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)

We propose a rapid enzymatic micromethod for the specific determination of lipase (EC 3.1.1.3) activity in serum and duodenal fluid. Free linoleic acid produced during 10-min incubation of 10 mul of sample with 1 ml of substrate (trillinolein emulsion) at 30 degrees C is converted by lipoxygenase (EC 1.99.2.1), in a coupled reaction, to its hydroperoxide, which is measured photometrically after solubilizing the reaction mixture in ethanol. Lipase activity is calculated from the rate of hydroperoxide formation, with linoleic acid as primary standard. The velocity of the reaction is greatest at pH 8.8, 35-37 degrees C, and a deoxycholate concentration of 3.6 mmol/liter. The energy of activation is 6.7 kcal/mol. The differing "apparent" Km values obtained for lipase in undiluted serum (4 X 10(-5) mol/liter) and in albumin-based diluents (1 X 10(-5) mol/liter) indicate the presence of a competitive inhibitor in the serum matrix. We detected no lipase activity in urine. Results by the proposed method correlate well with those by a copper soap extraction method (r = 0.95), but values are significantly higher for pancreatitis patients' sera (slope 1.6). The linear dynamic range extends to 1000 U/liter. Hemolysis, lipemia, and hyperbilirubinemia do not interfere. The normal range is 40-60 U/liter. Lipase activity of pancreatitis patients generally exceed 1000 U/liter during the acute phase and 250 U/liter for as long as 10 days after it.
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PMID:Lipoxygenic micromethod for specific determination of lipase activity in serum and duodenal fluid. 1 45

From 30 cases of mixed hyperlipidemia which were resistant to apparently correctly managed treatment, combining an adapted diet and Clofibrate, the authors confirmed that there is no specific clinical or laboratory picture in these cases: except for the constant presence of two beta-lipoproteins, with a high percentage of slow pre-beta, on electrophoresis on agarose, persisting throughout the length of inactive treatment. Analysis of the factors of resistance, whether exogenous and/or endogenous show that: bad adhesion to the "anticholesterol" diet (persistance of the supply of alcohol and/or sugar, insufficiency of unsaturated fats) and the incomplete reduction of a residual plethoric overload however minimal, constitute the two factors of resistance which are most easily picked out and overcome, but such factors are fat to be constantly causal. And in other cases, the contribution of drug interference or of considerable glycoregulation disorder remains to be excluded or discussed. In the absence of such factors or of their decisive role, a more specific cause of metabolic resistance had to be looked for. A disorder in Clofibrate mechanism, detected by gaseous chromatography in the form of an abnormal peak at C15 (clofibric acid) is found 12 hours or more after the last ingestion of the drug in certain cases. Binding of this molecule with VLDL, and perhaps with slow pre-betalipoprotens and nolonger with albumin, could explain the fault in metabolic clearance and in good metabolic utilization of this drug.
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PMID:[Mixed hyperlipidemia resistant to ordinary dietetic and medical treatment. 30 cases]. 17 69

Lipids, which serve as a source of energy and are an important constituent of cell membrane structure, are readily stored in the body. By definition they are insoluble in water. Specific proteins called apolipoproteins interact with lipids to form soluble lipid-protein complexes called lipoproteins. It is in this form that the major lipids--cholesterol, triglyceride and phospholipid--circulate in plasma. Unesterified fatty acids, another major lipid group, are bound to albumin in the circulation. The plasma lipoproteins are complex macromolecules composed of lipids, apolipoproteins and carbohydrates. The relative proportions of these components differ markedly between lipoprotein classes. Hyperlipidemia is a term used for increased concentrations of plasma cholesterol and/or triglycerides. Any one plasma lipid is present in several types of lipoproteins. Thus, hyperlipidemia implies the presence of hyperlipoproteinemia. The latter has important therapeutic implications. Most of the recent attempts at classification have been directed at the lipoprotein level of plasma lipid organization. Decreased concentrations of lipids in plasma can be achieved by altering the rates of metabolism of lipoproteins. Decrease in lipoprotein synthesis, increased catabolism or impaired release from cells into the blood stream may all result in a decrease of plasma lipids. Drugs which affect one or more of these factors are used to treat hyperlipoproteinemia. In order to elucidate the mechanism of action of hypolipidemic drugs it is necessary to understand the lipoprotein defect at the molecular level. This requires a more detailed knowledge of lipoprotein metabolism than is presently available for most of the hyperlipoproteinemias. This paper will review some of the generally accepted properties of the plasma lipoproteins, describe some difficulties which hamper the understanding of lipoprotein metabolism, and identify possible mechanisms by which drugs may affect lipoprotein metabolism.
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PMID:Importance of apolipoproteins in lipid metabolism. 20 49

