Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0242339 (dyslipidemia)
 13,927 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study aimed to reveal the relationships among C-reactive protein (CRP), obesity, blood pressure (BP), and serum lipids in children. Eighty-six obese and 58 non-obese boys aged an average of 11.2 years were examined. Serum CRP levels were measured by high sensitivity latex turbidimetric immunoassay and subjects with CRP levels below 0.3 mg/dl were adopted. Comparisons of serum CRP levels, BP, and serum lipids levels between age-matched obese and non-obese groups were performed. A comparison of serum CRP levels among the percentage of relative weight quartiles and the relationships among percentage of relative weight, BP, and serum lipids in CRP quartiles were analyzed. The relationships between CRP and other parameters were analyzed by simple and stepwise multiple regressions. Obese children had significantly higher high-sensitivity CRP (hs-CRP) levels than their non-obese counterparts. The mean hs-CRP level was 5.5-fold higher in the top quartile of the percentage of relative weight than in the bottom quartile. In the top quartile of CRP, the percentage of relative weight, systolic BP, diastolic BP, pulse pressure, and low density/high density lipoprotein-cholesterol (LDL-C/HDL-C) were significantly higher than in the bottom quartile. The percentage of relative weight, BP, LDL-C, and apolipoprotein B (ApoB) showed positive correlations and HDL-C showed a negative correlation with log CRP by simple regression. Stepwise multiple regression analysis indicated that only the percentage of relative weight was strongly related to CRP. In conclusion, this study revealed a significant relationship between CRP and obesity in children. Obese children tended to have high CRP levels, BP elevation, and slight dyslipidemia. These results support the findings that CRP is one of the useful indices of childhood obesity that would affect the progression to future atherosclerotic disease. We consider that a strategy of preventing obesity from childhood would contribute to a drop in the future incidence of metabolic syndromes.
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PMID:Elevation of serum C-reactive protein levels is associated with obesity in boys. 1292 21

Heart disease is a major cause of morbidity and mortality among patients with renal failure. Premature atherosclerotic coronary heart disease is driven by multiple risk factors, including dyslipidemia and oxidative stress. In the nondialysis population, there is overwhelming evidence that treatment of dyslipidemia can significantly improve cardiovascular outcomes. Accumulating data indicate that dialysis patients have atherogenic lipid abnormalities. Although LDL cholesterol (LDL-C) levels in patients who undergo hemodialysis are normal or near normal, increased oxidized LDL-C, triglycerides, and lipoprotein (a) [Lp(a)]; decreased HDL cholesterol (HDL-C); and triglyceride-rich VLDL have been noted. Patients who receive peritoneal dialysis have a more atherogenic lipid profile with increased LDL-C, apolipoprotein B, oxidized LDL-C, triglycerides, and Lp(a) and decreased HDL-C. Furthermore, the LDL particles of peritoneal dialysis patients are small and dense. However, there is a dearth of information regarding the goals, efficacy, and safety of dyslipidemia treatment among dialysis patients. Given the strong evidence of risk reduction and the benefits of lipid-lowering treatment in the nondialysis population, the emerging consensus is that dialysis patients should be treated aggressively for dyslipidemia to an LDL-C goal below 100 mg/dl. Although physicians and patients may be reluctant to add medications because of concerns about polypharmacy, potential decreased compliance, and increased cost, the use of agents such as sevelamer that can serve multiple functions, including phosphate control, lipid lowering (decreased LDL-C and total cholesterol), and anti-inflammatory effects (decreased high-sensitivity C-reactive protein), should be explored and considered for patients who would benefit from such treatment.
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PMID:Impact of dyslipidemia in end-stage renal disease. 1293 88

Metabolic abnormalities associated with the metabolic syndrome are also present in patients with type 2 diabetes mellitus and in those with familial combined hyperlipidemia (FCHL). These abnormalities include central obesity, insulin resistance with hyperinsulinemia, hypertension, increased plasma triglycerides, and decreased high-density lipoprotein cholesterol levels. Other characteristics associated with FCHL include the presence of small, dense low-density lipoprotein cholesterol and increased apolipoprotein B. Patients with these abnormalities are at an increased risk for premature coronary artery disease. Treatment of the dyslipidemia associated with type 2 diabetes and FCHL with a combination of a statin and a thiazolidinedione or niacin offers the most comprehensive modality to correct the various lipid abnormalities.
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PMID:Lipoprotein distribution in the metabolic syndrome, type 2 diabetes mellitus, and familial combined hyperlipidemia. 1295 24

