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)

Several parameters of lipoprotein metabolism were examined in 38 men with primary hypertriglyceridemia (phenotype IV). Family investigation showed that 17 men had familial combined hyperlipidemia (FCH), seven had familial hypertriglyceridemia (FHT), and 14 had unclassified hypertriglyceridemia (UNC). In all three groups, plasma high density lipoprotein (HDL) cholesterol and the concentrations of apolipoprotein A-I and A-II were decreased, and apolipoprotein B was increased, each to the same extent. These results are compatible with an increased risk of cardiovascular disease in both FCH and FHT patients. The mean concentration of LDL cholesterol and the ratio of LDL to HDL cholesterol were significantly higher in FCH subjects, which could explain their increased risk. Postheparin lipoprotein lipase and hepatic lipase were the same in both groups. Determination of apolipoprotein C composition, which may modulate lipoprotein lipase activity, did not reveal any abnormalities in the different groups. In both FCH and FHT, the mean turnover rate of plasma triglycerides was almost twice normal, indicating that overproduction of plasma triglyceride plays an important role in both disorders. However, there was an overlap with normal controls, indicating impaired triglyceride removal in some subjects. The underlying mechanism of hypertriglyceridemia in FCH and FHT therefore seems to be heterogeneous.
 ...
PMID:Plasma lipoproteins, apolipoproteins, and triglyceride metabolism in familial hypertriglyceridemia. 372 96

A case of familial hyperlipidemia incidentally found through a 16 year-old high school girl with type V hyperlipoproteinemia and abdominal bouts consistent with this type of hyperlipemia is reported for the first time in Japan. The laboratory findings of the plasma of her father revealed typical hyperlipoproteinemia of type IIa. Nineteen of her 26 kindred were investigated. Type V was seen only in the proband, type IIa in father, paternal grandmother, two paternal aunts, and two paternal cousins, type IV in three paternal cousins. The serum apolipoprotein (apo A-I, A-II, B, C-II, C-III, and E) concentrations were determined by the single radial immunodiffusion technique. The apolipoprotein concentrations were not different from those of normolipidemic control subjects except for apo B, which was higher in the hyperlipidemic members, and apo C-II, C-III, and E, which were higher in the proband.
 ...
PMID:A kindred of familial combined hyperlipidemia (FCHL) with proband showing type V hyperlipoproteinemia. 377 23

A quantitative automated immunoturbidimetric procedure for the analysis of apolipoprotein A-II (Apo A-II) in human serum is described. Dilution of antibody with a 5% solution of PEG 6000 enhanced the quantification. The within- and between-assay coefficients of variation were less than 5%. Results correlated well with those obtained by classic electroimmunodiffusion and immunonephelometry. No extraction of samples with organic solvent was necessary, whatever the triglyceride concentration. Large lipoproteins such as VLDL and immunocomplexes did not affect the method, nor was there interference from icteric or hemolyzed serum or from serum with excessive hyperlipemia. Physiological values of Apo A-II were determined in a normal population. Concentrations were found to be age-dependent, and higher in women than in men. The procedure is very suitable for the rapid, precise, reproducible and inexpensive assay of Apo A-II.
 ...
PMID:Automated immunoturbidimetric assay of serum apolipoprotein A-II using the Cobas-Bio centrifugal analyser: influence of hyperlipoproteinemia. 393 44