An analbuminemic colony was established from Sprague-Dawley rats. Analbuminemia was inherited as an autosomal recessive trait. The rates of growth and reproduction of the mutant rats were no different from those of normal rats. Biochemically, the mutant was characterized by an extraordinarily low serum albumin content and a hyperlipidemia. Total serum protein in the mutant rat was similar to that of control Sprague-Dawley rats, with increased globulin. Serum cholesterol was inversely correlated with a decrease in albumin; the correlation coefficient for ablumin was --.92. These mutant rats may serve as a model of human familial analbuminemia and may also be useful in elucidating the functional roles of albumin.
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PMID:Albumin-deficient rat mutant. 45 21

Fasting plasma concentrations of triglycerides (TG), cholesterol, immunoreactive insulin (IRI), and blood glucose were raised in 16 children with chronic renal failure on regular haemodialysis compared with 18 healthy children. In the patients plasma IRI correlated positively with plasma TG, while blood glucose did not correlate with IRI or lipid concentrations. Dietary intake, expressed as percentage of recommended intake for height-age, did not correlate with plasma lipids, but there was a positive correlation between plasma TG and the proportion of calories derived from carbohydrate. The children were not malnourished as evidenced by normal plasma albumin and transferrin concentrations. The mechanism of the hyperlipidaemia is unclear but it may be related to the glucose intolerance with hyperinsulinaemia which is found in uraemia. In view of the risk of premature atherosclerosis, plasma lipid concentrations should be monitored in children with chronic renal failure and attempts made to ameliorate hyperlipidaemia with appropriate dietary manipulations.
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PMID:Hyperlipidaemia in children on regular haemodialysis. 60 69

Fasting serum triglyceride and cholesterol measurements, and lipoprotein characterization by ultracentrifugation, were performed in four groups of patients with chronic renal disease (uraemic, short- and long-term haemodialysis and renal transplant recipients) and the results compared with those obtained from age- and sex-matched control subjects. Basal insulin and growth hormone levels, and serum creatinine and albumin concentrations were measured in, and detailed dietary histories taken from patients in each group. The predominant lipid abnormalities were hypertriglyceridaemia and increased very low density lipoproteins (type IV hyperlipoproteinaemia) in both uraemic and haemodialysis patients. Following renal transplantation, a different pattern of hyperlipidaemia was found. Hypercholesterolaemia was more common and hypertriglyceridaemia less common than in the uraemic and haemodialysis group. The lipoprotein abnormalities were increased low density and/or very low density lipoproteins, with types IIa IIb and IV hyperlipoproteinaemia occurring equally frequently. In uraemic and haemodialysis patients, the proportion of carbohydrate in the diet was high, and may have played a role in the genesis of hypertriglyceridaemia. There was a positive correlation between relative body weight and serum triglyceride in the long-term dialysis group. In renal allograft recipients hypertriglyceridaemia could be attributed, at least in part, to obesity, prednisone dosage and the degree of impairment of graft function. The aetiology of hypercholesterolaemia in the transplant recipients was unclear. Neither basal insulin nor growth hormone levels were elevated in any patient group. Uraemic hypertriglyceridaemia is a clearly defined and well documented metabolic abnormality which is not corrected by dialysis. Post-transplantation hyperlipidaemia however, is a condition of variable presentation and multifactorial aetiology.
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PMID:Studies on the nature and causes of hyperlipidaemia in uraemia, maintenance dialysis and renal transplantation. 110 47

