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Biomedical subjects

G Assmann

Publications and source records attributed to G Assmann.

At least 415 records · Page 23Linked to original sources
PubMed1981

Effect of polyenephosphatidylcholine on cholesterol uptake by human high density lipoprotein.

The lipid and protein composition of human HDL was changed by incorporation of polyenephosphatidylcholine (PPC) into HDL in vitro. HDL with incorporated PPC (HDL-PPC) had a higher molar PC/apoprotein ratio than native HDL. PPC accounted for up to 50% of the PC fraction of HDL. The fluidity of HDL-PPC was higher than that of native HDL but lower than that of PPC liposomes. Zonal ultracentrifugation separated HDL-PPC into a major and a minor component. The AI/AII ratio of the major fraction was reduced compared with native HDL. The storage capacity of HDL-PPC and native HDL for cholesterol was studied by incubation of these fractions with [14]cholesterol-LDL. Significantly more cholesterol (55%) was taken up by HDL-PPC from LDL than by native HDL. The transfer of cholesterol from LDL to HDL in human serum was studied by an in vitro [14C]cholesterol distribution test. In this test the lipoproteins of serum were labelled with [14C]cholesterol. An analytical procedure was developed to quantify the transfer of cholesterol from LDL to HDL after addition of PC. The transfer depended on the fluidity and the dose of the PC fraction used as well as on the initial LDL + VLDL/HDL ratio and was independent of LCAT activity.

Carbon Radioisotopes↗
PubMed1981

Serum ferritin, transferrin, haptoglobin, and iron in middle- and long-distance runners, elite rowers, and professional racing cyclists.

Serum ferritin, transferrin, haptoglobin, and iron were measured in well-trained middle- and long-distance runners, elite rowers of the West German national team, and professional racing cyclists during the summer training and the winter rest period. None of the male athletes examined, with the exception of the racing cyclists during the summer period, received oral or parenteral iron. The runners were found to have significantly lower ferritin (P less than 0.00001), iron (P less than 0.001), and haptoglobin values (P less than 0.01) than the controls. Their transferrin levels were elevated, however not significantly. Rowers showed significantly higher ferritin levels (P less than 0.01) than the controls. The reduced haptoglobin concentrations in runners are presumed to be caused by a running-induced hemolysis. It is speculated that a recurring hemoglobinuria produced diminished iron reserves in middle- and long-distance runners.

Adult↗
PubMed1981

Displacement of the human apoprotein A-I by the human apoprotein A-II from complexes of (apoprotein A-I)-phosphatidylcholine-cholesterol.

Reassembly experiments, involving isolated human apoproteins A-I and A-II and (dimyristoylglycerophosphocholine)-cholesterol vesicles were performed with apoprotein mixtures at apoprotein A-I/A-II molar ratios varying between 0 and 3. The apoproteins were incubated at 24 degrees C. 28 degrees C and 32 degrees C with either pure dimyristoyl-glycerophosphocholine vesicles or with dimyristoylglycerophosphocholine cholesterol vesicles containing 2, 5, 10, 15 mol/100 mol cholesterol. The kinetics of association were followed by measuring the increase of the fluorescence polarization ratio after labeling the lipids with diphenyl hexatriene. The complexes were separated from the free protein by gradient ultracentrifugation. Total protein was assayed and the apoproteins A-I and A-II were quantified separately by immunonephelometry. The content of apoprotein A-I was also monitored by measuring the intrinsic tryptophan fluorescence. The results suggest that apoprotein A-II has a greater affinity than apoprotein A-I for the phospholipid-cholesterol vesicles and that apoprotein A-II is able to quantitatively displace apoprotein A-I from the lipid-protein complexes. The content of apoprotein A-II in the complexes increases proportionally to the concentration of apoprotein A-II in the incubation mixture until saturation is reached. At saturation the dimyristoylglycerophosphocholine/apoprotein A-II ratio in the complex is dependent upon the cholesterol content of the original vesicles and increases from 60 to 275 mol/mol between 0 and 15 mol/100 mol cholesterol. From these experiments one can calculate that 1 mol human apoprotein A-I is displaced by 2 mol human apoprotein A-II.

Apolipoprotein A-I↗
PubMed1981

[Cholesteryl ester storage disease in the liver (author's transl)].

Cholesteryl ester storage disease is a rare disorder if cholesterol metabolism characterized by excessive hepatic storage of cholesteryl esters. The underlying defect probably is decreased activity of alpha-naphtyl-acetatesterase, a lysosomal acid lipase. The leading symptom in the early stage is a pronounced enlargement of the liver without subjective complaints or other changes in the physical status. Diagnosis can be established by liver biopsy, which will yield characteristic findings, and by exclusion of other storage disease. Histologic examination of the biopsy specimen will show lipid droplets in hepatic parenchymal cells, vacuolated Kupffer cells and focal accumulation of foamy cells. Biochemical analysis of the biopsy specimen will show an increased content of cholesteryl esters. Investigation of media of culture fibroblasts will show decreased activity of lysosomal alpha-naphtyl-acetat-esterase. In addition adrenal calcification has to be ruled out, in order to exclude wolman's disease. The prognosis of the disease will depend upon the degree of liver insufficiency, since lympho-histiocytic infiltration as a secondary phenomenon may lead to septal fibrosis and cirrhosis in children or adolescents in most cases. A case report is given of a 13-year old girl suffering from this disease.

