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

The purpose of this study was to examine the change in apolipoprotein and lipoprotein levels in patients with normolipidemic untreated non-insulin-dependent diabetes mellitus (NIDDM). Fifteen untreated, non-obese male NIDDM patients without hyperlipidemia were chosen, and 15 healthy subjects, matched for age, sex, body weight, alcohol consumption and cigarette smoking served as the control group. We observed that the concentrations of plasma total cholesterol (TC), triacylglycerol (TG) and very low density lipoprotein cholesterol (VLDL-C) were identical in both NIDDM and control groups. The levels of low-density lipoprotein cholesterol (LDL-C) were slightly increased in the diabetic group, but the difference did not reach statistical significance in our study. High-density lipoprotein cholesterol (HDL-C) was lower in the NIDDM group than in the controls. Significantly increased TC/HDL-C and LDL-C/HDL-C ratios were found in NIDDM patients compared with controls. The apolipoprotein A-I (apo A-I) and apolipoprotein A-II (apo A-II) levels were decreased in NIDDM patients, while the apolipoprotein B (apo B) level remained similar to that of the control subjects. The ratio of apo A-I/apo B was decreased significantly in the NIDDM group. Our results suggest that NIDDM patients are at higher risk of coronary heart disease, even if they remain normolipidemic.
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PMID:Apolipoprotein levels in normolipidemic non-insulin-dependent diabetes mellitus. 135 44

In order to establish the reference ranges of lipids and apolipoproteins apoA-I and apoB in serum for different periods of pregnancy we examined 719 healthy pregnant women. 172 of them were in the first trimester, 227 in the second and 320 in the third trimester. The control group, consisting of 65 healthy nonpregnant women, was used to determine the magnitude and statistical significance of the lipid changes. All lipids and apolipoproteins apoA-I and apoB were significantly elevated during the second and the third trimesters. The most prominent change was a 2.7-fold triglyceride increase in the third trimester; in the same trimester the mean level apoB increased by 56%, total cholesterol by 43%, low-density lipoprotein (LDL) cholesterol by 36% and apolipoprotein A-I by 32%. High-density lipoprotein (HDL) cholesterol rose maximally (25%) in the second trimester. The 95th percentiles of the distributions in the second and the third trimesters are: total triglyceride: 2.87 and 4.68 mmol/l; total cholesterol: 8.24 and 9.83 mmol/l; LDL-cholesterol: 5.61 and 6.48 mmol/l; apoA-I: 2.48 and 2.61 g/l; apoB: 1.47 and 1.92 g/l. The fifth percentiles of HDL-cholesterol distributions are: 1.09 in the second trimester and 1.04 in the third one. The ratios of total cholesterol to HDL-cholesterol, of LDL-cholesterol to HDL-cholesterol and apoB to apoA-I were decreased in the first trimester, without change in the second, and increased in the third trimester. These data may indicate that hyperlipidaemia of pregnancy is not atherogenic.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Reference ranges of lipids and apolipoproteins in pregnancy. 161 59

The study objective was to determine the effects of monotherapy with clonidine and atenolol versus placebo on serum lipids, apolipoproteins, and blood pressure in patients with mild primary hypertension. The protocol comprised a double blind, randomized, placebo-controlled 5-month prospective study carried out in an outpatient general internal medicine clinic in a university medical center. There were 92 patients ages 18 to 70, with mild primary hypertension (sitting diastolic blood pressure of greater than 90 mm Hg and less than 105 mm Hg) without significant cardiac, renal, cerebrovascular, hepatic, neoplastic, or hematologic disorders. Patients with severe hyperlipidemia or peripheral vascular disease were also excluded. All factors known to effect serum lipids were held constant throughout the study (i.e., diet, weight, exercise, caffeine, tobacco). Atenolol and clonidine significantly reduced blood pressure when compared with placebo. Atenolol caused significant increases in serum triglycerides and apolipoprotein B (p less than 0.05) and significant reductions in high-density lipoprotein-cholesterol, apolipoproteins A-I and A-II (p less than 0.05). Atenolol also induced a significant adverse effect on all lipid ratios, increasing total cholesterol/high density lipoprotein-cholesterol, low density lipoprotein-cholesterol/high density lipoprotein-cholesterol, apolipoprotein B/apolipoprotein A-I and apolipoprotein B/apolipoprotein A-II ratios and decreasing low density lipoprotein-cholesterol/apolipoprotein-B ratio (p less than 0.05). Clonidine caused significant reductions in high-density lipoprotein-cholesterol, apolipoproteins AI and AII (p less than 0.05 but was neutral on all other lipids, lipid subfractions, and apolipoproteins. Clonidine did not significantly alter any of the lipid ratios.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effects of clonidine hydrochloride versus atenolol monotherapy on serum lipids, lipid subfractions, and apolipoproteins in mild hypertension. 219 93

