Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Low doses of heparin were injected into the brachial artery of three volunteers. The lipase activities in the deep vein of the same forearm, draining mainly muscle tissue, and in the artery were monitored over a 10-min period. Lipase activity, rapidly released by heparin in the deep vein, was immunologically similar to lipoprotein lipase (E.C. 3.1.1.3), i.e. (1) it did not react with antiserum against human post-heparin plasma hepatic lipase and (2) it was inhibited by an antiserum against bovine milk lipoprotein lipase, which cross reacts with human post-heparin plasma lipoprotein lipase. The evidence that human muscle contains lipoprotein lipase is discussed.
Atherosclerosis 1977 May
PMID:Heparin-induced release of lipase activity in the human forearm: an immunological study. 32 91

Needle biopsies of adipose tissue and blood samples were obtained before and at short intervals after a "bolus" injection of 10% Intralipid. Lipoprotein lipase activities were measured in acetone--ether extracts of the tissue samples. Levels of serum triglyceride began to fall less than 5 min after the injection of the Intralipid with a half-life of 20 min. During this time interval, no significant changes were observed in the activities of lipoprotein lipase in adipose tissue. A patient with a severe hypertriglyceridaemia (Type V) underwent plasma exchange with a reduction in serum triglyceride levels from 11 to 4 mm/l. There was a parallel fall in adipose tissue lipoprotein lipase activity. We conclude that lipoprotein lipase in adipose tissue is unaltered during experimental hypertriglyceridaemia and that the activity of the enzyme in adipose tissue is probably not reduced as a secondary feature of an elevated plasma triglyceride level.
Atherosclerosis 1979 Jun
PMID:Lipoprotein lipase activity in human adipose tissue during induced hypertriglyceridaemia. 47 83

Two processes regulate the removal of lipoprotein triglycerides from plasma: (1) hydrolysis of triglycerides by lipoprotein lipase to fatty acids in the capillaries; (2) local uptake and esterification of fatty acids by adipose tissue, muscle and other tissues. This second process has been studied on needle biopsy specimens of adipose tissue from normotriglyceridemic and hypertriglyceridemic subjects. Hypertriglyceridemie was found to be associated to low fatty acid incorporation into adipose tissue.
Atherosclerosis 1978 Jan
PMID:Fractional fatty acid incorporation into human adipose tissue (FIAT) in hypertriglyceridemia. 62 25

Intimal tissue from human atherosclerotic aortae was collected by the Dermatome procedure. The tissue was extraved with 5 mM Tris.HCl buffer containing 0.3 M NaCl and 1 mM EDTA, pH 7.4. The ammonium sulfate precipitate between 0.4--0.8 saturation obtained from the extract was fractionated on a DEAE-cellulose column and the effluent was monitored for lipoprotein lipase inhibition employing purified bovine milk enzyme. The substrate used was an emulsion of purified olive oil and tritiated triolein. Human serum was the source of activator of the substrate. A peak of inhibitory activity was eluted between 0.15--0.17 M NaCl. The major component in the purified material had properties similar to a glycoprotein (lipolipin) which has previously been purified from porcine aorta and shown to inhibit lipoprotein lipase activity. The partially purified human inhibitor decreased both the basal and the serum-stimulated activity of milk lipoprotein lipase. The inhibition was non-competitive with respect to serum. However, high levels of triglyceride substrate appeared to relieve the inhibitory effect. It is postulated that the inhibitor may be involved in an interaction with the emulsified lipid denying the enzyme access to its substrate.
Atherosclerosis 1978 Feb
PMID:The in vitro inhibition of bovine milk lipoprotein lipase by a glycoprotein preparation from human atherosclerotic intima. 64 49

