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)

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.
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PMID:A kindred of familial combined hyperlipidemia (FCHL) with proband showing type V hyperlipoproteinemia. 377 23

Alterations in plasma lipoprotein lipid and apoprotein accompanying the hyperlipidemia of rats bearing Morris hepatoma 7288C were characterized. In tumor-bearing animals all plasma lipid classes except cholesterol ester (CE) were elevated, particularly free cholesterol (FC) and triglyceride (TG), which increased by 57 and 63%, respectively. Fasting only partially reduced the tumor-induced hyperlipidemia and had no effect on the ratios of FC/CE and TG/CE. Analysis of plasma lipoproteins revealed an elevation of VLDL, IDL, and LDL in host rats, with more than a 2-fold increase in both lipid and protein of VLDL. In contrast, the three high density fractions, HDL2, HDL3, and d greater than 1.21 g/ml, were reduced. The inverse changes in concentration of host lipoproteins of lower versus higher density indicate a defective catabolism of TG-rich lipoprotein. This possibility is supported by the analysis of apolipoprotein. The percentage of total apoprotein contributed by apo C-I and C-II was reduced in all host fractions except HDL2, while the C-IIIs remained unchanged except for a small decrease in C-III-3 of host VLDL and a slight increase in the combined C-IIIs of HDL2. These changes were reflected in the decreased C-I+C-II/C-III ratios of all host lipoprotein fractions. Apo E levels remained similar to control values except for a significant decrease in HDL2. Host VLDL showed increased apo A-IV and A-I content, while A-IV was decreased in HDL2. Changes in apo B profiles were also observed.
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PMID:Characterization of alterations in plasma lipoprotein lipid and apoprotein profiles accompanying hepatoma-induced hyperlipidemia in rats. 394 72

Diet is the common denominator in the treatment of hyperlipidemia. Calorie and alcohol restriction are often prescribed for hypertriglyceridemic subjects. When these subjects lose weight their serum triglycerides often decrease, secondary to a diminution in hepatic triglyceride secretion. There is also a reduction in insulin resistance leading to an improvement in carbohydrate tolerance. Because some hypertriglyceridemic subjects over-synthesize triglycerides after alcohol ingestion, alcohol restriction is important in the dietary therapy of these patients. Although controversial, the restriction of cholesterol and saturated fat intake is often prescribed for hypercholesterolemic subjects. Recent evidence show (a) As the daily absolute cholesterol intake increases, the % absorbed is decreased but the amount absorbed per kg body weight is increased. (b) Hypercholesterolemic subjects differ from normal subjects in their response to cholesterol and fat intake. (c) A high cholesterol and high saturated fat diet increases the cholesterol concentration in all lipoprotein fractions. A low cholesterol and high polyunsaturated fat diet has the opposite effect. (d) These diets also affect serum apoprotein levels (apo B and apo A-I). It is becoming evident that hyperlipidemic subjects respond differently from normal subjects to dietary changes. For these subjects, at greater risk of developing atherosclerosis, dietary therapy is important.
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PMID:Dietary therapy of hyperlipoproteinemias: new understandings. 628 14

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.
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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.
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PMID:Plasma lipoproteins in familial combined hyperlipidemia and monogenic familial hypertriglyceridemia. 640 42

Serum lipids, apoprotein and lecithin-cholesterol acyltransferase activities were studied in 27 renal transplant recipients with stable and normal renal function (serum creatinine 0.16 mM/l or less) sustained for more than 1 year following grafting. Hypertriglyceridemia, which was characteristic of hyperlipidemia in 18 hemodialyzed patients with chronic renal failure, was no longer manifest in transplant recipients. On the other hand, de novo hypercholesterolemia was observed posttransplant with mean serum levels of 5.82 +/- 1.34 versus 5.01 +/- 0.88 mM/l in 575 normal controls. As to the high-density lipoprotein metabolism, the cholesterol content (1.72 +/- 0.56 mM/l) was significantly higher in transplant patients than in hemodialyzed patients (0.82 +/- 0.31 mM/l). In contrast, no variation in apoprotein A-I levels was found between both groups of patients, which produced an elevated high-density lipoprotein cholesterol:apoprotein A-I ratio. Thus, derangement in the serum lipid profile, although qualitatively different, continued to be present following transplantation, and its relevance to the cardiovascular morbidity in these patients remains to be evaluated.
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PMID:De novo development of hypercholesterolemia and elevated high-density lipoprotein cholesterol: apoprotein A-I ratio in patients with chronic renal failure following kidney transplantation. 641 53

