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Biomedical subjects

H G Morgan

Publications and source records attributed to H G Morgan.

At least 55 records · Page 3Linked to original sources
PubMed1982

High-density lipoprotein subfractions as measured by differential polyanionic precipitation and rate zonal ultracentrifugation.

Recent interest in the putative protective role of high-density lipoprotein (HDL) and its subfractions against atherosclerosis has highlighted the need for a rapid, simple subfractionation procedure. Here we compared HDL subfractionation by two recently developed polyanionic-precipitation methods with the values obtained by rate zonal ultracentrifugation. A similar result for total HDL cholesterol was obtained by all three methods. However, HDL2 cholesterol as measured by the precipitation procedures was significantly higher than the zonal value, and HDL3 was lower. This reflects the different underlying principles involved in the separations and highlights the need for a clearer understanding of the functional roles of the HDL fractions.

Adult↗
PubMed1982

Anorexia nervosa.

Explore the source record for details and available documents.

Adolescent↗
PubMed1980

Cholestyramine promotes receptor-mediated low-density-lipoprotein catabolism.

We studied the influence of cholestyramine (24 g per day) on receptor-mediated and receptor-independent low-density-lipoprotein catabolism in five women with heterozygous familial hypercholesterolemia. Cholestyramine lowered the level of circulating low-density-lipoprotein apoprotein by doubling (P less than 0.01) its fractional clearance via the receptor path, but fractional catabolism by the receptor-independent route remained unchanged. Moreover, although the absolute rate of catabolism of the apoprotein was not affected by treatment, the amounts handled by each pathway altered. Catabolism via the physiologically controllable receptor route increased by 71 per cent (P less than 0.05), but there was a 12 per cent drop in clearance by the nonreceptor pathway. These data demonstrate the utility of cholestyramine in promoting low-density-lipoprotein catabolism via its specific physiologic clearance pathway. They also show that heterozygotes with familial hypercholesterolemia can increase the activity of their low-density-lipoprotein receptors when presented with an appropriate stimulus.

Adult↗
PubMed1980

The relationship between the cholesterol content and subfraction distribution of plasma high-density lipoproteins.

High density lipoprotein subfractions (HDL2 and HDL3) were separated from the plasma of 25 healthy volunteers (13 males, 12 females) rate zonal ultracentrifugation. The rotor elution profile, measured at 280 nm, was used with the specific extinction coefficient for each subfraction (HDL2, 0.60 +/- 0.11 mg protein/A280nm, HDL3, 0.86 +/- 0.10 mg protein/A280nm (n=25) to calculate their plasma concentration. Their protein and lipid composition were also determined by chemical analysis. Plasma lipids, lipoprotein cholesterol, apolipoprotein A-I, apolipoprotein A-II and apolipoprotein B levels were measured in the same subjects and correlated with the HDL subfraction concentrations. HDL cholesterol and apolipoprotein A-I concentrations correlated significantly (p less than 0.01 and 0.02 respectively) with plasma HDL2, but not with HDL3. Indeed, the significantly higher levels of HDL cholesterol and apolipoprotein A-I in the female group could be attributed entirely to an increase in circulating HDL2. This data supports the proposal that the latter subfraction is the major contributor to the anti-atherogenic role of plasma HDL.

Adult↗
PubMed1980

Combined drug therapy for familial hypercholesterolemia.

Six familial hypercholesterolemic subjects were treated with a combination of cholestyramine (16 g/day) and nicotinic acid (3 g/day). This therapy consistently lowered plasma cholesterol and triglyceride by, on average, 41% and 37% respectively. Very low density and low density lipoprotein cholesterol fell, while high density lipoprotein cholesterol rose significantly. Plasma apolipoprotein levels were also affected by treatment. Apolipoprotein A-I rose 26% and apolipoprotein B fell 31%. In addition, there was a fourfold increase in plasma high density lipoprotein subfraction2 (HDL2), although HDL3 remained unaltered. These favorable changes in a number of atherosclerotic risk indices commend the use of this drug combination in the treatment of heterozygous familial hypercholesterolemia.

Adult↗
PubMed1979

The effects of cholestyramine on high density lipoprotein metabolism.

