%, percentage of baseline) and vasoconstriction in the hyperlipidemic group (-9+/-2%) and in transplant recipients (-15+/-3%). After intracoronary infusion of L-arginine (40 mg/min for 14 minutes), serotonin-induced constriction was attenuated in the hyperlipidemic group but not in transplant recipients. Thus, the response to bradykinin is preserved in the early stages of graft vasculopathy. However, in contrast to patients with hyperlipidemia, the absence of an L-arginine effect on the responses to serotonin suggests the involvement of mechanisms other than a decrease in endothelium-derived nitric oxide availability. Immune processes promoting the release of endothelium-derived contracting factors such as endothelin and/or superoxide anion may play a role.
 ...
PMID:Absence of L-arginine effect on coronary hypersensitivity to serotonin in cardiac transplant recipients. 1056 27

Insulin resistance has been associated with hypertriglyceridemia, combined hyperlipidemia, and familial combined hyperlipidemia (FCHL). Whether all FCHL patients with different types of dyslipidemia have low insulin sensitivity has not been evaluated. We measured insulin sensitivity by the hyperinsulinemic euglycemic clamp with indirect calorimetry in 110 healthy controls and in 105 nondiabetic, FCHL family members: in 50 without dyslipidemia, in 19 with hypercholesterolemia (total cholesterol >/=7.7 mmol/L), in 22 with hypertriglyceridemia (total triglycerides >/=2.4 mmol/L in men 2.4 mmol/L in women), and in 14 with combined hyperlipidemia. During the hyperinsulinemic clamp, FCHL family members had higher free fatty acid levels than did controls (0.06+/-0.06 [mean+/-SD] in controls versus 0.16+/-0.11 in relatives without dyslipidemia versus 0.15+/-0. 07 in hypercholesterolemic patients versus 0.29+/-0.14 in hypertriglyceridemic patients versus 0.27+/-0.17 mmol/L in patients with combined hyperlipidemia; P<0.001 after adjustment for age, sex, and body mass index). Relatives without dyslipidemia (16.4+/-4.4 micromol. kg(-1). min(-1), P=0.001) and patients with hypertriglyceridemia (12.8+/-3.8 micromol. kg(-1). min(-1), P<0.001) and with combined hyperlipidemia (13.7+/-3.1 micromol. kg(-1). min(-1), P<0.001) had lower rates of insulin-stimulated glucose oxidation than did controls (19.4+/-4.7 micromol. kg(-1). min(-1)). Also, the rates of nonoxidative glucose disposal were lower in patients with hypertriglyceridemia (P=0.001) and combined hyperlipidemia (P=0.011) than in controls. In contrast, subjects with hypercholesterolemia and control subjects had similar rates of insulin-stimulated glucose uptake. We conclude that a defect in free fatty acid suppression during hyperinsulinemia, probably located in adipose tissue, is characteristic for all FCHL patients with varying types of dyslipidemia, whereas insulin resistance in skeletal muscle is observed only in FCHL patients with elevated triglyceride levels.
 ...
PMID:Impaired free fatty acid suppression during hyperinsulinemia is a characteristic finding in familial combined hyperlipidemia, but insulin resistance is observed only in hypertriglyceridemic patients. 1063 13

The goal of the present study was to assess the impact of variability at the APOC-III insulin response element (APOC-III IRE) genetic locus on lipid, lipoprotein and complex lipoprotein particle levels as well as on the risk of dyslipidemia, in the population of northern France. To this end, 590 men and 579 women were randomly selected in the urban community of Lille in the framework of the MONICA project. Three polymorphisms, -482, -455 in the APOC-III insulin response element (IRE) and SstI in the 3'-noncoding region of the APOC-III gene locus were assessed. Compared to the most common alleles, the rare alleles of -482 and -455 were associated with increased levels of apoB-containing particles (LDL-cholesterol, apoB) and of triglyceride-related markers (apoC-III and LpC-III:B) in women, but not in men, suggesting a gender-related impact of APOC-III polymorphisms on these variables. Similarly, triglycerides, LpC-III:B and apoB were higher in women bearing the rare allele of SstI than in those with the most common allele. There was no evidence for any significant association between any of the -482, -455, and SstI alleles and lipid disorders (mixed hyperlipidemia, hypertriglyceridemia and hypercholesterolemia) in this sample of randomly selected men and women from northern France. In contrast, the prevalence of the haplotype that combined the rare alleles of the -482 and -455 sites was increased only in women with hypertriglyceridemia. Therefore, although the individual risk of hypertriglyceridemia is increased in women with the haplotype T, C at -482, -455, it appears that the -482, -455 and SstI APOC-III gene polymorphisms are not major contributors to the risk of dyslipidemia in the population of northern France.
 ...
PMID:Gender related association between genetic variations of APOC-III gene and lipid and lipoprotein variables in northern France. 1078 46