A causal link between hypercholesterolemia due to elevated plasma concentrations of LDL and VLDL remnants of CAPD patients has been established. The effects of 24 weeks of treatment with Simvastatin, a new HMG coenzyme A-reductase inhibitor (at 20 and 40 mg/day) on serum lipid, lipoprotein, and apolipoprotein A-I and B concentrations, as well as safety parameters and subjective side effects, were evaluated in eight patients (mean duration CAPD 24.80 +/- 7.50 months, age 54.50 +/- 13.70 years). Maximal effects on plasma lipoprotein and apolipoprotein concentrations were achieved after 4 weeks, and remained stable thereafter during the study. Mean fasting plasma cholesterol concentrations decreased from 280.5 +/- 60.2 mg% to 190.2 +/- 40.4 mg/dl (p less than 0.005) (-47%); mean plasma LDL-cholesterol concentrations also decreased from 257.6 +/- 13.4 mg% to 190.5 +/- 15.4 mg/dl (p less than 0.001) (-35%). Apolipoprotein A and B concentrations decreased significantly from 1.78 +/- 0.19 to 1.40 +/- 0.22 g/L (p less than .005) and 1.81 +/- 0.26 to 1.38 +/- 0.20 g/L (p less than .005). These data substantiate the view that Simvastatin is well tolerated and that no serious clinical or adverse laboratory effects have been observed. It appears to be a promising drug for the effective control of hyperlipemia in a large proportion of hypercholesterolemic patients, reducing their cardiovascular morbidity while on CAPD.
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PMID:Therapeutic effects of simvastatin on hyperlipidemia in CAPD patients. 225 55

In a long-term longitudinal study of gestational diabetes mellitus in Black women, risk factors that were identified were age, obesity, a family history of diabetes, and the presence of hypertension. Poor predictors were a history of a previous large-for-date infant, parity, and age at first pregnancy. The prevalence of smooth muscle and nuclear autoantibodies was higher in gestational diabetic subjects. Gestational diabetic subjects who required insulin for glycemic control were more obese, had a lower frequency of the Bf-F phenotype and a higher frequency of the Bf-F1 phenotype, and had a lower frequency of the type 2 allele at the polymorphic locus adjacent to the insulin gene. Restriction-fragment-length polymorphisms flanking the insulin and apolipoprotein A-I and C-III genes, although not associated with gestational diabetes mellitus, may be associated with hyperlipidemia and subsequent atherosclerosis.
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PMID:Risk factors for gestational diabetes in black population. 226 42

Many patients with high levels of serum total cholesterol have a concomitant elevation of serum triglyceride levels and thus have mixed hyperlipidemia. In this study, 13 patients with mixed hyperlipidemia were treated with the cholesterol-lowering drug lovastatin to determine its effectiveness. In 9 of these patients, lovastatin therapy used alone was compared with the drug combination of lovastatin and gemfibrozil. In the 13 patients, lovastatin therapy produced a 31% reduction in total cholesterol level and a 32% decrease in triglyceride levels compared with placebo. It lowered very-low-density plus intermediate-density lipoprotein cholesterol levels by 40%, low-density lipoprotein cholesterol levels by 36%, and total apolipoprotein B levels by 28%. Concentrations of high-density lipoprotein cholesterol and apolipoprotein A-I were unchanged, but total cholesterol (and low-density lipoprotein cholesterol)/high-density lipoprotein cholesterol ratios were markedly reduced. Compared with lovastatin alone, lovastatin plus gemfibrozil produced greater decreases in very-low-density plus intermediate-density lipoprotein cholesterol levels and an increase in high-density lipoprotein cholesterol levels, but, in view of the higher risk for severe myopathy with this combination, lovastatin used alone may be adequate therapy for many patients with mixed hyperlipidemia.
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PMID:Management of primary mixed hyperlipidemia with lovastatin. 235 64