The relation between K2 and PHLA was studied in human subjects with special reference to clinical data determined by routine laboratory and physical examinations. The results obtained by Multiple Regression Analysis indicated that those factors which may contribute to K2 variation were fasting triglyceride level and age. There was an inverse partial correlation between K2 and fasting triglyceride level and between K2 and age. The first and second principal components calculated by Principal Component Analysis indicated that K2 is closely related to obesity and hyperlipidemia, especially hypertriglyceridemia, while PHLA related to albumin. These two components also suggested that K2 fibes different clinical information from that obtained by PHLA measurement. There was no partial correlation between K2 and PHLA. The various lipoprotein paper electrophoretic patterns, type IIa, type IIb, type IV and normal patterns, were clearly characterized by such factors as K2, plasma triglyceride and degree of obesity which has high coefficients in the first principal component.
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PMID:Study of an intravenous fat tolerance test with Intralipid. II. The relation between K2 and PHLA with special reference to clinical data in human subjects. 112 24

Studies were carried out in two patients with multiple myeloma (immunoglobulin G, [IgG], K light chain), cryoglobulinemia and xanthomatosis with clinical features and lipid transport abnormalities which were quite different. One patient had nodular xanthomatosis and lipemia with delayed triglyceride and apolipoprotein removal. In vivo heparin resistance was present and heparin-paraprotein interaction was shown in vitro. The lipoprotein removal defect may have been due to impaired uptake of the "remnants" of glyceride-rich lipoproteins. Abnormalities were found both in primary platelet aggregation and in the platelet release reaction. The second patient had diffuse plane xanthomatosis with normal lipids. An orange cryoprecipitate contained IgG, beta- and prebeta lipoproteins, albumin, carotenoids and about half of the serumcholesterol. Triglyceride turnover was normal. These observations show that M-proteins may interfere with lipid transport by at least two mechanisms and illustrate the clinical diversity of xanthomatous myeloma.
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PMID:Multiple myeloma, cryoglobulinemia and xanthomatosis. Distinct clinical and biochemical syndromes in two patients. 120 39

We present a comparative evaluation of two commercial kits, the "Quantitope" and "GammaCoat," for radioimmunoassay of digoxin in serum. These kits, in which iodine-125 is used as a label, proved to suitable for digoxin assay as determined by their reproducibility, sensitivity, precision, and a regression analysis. Hemolysis, lipemia, and icterus did not affect results. However, in some cases hypoalbuminemia falsely lowered the assayed digoxin concentration. Recovery of pure digoxin added to native patients' sera having low albumin concentration (24-28 g/liter) ranged from 67-105% with the Quantitope kit and 70-110% with the GammaCoat kit. Low serum albumin concentration did not always decrease the recovery of digoxin; this effect varied from serum to serum, which may indicate that there are factors other than albumin that affect the assay of digoxin.
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PMID:Evaluation of two digoxin radioimmunoassay procedures in which 125I-labeled digoxin is used. 124 20

We tested whether apoprotein B is present in fasting and postprandial human duodenojejunal mucosa because lipoprotein-like particles are visualized by electron microscopy within the smooth endoplasmic reticulum and the Golgi cisternae of these absorptive cells. Duodenojejunal biopsies from normal volunteers were incubated in citrate buffer and were shaken in 1% EDTA so that absorptive cells could be freed from underlying tissue. Apoprotein B was determined by double-antibody radioimmunoassay in homogenates of absorptive cells. The preparations of absorptive cells were shown to be uncontaminated by plasma lipoproteins; they did not contain any albumin by immunodiffusion able to detect 2 mug/ml. They adsorbed less than 0.1% of 125I-low density lipoprotein which was added to the citrate buffer. Cell preparations from suction biopsies of human rectum contained no detectable apoprotein B. Duodenojejunal absorptive cells from 22 fasting subjects contained 3.2 +/- 0.5 mug of apoprotein B per 100 mg (wet wt) of biopsies or 1.3 mug of apoprotein B per mg of total cell protein. The amount of apoprotein B per milligram of cell protein fell to 0.3 mug in 14 of these individuals whose mucosa was also sampled 45 min after instilling fat intraduodenally. These experiments provide immunochemical evidence that human duodenojejunal absorptive cells contain apoprotein B. This technique should be valuable for studying the physiology of intestinal lipoproteins in absorption and in patients with hyperlipidemia.
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PMID:Apoprotein B in fasting and postprandial human jejunal mucosa. 125 33


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