Search PubMed⌕ Search

Biomedical subjects

H Greten

Publications and source records attributed to H Greten.

At least 199 records · Page 11Linked to original sources
PubMed1983

Familial lipoprotein lipase and apolipoprotein C-II deficiency. Lipoprotein and apoprotein analysis, adipose tissue and hepatic lipoprotein lipase levels in seven patients and their first degree relatives.

Plasma lipids, lipoproteins, tissue lipoprotein lipase (LPL) and hepatic lipase (H-TGL) were studied in 7 patients with familial hyperchylomicronemia from four different families. Their first-degree relative were also studied. The patients were heterogeneous for the genetic defect; LPL activity was absent in five patients (LPL deficiency) but normal in two. However, these two did not have apo C-II, the physiological activator of LPL (C-II deficiency). There were no significant differences in the clinical picture between patients with LPL deficiency and C-II deficiency. In both mutants, marked hypertriglyceridemia was due to an accumulation of lipoproteins of density less than 1.006 g/ml. The LDL fraction was very reduced and abnormal in composition, presenting a CH/TG ratio of 0.5. The plasma apolipoprotein B (apo B) level was low (67 +/- 5.5 mg/dl) and was transported mainly in the VLDL fraction (26 +/- 3.2 mg/dl) rather than in the LDL fraction (15 +/- 1.4 mg/dl). Very low levels of cholesterol and apolipoprotein A-I in HDL subfractions HDL2 and HDL3 were also recorded. Only 3 out of the 24 first-degree relatives of patients with LPL deficiency showed even a small increase in plasma triglycerides, but 15 had low or low to normal LPL values. H-TGL levels were normal in all subjects. The 4 first-degree relatives of C-II deficiency patients showed normal levels of plasma lipids. LPL and H-TGL, and 2 children of 1 patient showed normal distribution of apo C peptides in their VLDL. A block in chylomicron catabolism, due to the absence of LPL or apo C-II, may lead to a massive accumulation of lipoproteins with a density less than 1.006 g/ml, and a drastic reduction in the LDL and HDL fractions. Low LPL values in the first-degree relatives of LPL deficiency patients might represent a biochemical marker for healthy carriers of LPL deficiency.

Adipose Tissue↗
PubMed1982

In vitro modulation of the distribution of normal human plasma high density lipoprotein subfractions through the lecithin: cholesterol acyltransferase reaction.

The effect of the lecithin: cholesterol acyltransferase reaction on the chemical composition, morphology and distribution of normal human plasma high density lipoprotein (HDL) subclasses was studied in vitro. Incubation of plasma in the presence of polyenephosphatidylcholine (PPC) resulted in a 45 +/- 11% (n = 6) decrease in unesterified cholesterol after 20 h. This effect was abolished by prior heating of the plasma at 56 degrees C or by the addition of diisopropyl fluorophosphate (DIFP). Plasma triacylglycerol levels were constant. Analysis of the plasma lipoproteins by zonal ultracentrifugation and isopycnic equilibrium banding revealed a bimodal distribution of the HDL of native plasma and both heat-inactivated or DIFP-treated samples with peak maxima at d = 1.084 g/ml and d = 1.110 g/ml. Following the lecithin:cholesterol acyltransferase reaction essentially all of the HDL material had flotation characteristics typical of HDL2. The peak maximum was d = 1.086 g/ml. There were no apparent changes in the distribution of the lipoproteins of d less than 1.063 g/ml. The newly formed HDL were poor in PC and unesterified cholesterol but rich in cholesteryl ester, sphingomyelin and lyso-PC. The HDL apolipoprotein pattern was unaltered. HDL morphology was not affected by the lecithin:cholesterol acyltransferase reaction. Similar results were obtained in the absence of PPC. However, under these conditions the total phospholipid content of the HDL was reduced and lyso-PC was not demonstrable as a product of the lecithin:cholesterol acyltransferase reaction after 20 h. The results are interpreted to indicate that lecithin:cholesterol acyltransferase is involved in the transformation of HDL3 into HDL2.