Familial dyslipidemic hypertension (FDH) is a syndrome recently described from sibships selected for early familial hypertension and found to have one or more of three fasting lipid abnormalities [high triglycerides, low high density lipoprotein (HDL) cholesterol, high low density lipoprotein (LDL) cholesterol]. In further analyses of these same 131 hypertensive subjects, apolipoprotein A-I and B, fasting plasma insulin (adjusted for body mass index), and detailed anthropometrics were different in two subgroups of FDH. Of 63 FDH patients, 19 met the criteria for familial combined hyperlipidemia (FCHL); 44 did not, but still had high triglyceride and/or low HDL cholesterol levels. When compared to 20 normolipidemic hypertensive patients, the 19 hypertensive patients with FCHL had 196% higher very low density lipoprotein cholesterol (p = 0.0001), 33% higher apolipoprotein B (p = 0.0002), smaller LDL particles (p = 0.007), and 73% higher fasting insulin (p = 0.003), but no significant differences in body mass index or skinfold thicknesses. The other 44 FDH patients without FCHL had 33% lower HDL (p = 0.0001), with only 8% lower apolipoprotein A-I levels (p = 0.20); significantly higher subscapular skinfolds (p = 0.02), weights (p = 0.002), body mass index (p = 0.006), knee widths (p = 0.0007), and wrist circumferences (p = 0.0009); smaller, denser LDL subfractions (p = 0.001); and increased apolipoprotein B levels (p = 0.01) compared to the normolipidemic hypertensive group. Increased fasting insulin levels were similar to the normolipidemic group and significantly lower than the FCHL group after adjustment for body mass index, suggesting a relationship between obesity and fasting insulin levels only in the non-FCHL group. We conclude that FDH consists of at least two subgroups: 1) FCHL with high apolipoprotein B, small LDL particles, and increased fasting plasma insulin levels, and 2) a less well-defined residual having upper central obesity with low HDL cholesterol and high triglyceride levels. Elevated insulin levels found in both groups, but possibly originating through different physiological mechanisms, may provide the pathophysiological connections between dyslipidemia, obesity, and hypertension.
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PMID:Apolipoprotein, low density lipoprotein subfraction, and insulin associations with familial combined hyperlipidemia. Study of Utah patients with familial dyslipidemic hypertension. 249 19

Two DNA polymorphisms adjacent to the apolipoprotein A-I/C-III and insulin genes have been suggested to be associated with hypertriglyceridemia and increased risk of coronary heart disease. Using cloned apolipoprotein A-I and insulin gene probes, we determined the genotypes of 39 subjects from six different kindreds with familial clustering of hypertriglyceridemia, 20 additional unrelated subjects with hypertriglyceridemia, 39 patients with angiographically confirmed coronary heart disease (CHD) and 61 normolipemic control subjects. The S2 allele bearing an additional SstI restriction site in the apo A-I/C-III complex was found in 16% of healthy controls, 23% of patients with CHD and 62% (P less than 0.001 when compared to controls) of unrelated subjects with hypertriglyceridemia. Among CHD patients the S2 allele was present in 6 out of 14 hypertriglyceridemic patients but only 3 out of 25 normotriglyceridemic patients (P less than 0.05). The S2 allele was present in 64% of subjects from kindreds with hypertriglyceridemia but this allele did not determine the occurrence of hyperlipidemia. The frequencies of the large size or U allele of the polymorphic DNA region flanking the 5' end of the insulin gene in CHD patients (33%) and in controls (24%) were not significantly different. Neither of the polymorphisms studied was associated with changes in serum LDL or HDL cholesterol levels in patients with CHD or unrelated subjects with hypertriglyceridemia. The data suggest that, at least in the Finnish population, the S2 allele of the apolipoprotein A-I/C-III gene complex may serve as a genetic marker for hypertriglyceridemia, whereas both DNA polymorphisms studied are probably useless in determining individual risks of atherosclerosis.
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PMID:DNA polymorphisms of apolipoprotein A-I/C-III and insulin genes in familial hypertriglyceridemia and coronary heart disease. 311 75