The aim of the present cross-sectional angiographic study was to examine if there is a relationship between the severity of CAD and postprandial lipemia in patients with type 2 diabetes mellitus. Special emphasis was directed to determining the contribution of apolipoprotein B-48 (apoB-48)-containing and B-100 (apoB-100)-containing triglyceride-rich particles to the magnitude of postprandial lipemia and degree of CAD. The role of apolipoprotein E (apoE) phenotype as a modulator of postprandial lipemia was also evaluated. The severity of CAD was determined by a quantitative coronary angiography and the subjects were classified into two groups based on the presence (severe CAD) or absence (mild CAD) of at least 50% stenosis in a major coronary vessel. The study population consisted of 43 subjects (31 men and 12 women) with fair glycemic control and comparable fasting lipids and body mass index. Postprandial responses of TG, apoB-48 and apoB-100 in lipoprotein subfractions (chylomicrons, VLDL1, VLDL2 and IDL) were determined after a fat load. Type 2 diabetic patients exhibited the classical dyslipidemia of the insulin resistance syndrome and delayed clearance of both hepatic and intestinal particles. Fasting or postprandial lipid or lipoprotein measurements, including apoB-48 and apoB-100 concentrations, did not differ between the groups. The presence or absence of apoE-4 allele did not significantly influence postprandial lipemia. The severity of the most significant coronary stenosis in angiography correlated with plasma and with chylomicron area under curve (AUC) for TG (n=27) and chylomicron AUC for apoB-48 (n=20). The strongest correlate of maximal stenosis was area under incremental curve (AUIC) for apoB-100 in IDL fraction (r=0.548, P=0. 012, n=20). In conclusion, postprandial apoB-48 and apoB-100 metabolism in triglyceride rich lipoproteins is distorted in type 2 diabetic patients, even in those with only mild CAD. The data suggest that postprandial change in small remnant particle numbers may contribute to the severity of CAD in type 2 diabetes.
 ...
PMID:Postprandial metabolism of apolipoprotein B-48- and B-100-containing particles in type 2 diabetes mellitus: relations to angiographically verified severity of coronary artery disease. 1078 48

Obesity and Type 2 diabetes are now major public health issues in developed nations and have reached epidemic proportions in many developing nations, as well as disadvantaged groups in developed countries, e.g., Mexican-Americans, African-Americans, and Australian Aborigines. These groups all show hyperinsulinemia and insulin resistance, which have been demonstrated to be future predictors of Type 2 diabetes and have also been suggested as key factors in the etiology of the Metabolic Syndrome. It is now increasingly recognized that Type 2 diabetes is part of a cluster of cardiovascular disease (CVD) risk factors comprising the Metabolic Syndrome. This group is at very high risk of atherosclerosis because each of the risk factors in the Metabolic Syndrome cluster in its own right is an important CVD risk factor. They also contribute cumulatively to atherosclerosis. A key strategy in reducing macrovascular disease lies in the better understanding of the Metabolic Syndrome--glucose intolerance, hypertension, hyperlipidemia, and central obesity. Although it has been suggested that hyperinsulinemia/insulin resistance is the central etiological factor for the Metabolic Syndrome, epidemiological data do not support the idea that this can account for all of the cluster abnormalities. We have animal and human data suggesting that hyperleptinemia rather than, or synergistically with, hyperinsulinemia may play a central role in the genesis of the CVD risk factor cluster that constitutes the syndrome. Studies in Psammomys obesus (the Israeli sand rat) suggest hyperinsulinemia/insulin resistance is an early metabolic lesion in the development of obesity and Type 2 diabetes. This animal also develops other features of the Metabolic Syndrome, making it an excellent model to investigate etiology. Psammomys, when placed on an ad libitum laboratory diet, develops hyperinsulinemia, insulin resistance, impaired glucose tolerance, diabetes, and dyslipidemia. It also develops hyperleptinemia and leptin insensitivity, and hyperleptinemia is correlated with insulin resistance independent of changes in body weight. It is likely that a similar sequence occurs in the transition from the prediabetic state to Type 2 diabetes in humans. More recently, other potential players in the etiology of the Metabolic Syndrome have been suggested including endothelial dysfunction and acetylation-stimulating protein (ASP). It has been suggested that endothelial dysfunction may be an antecedent for both Type 2 diabetes and the Metabolic Syndrome. In addition, ASP is a serious new candidate for an important role in insulin resistance. The ASP pathway plays a critical role in fatty acid metabolism and storage, and it has been suggested that ineffective storage of fatty acids by adipocytes due to a defect in the ASP pathway may lead to insulin resistance and Type 2 diabetes.
 ...
PMID:Etiology of the metabolic syndrome: potential role of insulin resistance, leptin resistance, and other players. 1084 50

A number of risk factors for coronary artery disease are known to be present in hypertensive patients, the most important being hyperlipidemia. An analysis of the lipid profiles of 3,182 uncomplicated non-diabetic patients (2,425 males, 757 females) who attended two institutions of Patna city between 1992-1998 was conducted alongwith 4,131 controls. Mean total cholesterol was slightly higher (but statistically significant; p < or = 0.05) in hypertensives (191.8 mg/dL vs 190.1 mg/dL) as compared to the control group; mean total cholesterol-HDL ratio was also higher (4.65 vs 4.48) in hypertensives (p < or = 0.05). As per National Cholesterol Education Programme guidelines, 1,069 (33.6%) patients had cholesterol level above 200 mg/dL while 850 (26.7%) had triglycerides over 200 mg/dL among the hypertensive group. An abnormal total cholesterol-HDL ratio (> 4.5) was found in 1,600 (50.3%) of the hypertensives; this was by far the most common abnormality. With increasing severity of hypertension, the prevalence of elevated total cholesterol, LDL cholesterol and low HDL cholesterol was higher; triglyceride levels were less affected. These results indicate that an abnormal total cholesterol-HDL ratio is the most common variety of dyslipidemia in uncomplicated hypertension.
 ...
PMID:A study of lipid levels in uncomplicated hypertension. 1089 93


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>