Heparin-like glycosaminoglycans (GAG) were isolated from commerical Vessel and their biologic properties studied. Vessel was found to be a mixture of chondroitin sulfates, dermatan sulfate and heparin-like GAG. Chondroitin sulfates and dermatan sulfate in Vessel were hydrolyzed by chondroitinase ABC and the residual Vessel was fractionated on a Dowex-1 Cl- column eluting with a stepwise-increasing concentration of NaCl (1.2--4.0 M). The major fractions eluted at 1.6 M and 1.8 M NaCl were tentatively identified by chemical analysis as heparin-like GAG with somewhat lower sulfate content than standard heparin. Both fractions had lipoprotein lipase-releasing activity and anticoagulant activity similar to heparin, but 1.6 M NaCl fraction had a third of the anticoagulant activity of standard heparin. The 1.8 M NaCl fraction complexed with serum lipoproteins similarly to heparin. In preliminary studies cholesterol-fed rabbits treated with Vessel exhibited somewhat less atherosclerosis than controls.
Atherosclerosis 1978 Oct
PMID:Studies of glycosaminoglycan composition and biologic activity of Vessel, a hypolipidemic agent. 72 39

Fourteen normal dogs received continuous infusions of intravenous heparin for one year by means of an implantable infusion pump. Heparin wad admistered at an overall mean rate of 666 units/kg/day, a dose sufficient to prolong the Lee-White clotting time to greater than twice normal. Eight control, animals, under the same dietary and activity regimen, received continuous infusions of bacteriostatic water for one year by means of implanted pumps. Serum cholesterol concentrations rose to 50% above control values after one month of heparin infusion, and remained significantly (P less than 0.05) elevated at this level for the remaining 11 months. Serum triglyceride levels were unchanged. A possible mechanism for this elevation resides in the known effect of heparin to increase plasma free fatty acid concentrations by its activation of lipoprotein lipase. These results may have implications for the long-term use of heparin anticoagulation in the treatment of atherosclerotic states in man.
Atherosclerosis 1977 Jan
PMID:The effect of continuous heparin infusion for one year on serum cholesterol and triglyceride concentrations in the dog. 83 45

Autoimmune hyperlipidemia (AIH) may be induced a variety of antibodies which inhibit different stages of the lipolytic process by which the lipid load is removed from the circulating lipoproteins. In a patient having a monoclonal gammopathy and a nephrotic syndrome with a glomerulonephritis and a marked hypertriglyceridemia, it was found previously that the monoclonal IgG gamma Lac. reacted with human VLDL as well as with human serum albumin. Here it is demonstrated that the purified IgG gamma inhibits the lipolysis of triglyceride substrates by reacting with a substance (Lac. S) necessary for lipoprotein lipase activity. The interaction of IgG lambda Lac. with serum or HDL-activated triglyceride substrates inhibits the lipolytic activity of human and rat plasma post heparin and also adipose tissue lipases. It slightly inhibits the activity of swine pancreatic lipases. The Lac S. which reacts with IgG Lac. is associated to whole and delipidated VLDL and HDL and not to LDL or purified APo-A. It may be an Apo-C or a non-peptidic co-factor of the lipases which remains bound to the apoprotein core after delipidation. Its lack of species specificity and its presence as traces in HSA preparations favors the latter hypothesis. The Lac. substances is different from the Pg and As substances which were found to react with IgA anti-Pg and IgG anti-As antibodies in previously reported antilipoprotein AIH.
Atherosclerosis 1977 Jan
PMID:Inhibition of lipoprotein lipase activity by a monoclonal immunoglobulin in autoimmune hyperlipidemia. 83 49