Triglyceridemic response to a standard oral fat meal was determined in 28 healthy subjects and related to the levels of several lipids, lipoproteins, and apolipoproteins in the post-absorptive plasma. A fatty test meal was administered orally, and postprandial plasma triglyceride levels were determined. In the fasting blood samples, concentrations of apolipoproteins (apo) A-I, A-II, and B were determined by radioimmunoassay, and those of high density lipoprotein (HDL) subfractions HDL2 and HDL3, by zonal ultracentrifugation. The magnitude of triglyceridemic response showed a negative correlation with the plasma levels of HDL2 (r = -0.860, P less than 0.001), HDL-associated cholesterol (r = -0.605, P less than 0.001), and apoA-I (r = -0.459, P less than 0.02). No correlation was found between the triglyceridemic response and the levels of total cholesterol, HDL3, and apoA-II. Triglyceridemic response was correlated positively with fasting triglyceride concentrations (r = 0.450, P less than 0.02) and apoB levels (r = 0.396, P less than 0.03). In two subjects followed for 3 yr, when HDL2 levels rose or fell, the triglyceridemic response decreased or increased, respectively (r = -0.944; r = -0.863). Our data indicate that normolipidemic individuals with high HDL2 levels in the plasma are able to clear alimentary fat at a faster rate than normolipidemic subjects with low HDL2 levels. The pronounced difference in severity and duration of postprandial lipemia among subjects with varying HDL2 levels may help to explain the negative correlation between the risk of atherosclerosis and HDL cholesterol levels.
 ...
PMID:Inverse relationship between blood levels of high density lipoprotein subfraction 2 and magnitude of postprandial lipemia. 640 80

Plasma lipoprotein concentration, composition, and size were evaluated in two common familial forms of hypertriglyceridemia and compared with those in normal subjects. The very low density lipoproteins (VLDL) were triglyceride-enriched in familial hypertriglyceridemia (triglyceride/apoprotein B ratio: 25.7 +/- 8.9) as compared to normal (9.6 +/- 12.2, P < 0.001) or familial combined hyperlipidemia (9.7 +/- 3.3, P < 0.001). The diameter of VLDL was larger in familial hypertriglyceridemia (3.27 +/- 0.28 pm) than in familial combined hyperlipidemia (2.87 +/- 0.16 pm, P < 0.02). Although in familial hypertriglyceridemia VLDL tended to be larger, and in familial combined hyperlipidemia VLDL tended to be smaller than normal (3.08 +/- 0.48 pm), neither of these differences were significant. While VLDL was normally distributed in the control population, the size was skewed to larger particles in familial hypertriglyceridemia with fewer small particles (P < 0.05) and skewed to smaller particles in familial combined hyperlipidemia with fewer large particles (P < 0.05). VLDL was reciprocally related to low density lipoproteins (LDL) in familial combined hyperlipidemia (r = -0.80 to -0.87) suggesting that the concentrations of these individual lipoprotein groups were somehow interrelated. There was no significant relationship between these two lipoprotein classes in familial hypertriglyceridemia or in normals. In familial combined hyperlipidemia, the apoprotein A-I/A-II ratio was below normal (P < 0.01) suggestive of low HDL(2) levels. This change in apoprotein composition was independent of VLDL or LDL concentration. In familial hypertriglyceridemia, high density lipoprotein (HDL) cholesterol was reduced (33% below mean normal) and HDL triglyceride was increased (by 46%), while the concentration of apoA-I and apoA-II was normal. VLDL triglyceride was inversely related to HDL cholesterol in familial hypertriglyceridemia (r = -0.74, P < 0.005), but not in familial combined hyperlipidemia. The large, triglyceride-enriched VLDL observed in familial hypertriglyceridemia is compatible with the reported increase in VLDL triglyceride synthesis seen in this disorder. The increase in VLDL apoprotein B synthesis previously reported in familial combined hyperlipidemia was associated with VLDL of normal composition. The changes in HDL cholesterol in these two disorders might reflect exchange of triglyceride between VLDL and HDL or could be related to transfer of surface components during the catabolism of VLDL. The reciprocal relationship between various components of VLDL and LDL seen in familial combined hyperlipidemia, but not in familial hypertriglyceridemia or in normal subjects, might provide some insight into the pathological abnormalities in these disorders. The differences between these two common familial forms of hypertriglyceridemia provide further support that they are distinct entities.-Brunzell, J. D., J. J. Albers, A. Chait, S. M. Grundy, E. Groszek, and G. B. McDonald. Plasma lipoproteins in familial combined hyperlipidemia and monogenic familial hypertriglyceridemia.
 ...
PMID:Plasma lipoproteins in familial combined hyperlipidemia and monogenic familial hypertriglyceridemia. 640 42