The aim of this study was to investigate the relationship between plasma viscosity and lipoprotein and apolipoprotein pattern in normo- and hypercholesterolemic patients with peripheral occlusive arterial disease (POAD). 40 patients with POAD have been selected (8 females and 32 males, mean age: 54+/-3.2 years) with clinically evident superficial femoral occlusive artery disease. They were separated into two groups as normocholesterolemic (plasma total cholesterol <200 mg/dl) and hypercholesterolemic (plasma total cholesterol >200 mg/dl). Plasma total cholesterol, high density lipoprotein cholesterol (HDL-C), low density lipoprotein cholesterol (LDL-C), triglycerides, total protein, and albumin levels were determined by enzymatic methods using commercial kits. Levels of apolipoprotein AI (apo AI), and apolipoprotein B (apo B) were measured using a immunoturbidometric method. Plasma viscosity (PV) was measured by capillary viscometer. Classifying the patients with PAOD according to the cholesterol levels; hypercholesterolemic (mean total-cholesterol: 227.90+/-26.97 mg/dl) patients had significantly higher LDL-C, PV and triglyceride levels compared with nornocholesterolemic patients (p<0.001, p<0.001, p<0.001, respectively). HDL-C and apo B were significantly lower in hypercholesterolemic patients than in normocholesterolemic patients (p<0.001, p<0.001, respectively). PV was positively correlated with total cholesterol (r=0.485, p<0.05), atherogenic index (r=0.624, p<0.01), total-C/HDL-C ratio (r=0.624, p<0.05), and LDL-C/HDL-C ratio (r=0.707, p<0.001) in hypercholesterolemic patients with POAD. PV was higher in hypercholesterolemic patients with POAD than in normocholesterolemic patients with POAD. We suggest that POAD patients should be regarded as a heterogenous group with lipid and lipoprotein parameters in order to assess the microcirculation in the affected limb. In case of dyslipidemia in POAD patients an elevated plasma viscosity should be considered as coexisting risk factor.
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PMID:Impaired plasma viscosity via increased cholesterol levels in peripheral occlusive arterial disease [correction of disase]. 1456 98

Standard lipoprotein measurements may not adequately reflect the increased atherogenic risk found in patients with abnormalities in lipoprotein particle size and subfraction distribution such as disproportionate amounts of small, dense low-density lipoprotein particles, small high-density lipoprotein particles, or large very-low-density lipoprotein particles. Measurement or anticipation of patients most susceptible to lipoprotein subfraction abnormalities may influence therapeutic choices for the optimal management of dyslipidemia. Previously, the ADvicor Vs. Other Cholesterol-modulating Agents Trial Evaluation demonstrated that niacin extended release/lovastatin provided greater global improvement in lipid parameters such as low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, triglycerides, lipoprotein (a), apolipoprotein B, and apolipoprotein A-I blood levels compared with atorvastatin and simvastatin monotherapies. In this report, niacin extended release/lovastatin was also more effective than atorvastatin and simvastatin monotherapies in reducing small, dense low-density lipoprotein particles and improving low-density lipoprotein phenotype pattern at relative starting doses, and was more effective in increasing the proportion of high-density lipoprotein in the potentially cardioprotective 2b subclass at all doses.
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PMID:Once-daily niacin extended release/lovastatin combination tablet has more favorable effects on lipoprotein particle size and subclass distribution than atorvastatin and simvastatin. 1460 11

Human plasma platelet activating factor acetylhydrolase (PAF-AH) is an enzyme associated mainly with the apolipoprotein B (apoB)-containing lipoproteins and primarily with low-density lipoprotein (LDL). A small proportion of enzyme activity is also associated with high-density lipoprotein (HDL). PAF-AH activity is essential for the metabolism of PAF and oxidized phospholipids, i.e. bioactive lipids that are involved in the pathophysiology of atherosclerosis. Thus, PAF-AH may play a significant role in atherogenesis. Accumulating data indicate that PAF-AH associated with HDL particles plays a predominantly antiatherogenic role. By contrast, the role of LDL-associated PAF-AH remains controversial. Dyslipidemia induces a significant increase in total plasma PAF-AH activity and alters the enzyme distribution between proatherogenic apoB- and antiatherogenic apo AI-containing lipoproteins by increasing the PAF-AH activity associated with apoB-containing lipoproteins. The decreased rate of LDL removal from the circulation and the abnormal catabolism of triglyceride-rich lipoproteins play important roles in these abnormalities. Atorvastatin or fenofibrate therapy can restore, at least partially, the dyslipidemia-induced alterations in plasma PAF-AH by increasing the ratio of HDL-PAF-AH to plasma PAF-AH (or to LDL-cholesterol) levels, which may represent an important antiatherogenic effect of these hypolipidemic drugs.
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PMID:Effect of hypolipidemic drugs on lipoprotein-associated platelet activating factor acetylhydrolase. Implication for atherosclerosis. 1460 31