Adolescent↗
PubMed1981

[The detection of apolipoproteins AI and B in the liver of patients with and without hyperlipoproteinemia (author's transl)].

Liver sections as well as isolated liver cells from 5 patients with a normal liver and normal serum lipids and patients with familial hyperlipoproteinemia type IIa (n=6), type IIb (n=11), type IV (n=13) and type V (n=2) were studied for the presence of apolipoprotein (apo) AI and B by immunofluorescence technique. At the time of liver biopsy the actual serum concentrations of HDL- and LDL-cholesterol and triglycerides were determined. In patients without metabolic disturbances apo AI was detectable in hepatocytes in 2 out of 5 cases. Apo B was not found in the liver of these patients. The non-parenchymal liver cells did not show depositions of apoproteins. In the group of 32 patients with hyperlipoproteinemia 6 cases showed in the liver apo AI and 2 cases apo B. The apoproteins exhibited a granular fluorescence pattern in the cytoplasm of hepatocytes. There was no correlation between the apoproteins in the liver and the degree of fat depositions in hepatocytes or the concentrations of serum lipids. The results indicate that the fat droplets in hepatocytes of patients with hyperlipoproteinemia represent lipid particles free of apoproteins. The lack of apoproteins in the liver with elevation of lipids in serum can be explained with a disturbed hepatic clearance function for lipoproteins.

Adult↗
PubMed1981

[Accuracy of HDL-cholesterol and HDL-apolipoprotein A-I determinations after phosphotungstate/MgCl2-precipitation of apolipoprotein B-containing lipoproteins (author's transl)].

With optimal concentrations of reagents a complete precipitation of apolipoprotein B-containing lipoproteins and only a small coprecipitation of HDL can be achieved using the phosphotungstate/MgCl2 precipitation method. The accuracy of the precipitation is not influenced by triglyceride concentrations less than 4.0 mmol/l. Similarly, in most hypertriglyceridaemic sera (greater than 4.0 mmol/l) a complete precipitation of apolipoprotein B-containing lipoproteins and a complete recovery of HDL can be observed. In addition to the HDL cholesterol determination, apolipoprotein A-I was determined by kinetic nephelometry. In hypertriglyceridaemic sera (greater than 4.56 mmol/l) precipitation of apolipoprotein B-containing lipoproteins must be carried out prior to the nephelometric determination of apolipoprotein A-I.

Aging↗
PubMed1981

[Performance and limitations of the analysis of HDL-cholesterol (author's transl)].

Comparing published data, three methods for HDL-cholesterol determination (phosphotungstate/MgCl2, dextran sulphate 500/MgCl2 and heparin/MnCl2) are reviewed with respect to accuracy, precision, sensitivity and liability to interference. All three methods are specific (complete precipitation of apolipoprotein B-containing lipoprotein) and sufficiently sensitive (only significant coprecipitation of HDL). A disadvantage of the heparin/MnCl2 method is incomplete precipitation of apolipoprotein B-containing lipoprotein in hypertriglyceridemic sera. Limitations of the diagnostic value of HDL-cholesterol analysis are discussed.

Apolipoproteins↗
PubMed1980

Reassembly of human apoproteins A-I and A-II with unilamellar phosphatidylcholine-cholesterol liposomes. Association kinetics and characterization of the complexes.

The kinetics of association between the human apoprotein A-I and apoprotein A-II and cholesterol dimyristoyl phosphatidylcholine (DMPC) vesicles are compared in this study and the lipid-apoprotein complexes are characterized. The association kinetics are followed by turbidity measurements monitoring the decrease of the vesicular size and by fluorescence polarization measurements monitoring the decrease in the mobility of the phospholipid acyl chains during complex formation. The influence of the incubation temperature and of the cholesterol/DMPC ratio has been studied by both techniques. Under all incubation conditions the apoprotein A-II associates more readily with cholesterol-DMPC vesicles than apoprotein A-I, as the kinetics are faster and the complex yield larger. With both apoproteins optimal complex formation takes place around the phospholipid transition temperature and around 10 mol% cholesterol. The apoprotein A-I/lipid association seems restricted to this narrow range for the temperature and the cholesterol/DMPC ratio, while the apoprotein A-II still associates with vesicles containing 20 mol% cholesterol and at temperatures up to 32 degrees C. The lipid-apoprotein complexes were isolated by gradient ultracentrifugation and by gel chromatography. According to these data the apoprotein A-II associates more readily than apoprotein A-I with cholesterol-DMPC vesicles to form protein-rich complexes, whilst the optimal apoprotein A-I-lipid association requires a more disordered lipid structure.