In order to study the effects of chronic alcoholism, 3 groups of patients were investigated and compared to 10 healthy controls. Group I consisted of 9 heavy drinkers, who exhibited type V hyperlipidemia (HLP) under alcohol intake. Group II consisted of 7 patients, who previously had type V HLP under the influence of alcohol. At the time of the investigation, however, they had ceased alcohol drinking for at least 6 months and were normolipidemic. Group III consisted of 7 heavy drinkers without hyperlipidemia. Compared to controls, group I had significantly decreased plasma concentrations of high density lipoproteins2 (HDL2) and HDL3 (both P less than 0.01); activities of post-heparin lipoprotein lipase (LPL) and hepatic lipase (HTGL) as well were excessively decreased (both P less than 0.01). In group III LPL was also decreased (P less than 0.01), but HTGL was distinctly (P less than 0.01) higher than in controls. No such differences could be demonstrated for the patients of group II. Acute alcohol withdrawal from a patient suffering from alcoholism with HLP led to a sharp increase of LPL with a simultaneous decrease of VLDL within 2 days and a more delayed increase of LDL, HDL2 and HTGL, all reaching normal values within 12 days after cessation of alcohol drinking. With respect to the apolipoprotein (apo) composition of HDL2, patients of group I and group III exhibited a significantly lower percentual content of apo C-I at the expense of a significantly higher content of apo A-II as compared to controls and patients of group II. In group I and II, the percentual content of apo D in HDL2 was significantly higher than in controls and in group III. It is concluded that severe alcohol intake strongly impairs LPL in patients with HLP. The pronounced increase of HTGL in some patients (group III) may protect these individuals from HLP. The increased content of apo D in HDL2 may be a possible primary trait for alcohol-inducible HLP.
 ...
PMID:Post-heparin lipolytic activities and alterations of the chemical composition of high density lipoproteins in alcohol-induced type V hyperlipidemia. 649 35

Changes of plasma levels of apoproteins A-I, A-II and C-III were determined after oral and intravenous fat administration. The A-I levels increased in three out of four subjects after fat ingestion but no changes or even a slight decrease in the levels of A-I were observed after intravenous fat infusion. The A-II levels also increased after fat ingestion in two subjects but the levels either did not change or decreased slightly after fat infusion. The levels of C-III increased concomitantly with the increase of triglyceride levels after fat ingestion as well as fat infusion . After intravenous fat infusion, part of the C-III in the d greater 1.006 fraction shifted to the lighter fraction (d less than 1.006). These observations suggest that the increase in the levels of A-I and A-II after fat ingestion are a consequence of an increase in apoprotein synthesis in the intestine during fat absorption. The increase in the levels of C-III after fat ingestion as well as fat infusion seemed to be related to the capture of C-III inthe triglyceride rich particles, i.e. C-III accumulated in the circulation with triglyceride-rich particles. However, it appeared also to be possible that the rate of C-III synthesis increases during hyperlipidemia induced by fat infusion.
 ...
PMID:Effects of oral and intravenous fat administration on the levels of apoproteins A-I, A-II and C-III in human. 680 12

The effects of gemfibrozil on serum lipids and apolipoproteins were investigated in 60 male survivors of myocardial infarction (MI) (age range 29-48 years, mean 44). Fifteen had normal serum cholesterol (less than or equal to 7.0 mmol/l) and triglyceride (less than or equal to 1.7 mmol/l) levels, but most had low levels of high density lipoprotein (HDL) cholesterol (less than 1.00 mmol/l). Ten had type II A, 27 type II B and 8 type IV hyperlipidaemia. A double-blind placebo-controlled cross-over design was used with 3-month treatment periods. Gemfibrozil was given in daily doses of 1200 mg. The drug was well tolerated and there were no drop-outs attributable to its use. In all subjects, gemfibrozil reduced the mean serum total cholesterol by 17% and triglycerides by 54% and increased HDL cholesterol by 16%. The percentage HDL cholesterol of total cholesterol increased from 14 to 19%. The changes were similar in patients with normal serum cholesterol and triglyceride values and in those with classical hyperlipidaemias. In contrast, the changes during placebo treatment corresponded to those in healthy male untreated controls who were followed simultaneously. Apoprotein A-I remained unchanged, but A-II increased by 20% during gemfibrozil treatment. It is concluded that gemfibrozil corrects effectively dyslipidaemias in male MI patients but further long-term studies are warranted.
 ...
PMID:Gemfibrozil in the treatment of dyslipidaemias in middle-aged male survivors of myocardial infarction. 701 Sep 29