An esterifying activity of blood plasma (lecithin-cholesterol-acyl transferase, LCAT) was decreased in men with ischemic heart disease (IHD) and coronary atherosclerosis as compared with patients without any symptoms of IHD; the decrease of the activity was most distinct in patients with low level of cholesterol in high density lipoproteins (HDL) and with hyperlipidemia. In these patients phospholipid composition of HDL subfractions was altered: a decrease in the lecithin ratio, increase in the content of sphingomyelin and corresponding decrease in the ratio lecithin/sphingomyelin. Decrease in content of HDL cholesterol and in concentration of apo A-I in blood, plasma, alterations in phospholipid composition of HDL subfractions and in the rate of fatty acids unsaturation of HDL phospholipids in the patients with IHD were considered as factors responsible for the decrease of LCAT activity, which may aggravate the atherosclerotic impairment of arteries.
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PMID:[Esterifying activity of the plasma in patients with ischemic heart disease]. 652 15

The effects on serum lipoproteins were studied in 8 patients with familial heterozygous hypercholesterolemia and 9 patients with familial combined hyperlipidemia during an 8-week treatment with fenofibrate. VLDL, IDL, LDL and HDL were isolated by ultracentrifugation and precipitation. Lipids and apolipoproteins A-I and B were determined by enzymatic and immunonephelometric techniques, respectively. In hypercholesterolemia, administration of fenofibrate resulted in decreases of VLDL, IDL, and LDL (cholesterol -58.3%, -28.6%, and -24.4%), while, in combined hyperlipidemia, treatment with the drug lowered VLDL and IDL (-33.3% and -42.9%). HDL cholesterol and apolipoprotein A-I increased only in hypercholesterolemia (+22.9% and +6.9%).
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PMID:Effect of fenofibrate on serum lipoproteins in subjects with familial hypercholesterolemia and combined hyperlipidemia. 652 48

Hyperlipidemia associated with hypothyroidism is well documented in man and several animal species. The effect of hypothyroidism on apolipoprotein metabolism in the absence of complicating factors such as high cholesterol or fat content in the diet is virtually unknown. Hypothyroidism was therefore induced in male Sprague-Dawley rats by radiothyroidectomy (RTx-treated) or treatment with propylthiouracil (PTU-treated). Both treatments resulted in an over 90% decrease in circulating thyroid hormone concentrations accompanied by a 50-100% increase in plasma cholesterol and a 20-40% reduction in plasma triglyceride concentrations. Plasma apo E and apo B concentrations increased by 100% in the PTU-treated group and 40-50% in the RTx-group. Apo A-I increased 10 and 30% in the RTx- and PTU-treated rats, respectively, while the concentration of apo A-IV was not altered. A large increase in the low-density (LDL) and high-density lipoprotein (HDL) protein was observed and accompanied by a marked reduction of very low density lipoprotein (VLDL) in the hypothyroid rats. The electrophoretic pattern of plasma lipoproteins in the hypothyroid rats was changed by the appearance of a slow pre-beta band shown to be beta-VLDL. A redistribution of apo B occurred within the lipoprotein fractions. Apo B content in the VLDL fraction decreased and a large increase was noted in LDL. The major portion of the apo E and apo A-I increment was recovered in the HDL and to a lesser degree in LDL. An accumulation of apo E-rich larger HDL particles, resembling HDLc in apolipoprotein composition and distinct from the apo A-I-containing species, was observed by column chromatography. The results presented are consistent with the hypothesis that hypothyroidism in the rat may induce an accelerated production of VLDL catabolic remnants, including LDL, but at the same time reduce the rate of removal of these lipoproteins from the circulation.
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PMID:Rat plasma lipoproteins and apolipoproteins in experimental hypothyroidism. 678 58

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.
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PMID:Effects of oral and intravenous fat administration on the levels of apoproteins A-I, A-II and C-III in human. 680 12


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