The hydrolysis of lipoprotein triglycerides is catalyzed by lipoprotein lipase (LPL), an enzyme found in many tissues. We have examined tissue LPL activity (LPLA) in rats with experimentally-induced hyperthyroidism. In younger, lighter rats, hyperthyroidism was accompanied by a decrease in LPL in adipose tissue whereas heart and diaphragm muscle LPL activities were increased. These changes are consistent with the hypothesis that the hypercatabolism and increased beta-adrenergic activity of hyperthyroidism result in characteristic changes in tissue LPLA. In older, heavier hyperthyroid animals, however, adipose tissue LPLA was increased and heart and diaphragmatic LPLA were similar to control activities. Propranolol feeding abolished the thyroxine-induced increase in adipose tissue LPLA. In euthyroid animals of similar size the response of muscle LPLA to short-term starvation was also attenuated. These changes in tissue LPLA may provide a mechanism for shunting triglyceride fatty acids away from adipose tissue for utilization by muscle in the hyperthyroid state. During growth and aging, these adaptations are modified.
Atherosclerosis 1977 Mar
PMID:Tissue lipoprotein lipase in the hyperthyroid rat. Effect of growth and aging. 84 80

Three different assays for selective measurement of plasma lipoprotein lipase (LPL) and hepatic triglyceride lipase (H-TGL) were compared. These were: an immunochemical method based on enzyme antibody precipitation (IM), a procedure in which both enzymes were separated by affinity chromatography on small heparin--Sepharose columns (HS), and an assay in which one enzyme was inhibited by protamine sulfate (PS). Good correlations were found between the immunochemical and the heparin--Sepharose method, but not between these and the protamine sulfate assay procedure. The IM was then used to evaluate the effect of clofibrate on the two lipolytic enzymes. It was found that both in normals and in patients with Type IV hyperlipoproteinemia, clofibrate treatment leads to a specific increase of plasma LPL while H-TGL activity remains almost unaffected. The magnitude of the LPL response was different in normals and in patients with endogenous hyperlipoproteinemia. Furthermore, in normals the maximal increase of LPL activity was already reached one week after drug treatment was begun, while in hypertriglyceridemic patients, this effect was not evident prior to four weeks of clofibrate treatment. The marked enzyme increase following clofibrate administration indicates that an increased peripheral removal rate for triglycerides is one major mechanism responsible for the lipid-lowering effect of this drug.
Atherosclerosis 1977 Apr
PMID:Comparison of assay methods for selective measurement of plasma lipase. The effect of clofibrate on hepatic and lipoprotein lipase in normals and patients with hypertriglyceridemia. 85 26

The ontogenic development of lipoprotein lipase and liver triglyceride hydrolase was studied in the rat. The enzyme activity measured in extrahepatic tissues fulfilled the criteria of lipoprotein lipase from the onset of measurable activity, i.e. it was inhibited by protamine and 1 M NaCl and showed requirement for serum and heparin for optimal activity. In the liver, measurable amounts of triglyceride hydrolase, active at pH 8.6 were detected 6 days prior to birth. However, till the fourth postnatal day about 50% of this activity was inhibited by NaCl and its sensitivity towards protamine was also higher than that of the enzyme in adult liver. Three patterns of development of enzymic activity were observed in extrahepatic tissues. In the lung, the lipoprotein activity reached the adult values one day prior to birth, while in the kidney only 30% of adult activity were found at birth. A linear increase of enzyme activity was observed in the heart; only 25% of adult activity were detected at birth and 100% were reached only 20 days after birth. The increase in lipoprotein lipase activity in the heart was accompanied by morphological differentiation of cardiocytes and by a progressive development of the capillary bed, which might be related to the pattern of development of enzyme activity in this organ. Adipose tissue lipoprotein lipase activity in inguinal fat fell from values 15 times than adult values between the 4th and 40th postnatal days. The enzyme activity in epididymal fat increased steeply between day 10 and 40, at which time it exceeded the adult values very considerably. These findings indicate that the regulation of the development of lipoprotein lipase activity in extrahepatic tissues is governed by local factors, which can differ even in the same type of tissue, as exemplified by the difference between inguinal and epididymal fat.
Atherosclerosis 1977 Apr
PMID:Pre- and post-natal development of lipoprotein lipase and hepatic triglyceride hydrolase activity in rat tissues. 85 10


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