Apolipoprotein A-I↗
PubMed1980

[HDL cholesterol: biochemical aspects (author's transl)].

High density lipoproteins are a heterogeneous mixture of spherical macromolecules which differ in size (80-120 A), chemical composition (apolipoprotein A-I: 30-35%; apolipoprotein A-II: 10-15%; apolipoprotein C: 3-5%; phospholipids 25-30%; cholesterol/cholesterol esters: 15-20%; triglycerides: 3-5%) and physico-chemical properties. They can be isolated through selective precipitation of apolipoprotein B-containing lipoproteins (very low density lipoproteins, low density lipoproteins, lipoprotein (a)) and, under routine conditions, quantitation can be performed by the determination of their cholesterol or apolipoprotein content. A considerable portion of high density lipoproteins originates in plasma from discoidal phospholipid-apolipoprotein bilayers (thickness: 46 A; diameter: 190 A). These bilayers are in part synthesized by the liver and in part derived from the surface of chylomicrons during lipolysis. The role of discoidal precursors of high density lipoproteins in cholesterol-uptake from peripheral cells will be discussed.

Apoproteins↗
PubMed1980

[HDL cholesterol: clinical and pathobiochemical aspects (author's transl)].

The determination of high density lipoprotein (HDL)-cholesterol in patients with mild hypercholesterolemia (240-300 mg/dl) allows one to distinguish between hyperbetalipoproteinemia (= high atherogenic risk) and hyperalphalipoproteinemia (= low atherogenic risk). In addition, analysis of HDL-cholesterol is of value in the prediction and early recognition of coronary heart disease, particularly in combination with known risk factors (hypertriglyceridemia, adipositas, smoking). This prognostic value of HDL-cholesterol is a result of its negative correlation to coronary heart disease which has been recognized in epidemiologic and clinical studies. The study of Tangier disease (analphalipoproteinemia) and tissue culture experiments will provide opportunities for the further elucidation of the role of HDL in atherogenesis.

Apoproteins↗
PubMed1980

[Screening and therapy control of lipid metabolism disturbances in general practice (author's transl)].

The determination of total cholesterol and triglycerides in fasting serum is the basic program for routine diagnosis and therapy control of lipid metabolic defects. With the introduction of routine determination of HDL-cholesterol and LDL-cholesterol into the laboratory of the general practitioner, differential diagnosis of lipid metabolism disorders and therefore an improved recognition of the coronary risk becomes possible. The combination of hypertriglyceridemia and a low HDL-cholesterol as a possible indicator of diminished intravascular lipolysis is especially significant for the recognition of individual risks. The indications for the diagnosis and therapeutic control of hyperlipidemia as well as the value of the lipid parameters for the prediction and early diagnosis of coronary heart disease is discussed.

Adult↗
PubMed1980

Role of low-density and high-density lipoproteins in atherogenesis.

Among the cholesterol-carrying lipoproteins, low-density lipoproteins (LDL) have been associated with coronary heart disease as a risk factor while high-density lipoproteins (HDL) appear to protect against coronary heart disease. According to studies with cells in tissue culture, control mechanisms of receptor-mediated LDL uptake are important in maintaining the cholesterol balance within the arterial cells. HDL may be a vehicle for transporting cholesterol from peripheral cells to the liver. Recent results, derived from studies of patients affected with Tangier disease (absence of HDL in plasma), favor the hypothesis that HDL precursors (e.g. surface remnants of chylomicrons) may be more potent in cholesterol uptake than mature HDL.

Cholesterol↗
PubMed1980

Lipoproteins and apolipoprotein patterns in rat plasma after liver injury induced by D-galactosamine.

The effect of galactosamine administration on the concentration and composition of plasma lipoproteins was studied in female rats. After a single intraperitoneal injection of 3.48 mmol galactosamine/kg the following alterations occurred within 24 h: Disappearance of alpha-lipoproteins as shown by agarose electrophoresis, increase of abnormal lipoproteins in the beta- and pre-beta-region. These changes corresponded to a two- to three-fold increase of VLDL and LDL and a decrease of HDL to 20-30% of normal after sequential ultracentrifugation. When compared to control animals, galactosamine-treated rats exhibited an abnormal chemical composition of their plasma lipoproteins: A nearly total loss of cholesterol esters, but an increase of free cholesterol and phospholipids, particularly in the LDL and HDL density classes. Moreover, polyacrylamide gel electrophoresis in 8M urea revealed a clear diminution of all C-apoproteins in the VLDL and HDL density class and a complete disappearance of the A II band in the HDL fraction 24-48 h after galactosamine administration. These lacking apoprotein bands reappeared 72-168 h after galactosamine treatment. The same effects could be obtained by lower doses of galactosamine (2.32 and 1.16 mmol/kg, respectively) which led only to slight increases of hepatocellular enzymes in the plasma. It is concluded therefore, that galactosamine administration in experimental animals leads to profound, but reversible alterations in the synthesis and/or secretion of plasma lipoproteins.

Animals↗