The Program on the Surgical Control of Hyperlipidemias (POSCH) is a multicentered, randomized, secondary intervention trial assessing the effect of lipoprotein modification achieved by partial ileal bypass (PIB) on overall mortality rates and the course of coronary heart disease. Of the 838 participants, 396 (196 control and 200 surgical patients) have complete 5-year lipoprotein results and are the basis of this report. After PIB, total cholesterol level decreased 24 +/- 1.2% (mean +/- SEM) and low-density lipoprotein cholesterol level fell 38 +/- 1.5% in comparison with control subjects. High-density lipoprotein (HDL) cholesterol level was not changed by PIB; however, a significant decrease in HDL occurred over 5 years in the control group (41.7 +/- 0.7 mg/dl versus 39.5 +/- 0.6 mg/dl, p less than 0.05). This led to consistently higher HDL levels in the surgical group in comparison with control subjects after PIB. Very low-density lipoprotein cholesterol and triglyceride levels were higher in the surgery group than in control subjects (24 +/- 7.6% and 21 +/- 5.4% at 5 years). Apolipoprotein B-100 was significantly lower, and apolipoprotein A-I and HDL-2 were significantly higher in the surgery group. These lipoprotein changes are greater than have been reported from any previous trial of dietary or pharmacologic intervention, including the Lipid Research Clinics-Coronary Primary Prevention Trial, which used cholestyramine. Based on available epidemiologic data, these changes predict a marked reduction in morbidity and mortality rates associated with coronary heart disease after PIB.
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PMID:Lipoprotein modification achieved by partial ileal bypass: five-year results of The Program on the Surgical Control of the Hyperlipidemias. 330 2

We investigated the effects of omega-3 fish oil (FO) supplementation on lipid metabolism, glycemic control, and blood pressure (BP) in patients with type II diabetes mellitus. In 22 diabetic patients without overt hyperlipidemia, serum triglyceride, total cholesterol, high density lipoprotein (HDL)-cholesterol, HDL2-cholesterol, HDL3-cholesterol, and apolipoprotein A-I (apo A-I) levels did not change during omega-3 FO supplementation for 8 weeks. The mean serum apo B concentration increased significantly [baseline, 2.56 +/- 0.11 (+/- SEM) mmol/L; 4 weeks, 2.82 +/- 0.13 mmol/L; 8 weeks, 2.80 +/- 0.13 mmol/L; P less than 0.01]. The mean plasma postheparin lipoprotein lipase activity increased transiently during the fourth week (baseline, 168 +/- 17 U/mL; 4 weeks, 182 +/- 18 U/mL; P less than 0.05), whereas postheparin hepatic triglyceride lipase activity did not change. Glycemic control worsened transiently during the fourth week, (baseline, 7.7 +/- 0.4%; 4 weeks, 8.4 +/- 0.3%; P less than 0.05). Both systolic and diastolic BP decreased significantly throughout the study (systolic BP: baseline, 142 +/- 5 mm Hg; 8 weeks, 128 +/- 5 mm Hg; diastolic BP: baseline, 88 +/- 4 mm Hg; 8 weeks, 80 +/- 3 mm Hg; P less than 0.01). These findings suggest that in type II diabetics without overt hyperlipidemia, omega-3 FO supplementation does not improve either the glycemic control or serum lipids, and it is associated with a potentially detrimental rise in serum apo B concentrations. Until more information is available, use of such supplementation should be discouraged.
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PMID:Effects of omega-3 fish oils on lipid metabolism, glycemic control, and blood pressure in type II diabetic patients. 337 25


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