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K R Norum

Publications and source records attributed to K R Norum.

At least 163 records · Page 9Linked to original sources
PubMed1975

Substrate specificity of lecithin:cholesterol acyltransferase. Esterification of desmosterol, b-sitosterol, and cholecalciferol in human plasma.

Desmosterol and beta-sitosterol were esterified when incubated with normal human plasma. The initial rate of demosterol esterification was 1.7 times faster, and that of beta-sitosterol 0.4 times slower, than the esterification rate of cholesterol. These ratios were found to be almost the same when plasma from different normal individuals was tested. Plasma from a patient with familial lecithin:cholesterol acyltransferase deficiency did not esterify any of the sterols. The esterification of desmosterol and beta-sitosterol was considerably slower in normal plasma in which in vitro cholesterol esterification previously had taken place. The different esterification rates could not be explained by a different affinity of the plasma lipoproteins for the sterols tested. Cholecalciferol added to normal plasma did not become esterified.

Acyltransferases↗
PubMed1973

[School meals].

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Child↗
PubMed1973

Plasma lipoproteins in familial lecithin: cholesterol acyltransferase deficiency. Further studies of very low and low density lipoprotein abnormalities.

Plasma lipoproteins of d<1.006 g/ml, d 1.006-1.019 g/ml, and d 1.019-1.063 g/ml from patients with familial lecithin:cholesterol acyltransferase deficiency yielded abnormal subfractions upon being separately filtered through 2% agarose gel. A subfraction that emerged with the void volume and contained unusually large amounts of unesterified cholesterol and phosphatidylcholine was present in each lipoprotein group, and in each group this subfraction was less prominent in the nonlipemic plasma of one patient than in the lipemic plasma of other patients. A subfraction containing smaller lipoproteins also was present in each lipoprotein group. These lipoproteins were of the same size as normal lipoproteins of the corresponding density, but contained abnormally small amounts of cholesteryl ester. The lipoproteins of 1.019-1.063 g/ml contained abnormal components of intermediate molecular weight as well as large and small abnormal components similar to those described previously. The intermediate components were more prominent in the nonlipemic plasma but were easily recognized in the hyperlipemic plasma as a peak of S(f) 20-30 in the analytical ultracentrifuge. Also they could be recognized, upon electron microscopy of the lipoproteins of d 1.019-1.063 g/ml, as particles 340-1000 A in diameter. The data suggest that related large, abnormal particles pervade the patients' very low and low density lipoproteins, and that the large particles are affected by, but are not dependent on, the lipemia that frequently accompanies the disease. The smaller very low and low density lipoproteins appear to be counterparts of lipoproteins present in normal plasma. Their abnormal composition is compatible with the possibility that lecithin:cholesterol acyltransferase normally decreases the triglyceride and phosphatidylcholine and increases the cholesteryl ester of very low density and low density plasma lipoproteins in vivo.

Acyltransferases↗
PubMed1971

Plasma lipoproteins in familial lecithin: cholesterol acyltransferase deficiency: physical and chemical studies of low and high density lipoproteins.

LOW DENSITY LIPOPROTEINS (LDL) AND HIGH DENSITY LIPOPROTEINS (HDL) FROM THE PLASMA OF PATIENTS WITH FAMILIAL LECITHIN: cholesterol acyltransferase (LCAT) deficiency have been characterized by gel filtration, analytical ultracentrifugation, and gel electrophoresis, and their relative content of lipid and protein has been determined. The LDL of d 1.019-1.063 g/ml show marked heterogeneity. A subfraction of the LDL emerges from columns of 2% agarose gel with the void volume, has corrected flotation rates (S(f) degrees ) in the range of 20-400, and contains 4-10 times as much unesterified cholesterol, phosphatidylcholine, and triglyceride per mg protein as normal LDL. A major subfraction of the LDL emerges from the gel in the same general position as normal LDL, but exhibits somewhat higher flotation rates and contains 1.5-3 times as much unesterified cholesterol and phosphatidylcholine and 13 times as much triglyceride per mg protein. The HDL, shown to be heterogeneous in earlier studies, are mainly comprised of molecules which have flotation rates of F(1.20) 3-20, migrate in the alpha(1)-alpha(2) region on electrophoresis, and contain about 12 times as much unesterified cholesterol and 5 times as much phosphatidylcholine per mg protein as normal HDL. Smaller molecules are also detected, which have flotation rates of F(1.20) 0-3, migrate in the prealbumin region on electrophoresis, and contain only slightly more unesterified cholesterol and phosphatidylcholine per mg protein than normal HDL.

Acyltransferases↗
PubMed1971

Plasma lipoproteins in familial lecithin: cholesterol acyltransferase deficiency: structure of low and high density lipoproteins as revealed by elctron microscopy.

The low density lipoproteins (LDL) of d 1.019-1.063 g/ml of patients with familial lecithin: cholesterol acyltransferase (LCAT) deficiency show marked heterogeneity when viewed with the electron microscope. At least two types of particles are present, one large and the other small. The large particles predominate in a LDL subfraction of large molecular weight isolated by gel filtration on 2% agarose gel. They appear to be flattened structures with diameters mainly in the range of 900-1200 A. The small particles predominate in a LDL subfraction of smaller molecular weight isolated by filtration on the same type of gel. They are 210-250 A in diameter and are similar to normal LDL in size and shape. The high density lipoproteins (HDL) also are heterogeneous. The majority of particles are disc-shaped structures 150-200 A in diameter. The discs are mainly present in stacks which have a periodicity of 50-55 A and a variable length. Each disc appears to be made up of a rosette of smaller globular units 50 A in diameter. The appearance of these large molecular weight HDL contrasts with that of normal HDL, which are 70-100 A in diameter and aggregate in monolayers that show hexagonal packing of particles. A small percentage of the patients' HDL consists of structures 45-60 A in diameter. These predominate in a smaller molecular weight HDL subfraction isolated by gel filtration on Sephadex G200. The particles are present in monolayer aggregates but never form stacked structures similar to those seen in the large molecular weight HDL subfraction.

Adult↗