Female↗
PubMed1982

Effect of catecholamines on sterol synthesis in human mononuclear cells.

The effect of adrenaline, noradrenaline, isoproterenol and dibutyryl cyclic AMP on the rate of sterol synthesis was studied in freshly isolated human mononuclear cells. Incubation of cells in a medium containing lipid depleted serum led to a two-fold rise in the rate of sterol synthesis from [14C]acetate. Adrenaline, nor-adrenaline and isoproterenol added in a concentration of 2 X 10(-5) mol/l at zero-time resulted in an inhibition of 30% of this increase in sterol synthesis after 4 h, but had no effect when the hormones were given at 4 h. This indicates that the catecholamines require some time to exert their inhibitory action on sterol synthesis. The action of catecholamines on the incorporation of [14C]acetate into sterols could be mimicked by dibutyryl cyclic AMP. Propranolol added in increasing concentrations to the incubation medium diminished or totally prevented the inhibitory effect of adrenaline, noradrenaline and isoproterenol on sterol synthesis. The results indicate that cholesterol synthesis in extrahepatic human cells, regulated predominantly by low density lipoprotein derived from plasma, is under additional control of catecholamines which may act via cyclic AMP.

Bucladesine↗
PubMed1982

Increased serum phospholipids in epileptic children treated with phenobarbitone.

Plasma lipid concentration and post-heparin lipolytic activity in twenty-two epileptic children treated either with phenobarbitone or sodium valproate were evaluated. An increase of phospholipid was observed in whole blood as well as in the low-density nd high-density lipoproteins in patients undergoing phenobarbitone treatment. No change was found in subjects treated with sodium valproate. The enzyme activities were slightly, but not statistically significantly, increased in the two groups compared with the control subjects.

Child↗
PubMed1981

Function of hepatic triglyceride lipase in lipoprotein metabolism.

Rat hepatic triglyceride lipase (H-TGL) was purified from liver tissue extracts by affinity chromatography on Sepharose 4B with covalently linked heparin. The purified rat H-TGL exhibited the properties previously described for this enzyme. Enzyme protein was injected into rabbits for anti-H-TGL antibody production. Antirat-H-TGL did not react against rat lipoprotein lipase (LPL) but inhibited H-TGL-activity both in vitro and in vivo greater than 90%. These antibodies were injected into rats and lipoprotein analyses were performed over a 36-hr period. It could be shown that inactivation of H-TGL by anti-H-TGL gamma-globulins in vivo led to an increase in total triglyceride concentration from 70 mg/dl to 230 mg/dl due to an increase in very low density lipoprotein (VLDL) and low density lipoprotein (LDL) triglycerides 4 hr after antibody injection; a marked increase in high density lipoprotein (HDL) phospholipid concentration was observed with almost no change in HDL-cholesterol and HDL-triglycerides. This study documents the ability of antirat-H-TGL-gamma-globulins to inhibit H-TGL in vitro and in vivo. Furthermore, the inhibition of triglyceride removal in vivo demonstrated that this enzyme together with LPL is responsible for the catabolism of VLDL-triglyceride.

Adipose Tissue↗
PubMed1980

Purification of human plasma lipoprotein lipase.

Human plasma lipoprotein lipase was purified in a highly active form. Addition of the non-ionic detergent Triton X-100 led to stabilization of enzyme activity during the purification procedure. Antithrombin III, the major contaminant after affinity chromatography with heparin-Sepharose 4B, could be removed by gel filtration on Bio-Gel A-5m. The application of Tris-glycine buffer in the absence of denaturating agents allowed identification of the protein band corresponding to lipoprotein lipase activity on polyacrylamide gels.

Buffers↗
PubMed1980

[Lipid lowering treatment and regression of arteriosclerosis (author's transl)].