The paradigm of obesity leading to insulin resistance and type 2 diabetes is examined in relation to dyslipidemia, which typically consists of high levels of triglycerides (TG) and low levels of high-density lipoprotein (HDL). Kinetic studies with stable isotope-labeled amino acid precursors have shown that the development of visceral obesity, as well as type 2 diabetes, leads to overproduction of the apolipoprotein B-100 and TG in very low-density lipoproteins. Elevated plasma levels or increased flux of albumin-bound free fatty acids to the liver appear to be underlying metabolic events in this process. Low levels of HDL are due to increased catabolism, which can be related to TG enrichment.
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PMID:Lipoprotein metabolism in obesity and diabetes: insights from stable isotope kinetic studies in humans. 1467 71

Patients with type 2 diabetes mellitus or the metabolic syndrome have a unique dyslipidemia characterized by hypertriglyceridemia; elevated blood levels of apolipoprotein B; small, dense low-density lipoprotein (LDL) cholesterol; and low levels of high-density lipoprotein (HDL) cholesterol, in particular HDL(2)-C. Treatment of the dyslipidemia associated with these disorders should focus on correcting the abnormal lipoprotein levels as well as LDL and HDL heterogeneity. Statins and fibrates are useful for treating elevated LDL in patients with and without diabetes or the metabolic syndrome. In addition, thiazolidinediones or niacin in combination with a statin show promise for correcting defects in LDL and HDL heterogeneity. The ultimate goal of treatment in this patient population is to prevent the development and progression of coronary artery disease.
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PMID:Dyslipidemia in the metabolic syndrome and type 2 diabetes mellitus. 1467 62

The dyslipidemia and insulin resistance of type 2 diabetes can be improved by aerobic exercise. The effect of 6 months supervised exercise on very low-density lipoprotein (VLDL) apolipoprotein B metabolism was investigated in patients with type 2 diabetes. Moderately obese patients (n = 18) were randomized into supervised (n = 9) and unsupervised (n = 9) exercise groups. All patients were given a training session and a personal exercise program and asked to exercise four times per week at 70% maximal oxygen uptake for 6 months. Patients in the supervised group had a weekly session with an exercise trainer. VLDL apolipoprotein (apo)B metabolism was measured with an infusion of 1-(13)C leucine before and after 6 months of the exercise program. Supervised exercise for 6 months resulted in a significant within-group decrease in percent hemoglobin A1c (P < 0.001), body fat (P < 0.004), nonesterified fatty acid (P < 0.04), and triglycerides (P < 0.05) and an increase in insulin sensitivity (P < 0.01). There was a decrease in VLDL apoB pool size (160.8 +/- 42.6 to 84.9 +/- 23.2 mg, P < 0.01) and VLDL apoB secretion rate (11.3 +/- 2.6 to 5.5 +/- 2.0 mg/kg.d, P < 0.05) with no change in fractional catabolic rate. In a between-group comparison, the decrease in VLDL apoB secretion rate in the supervised group did not achieve significance. This study demonstrates that in type 2 diabetes, a supervised exercise program reduces VLDL apoB pool size, which may be due to a decrease in VLDL apoB secretion rate.
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PMID:The effect of a six-month exercise program on very low-density lipoprotein apolipoprotein B secretion in type 2 diabetes. 1476 82

Several animal models have been used to investigate the mechanisms of atherogenesis. Each animal species has advantages and disadvantages with regard to similarity with human lipoprotein metabolism. In humans, fractional esterification rate in apolipoprotein B-depleted plasma (FER(HDL)) has been shown to correlate with the quality of high density lipoprotein particles. Increased values of FER(HDL) indicate an atherogenic lipoprotein profile. Such an association has not been defined in animal models. Thus, we have characterized plasma lipoprotein profile and FER(HDL) values in four animal species namely, cats, pigs, guinea pigs and rabbits. These animal species have been used in experimental dyslipidemia and atherosclerosis. Our data indicate a wide rage of variations among various animal species. High-density lipoprotein (HDL) particles contain approximately 40% of total plasma cholesterol concentrations in rabbits, pigs and cats <10% in guinea pigs. A negative association between FER(HDL) values and plasma HDL-cholesterol levels was observed in pigs, rabbits and guinea pigs. On the other hand, FER(HDL) values showed a positive association with plasma triglyceride levels in all animal species tested. These findings are in agreement with data reported in humans. More research is needed to identify the better animal models which closely resemble human lipoprotein metabolism.
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PMID:Species-related variations in lipoprotein metabolism: the impact of FER(HDL) on susceptibility to atherogenesis. 1499 21


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