The relationship of VLDL-, LDL-, HDL-cholesterol, VLDL-triglycerides and of apolipoproteins A-I, A-II and apo-D has been studied in 89 survivors of myocardial infarction and in 80 age- and sex-matched controls. The two groups as a whole were analysed as well as sub-groups of subjects divided according to their lipid phenotype (normolipidaemic, IIA, IIB and IV). The data support the view that plasma levels of apo-B and apoA-I as well as their ratio and the TC/apo-B and LDL-C/apo-B ratios are better indicators of lipid derangement in survivors of myocardial infarction than the levels of LDL-cholesterol and HDL-cholesterol. Total cholesterol, total triglycerides, VLDL-cholesterol and VLDL-triglycerides are of no help in discriminating between the two series. The VLDL-C/VLDL-TG ratio in survivors is, however, very close to the ratio thought to be peculiar to type III hyperlipidaemia.
 ...
PMID:Relationship between apolipoproteins and chemical components of lipoproteins in survivors of myocardial infarction. 742 89

In view of the evidence linking plasma high density lipoprotein (HDL)-cholesterol levels to a protective effect against coronary artery disease and the widespread use of fibrates in the treatment of hyperlipidemia, the goal of this study was to analyze the influence of fibrates on the expression of apolipoprotein (apo) A-II, a major protein constituent of HDL. Administration of fenofibrate (300 mg/d) to 16 patients with coronary artery disease resulted in a marked increase in plasma apo A-II concentrations (0.34 +/- 0.11 to 0.45 +/- 0.17 grams/liter; P < 0.01). This increase in plasma apo A-II was due to a direct effect on hepatic apo A-II production, since fenofibric acid induced apo A-II mRNA levels to 450 and 250% of control levels in primary cultures of human hepatocytes and in human hepatoblastoma HepG2 cells respectively. The induction in apo A-II mRNA levels was followed by an increase in apo A-II secretion in both cell culture systems. Transient transfection experiments of a reporter construct driven by the human apo A-II gene promoter indicated that fenofibrate induced apo A-II gene expression at the transcriptional level. Furthermore, several other peroxisome proliferators, such as the fibrate, Wy-14643, and the fatty acid, eicosatetraynoic acid (ETYA), also induced apo A-II gene transcription. Unilateral deletions and site-directed mutagenesis identified a sequence element located in the J-site of the apo A-II promoter mediating the responsiveness to fibrates and fatty acids. This element contains two imperfect half sites spaced by 1 oligonucleotide similar to a peroxisome proliferator responsive element (PPRE). Cotransfection assays showed that the peroxisome proliferator activated receptor (PPAR) transactivates the apo A-II promoter through this AII-PPRE. Gel retardation assays demonstrated that PPAR binds to the AII-PPRE with an affinity comparable to its binding affinity to the acyl coA oxidase (ACO)-PPRE. In conclusion, in humans fibrates increase plasma apo A-II concentrations by inducing hepatic apo A-II production. Apo A-II expression is regulated at the transcriptional level by fibrates and fatty acids via the interaction of PPAR with the AII-PPRE, thereby demonstrating the pivotal role of PPAR in controlling human lipoprotein metabolism.
 ...
PMID:Fibrates increase human apolipoprotein A-II expression through activation of the peroxisome proliferator-activated receptor. 763 67


<< Previous 1 2 3 4 5 Next >>