The pathogenesis of arteriosclerosis is unknown. As etiological factors which are associated with early development of arteriosclerosis hyperlipemia, cigarette smoking and hypertension are undisputed. More recently studies which show substantial pointers to regression of arteriosclerosis have become more numerous. It has been demonstrated by animal experiments that arteriosclerotic changes can be induced by a diet rich in cholesterol and furthermore can be brought to remission by low fat feeding and/or lipid lowering substances. Indirect pointers to regression, slower or no progressiveness of arteriosclerosis in man have been provided by autopsy findings and epidemiological studies. It has also been recorded angiographically that arteriosclerotic changes can be made to regress by a lipid lowering treatment.

Animals↗
PubMed1980

The effect of polyunsaturated phosphatidylcholine on plasma lipids and fecal sterol excretion.

Highly polyunsaturated phosphatidylcholine (PC) was orally administered to patients with familial hypercholesterolemia and normal controls. Plasma lipid and lipoprotein composition as well as fecal sterol excretion and bile lipid composition were analyzed. Two dietary regimens were given, containing similar amounts of calories, cholesterol and polyunsaturated fatty acids in order to evaluate the specific effect of phosphorylcholine. No change in plasma lipid or lipoprotein concentration was observed. However, fecal sterol excretion was substantially increased in all subjects when PC was added to the diet. Bile acids, phospholipid and cholesterol content in bile did not vary.

Adolescent↗
PubMed1979

Activation and inhibition of lipoprotein lipase. Studies with artificial lipoproteins.

Human plasma very low density apolipoproteins C-I, C-II and C-III were recombined in vitro with triolein. The lipid-protein complexes were analyzed by ultracentrifugal flotation, agarose gel electrophoresis, immunoelectrophoresis and electron microscopy. Maximal protein/triolein ratios for apoprotein C-I, C-II, C-III-1 and C-III-2 were 50, 45, 95 and 55 microgram/mg, respectively. Electron micrographs exhibited spherical particles with diameters ranging from 200--2000 A comparable to native VLDL and chylomicrons. On agarose gel electrophoresis these complexes showed alpha-mobility. Kinetics of triolein hydrolysis by purified human plasma lipoprotein lipase were studied using these artificial lipoprotein substrates with different apoprotein/triolein ratios. The reaction followed the Michaelis-Menten equation. With increasing amounts of apo C-II, the apparent Km decreased from 0.60 to 0.11 mM. Incubation of the substrate with either rabbit anti-apo C-II gamma-globulins or digestion with trypsin prior to hydrolysis reversed this lowering effect on apparent Km. V was not altered significantly. Increasing amounts of apo C-I, apo C-III-1 or apo C-III-2 without apo C-II caused inhibition of triolein hydrolysis. In the presence of apo C-II, however, similar kinetic parameters were obtained as described above.

Apolipoproteins↗
PubMed1979

A bile-acid-rich high-density lipoprotein (HDL) in acute hepatitis.

Severe liver dysfunction is often associated with alterations of plasma lipids and lipoproteins. In this study the high-density lipoprotein (HDL) class has been further investigated. HDL from patients with acute, cholestatic hepatitis (n = 10) was isolated and compared with that of normals. Lipid and protein analyses were performed during the acute stage of the disease, with consequent follow-up studies. It was found that (1) only apo A-I was decreased by 50% in the isolated HDL fractions, whereas apo A-II remained unchanged; apo A-I in total plasma was normal; (2) immunoelectrophoresis of hepatitis HDL against monospecific anti-A-II revealed one precipitin line but two or more bands against anti-A-I; (3) concomitant with an increase of phospholipids and a decrease of triglycerides and the total cholesterol fraction, hepatitis HDL contained 10--12 times more bile acid than normal HDL. Chenodeoxycholic acid was the predominant bile acid. These alterations were fully reversible when patients recovered. These parameters seem to be sensitive markers for the degree of disturbance and restoration of liver function. The structural-functional implications of the observed compositional changes of HDL during cholestasis are discussed.

Acute Disease↗