This study on 4 type II hyperlipoproteinaemic subjects examines the effects of pharmacologic doses (8 g twice daily) of the bile acid sequestrant cholestyramine on the plasma distribution and chemical composition of the high density lipoprotein subfractions, HDL2 and HDL3, and describes the influence of the drug on the metabolism of the major HDL aporoteins, apolipoprotein A-I and A-II. Cholestyramine lowered plasma low density lipoprotein cholesterol (32%; P less than 0.05) without affecting the level of that lipid in very low density or high density lipoproteins. However, the plasma HDL2/HDL3 ratio and apolipoprotein A-I concentration rose significantly on treatment, while apolipoprotein A-II remained unchanged. The rise in apolipoprotein A-I derived from an increase in its synthetic rate and produced a relative enrichment of the protein with respect to apolipoprotein A-II in both HDL subfractions. These results demonstrate the cholestyramine treatment affects HDL metabolism in a way which, according to current concepts, may prove beneficial to the recipient.

Apolipoproteins↗
PubMed1979

Severe hypokalemia in hospitalized patients.

Profound hypokalemia was observed in 73 patients in a major university teaching hospital during a three-year period. When compared with hospitalized subjects used as controls, these patients experienced a greater mortality, were substantially more likely to be female, but were not more likely to suffer from cardiovascular disease. Use of a diuretic appeared to precipitate profound hypokalemia infrequently, and when it did, the clinical situation was extremely complex. Over 10% of the patients with hypokalemia had acute myeloid leukemia, an incidence 22 times greater than that expected. Hypokalemia should be sought in all patients with this disease, since it is an avoidable cause of death. Further studies into the mechanism of hypokalemia are required to explain its striking preponderance in women.

Cardiovascular Diseases↗
PubMed1977

Lipoprotein concentrations in untreated adult onset diabetes mellitus and the relationship of the fasting plasma triglyceride concentration to insulin secretion.

Plasma lipoprotein concentrations in 64 untreated adult onset diabetics were compared to the lipoprotein levels found in non diabetics. No significant difference was found. The relationship of the fasting plasma triglyceride concentration to the plasma immunoreaction insulin response to 50 g glucose orally was investigated. Using correlation analysis a significant and insulin response in the non diabetics but not in the diabetics.

Cholesterol↗
PubMed1976

Radioimmunoassay for human plasma apolipoprotein B.

We have developed a simplified double antibody radioimmunoassay for human apolipoprotein beta. The purified antigen, a narrow density subclass of beta lipoprotein (d 1.030-1.050 g/ml; was isolated by a combination of gel filtration and ultracentrifugationmthis material gave a single immunoprecipitin arc on crossed immunoelectrophoresis into an antibody to whole human serum. The antigen was radiolabelled using iodine monochloride at pH 10. The iodinated antigen was indistinguishable immunochemically from native material and eluted as a single radioactive peak from a Sephadex G-200 column. The lower limit of sensitivity of the assay was 15 ng protein, and the working range, 15-200 ng. The mean apolipoprotein B level (+/-1 S.D.) in 128 healthy control subjects was 86.6 +/- 29.6 mg/100ml and is in agreement the values published by other workers using unmodified assays.

Apoproteins↗
PubMed1976

Radioiodination of human low density lipoprotein: a comparison of four methods.

A comparison has been made of four labelling techniques used to radioiodinate human low density lipoprotein (LDL). (1) Chloramine T iodination at pH 7.4 was 20-25% efficient and gave a product immunologically indistinguishable from native LDL. Approximately 30% of the incorporated radioactivity, however, was found in LDL lipids, and the metabolic decay of the labelled complex in rats did not obey first order kinetics. Radiolabelling at pH 10 reduced the uptake of 125I into lipids to 10% but also cut the overall incorporation of radioiodine by a factor of 7. (2) Lactoperoxidase labelling and (3) conjugation with iodinated N-succinimidyl-3-(4-hydroxyphenyl)propionate were highly efficient (100%), but incorporation of radioactivity into the lipid moiety was unacceptably high (approximately 30%). (4) The efficiency of iodine monochloride labelling was highly reproducible and the product was immunologically indistinguishable from native LDL. Incorporation of radioactivity into the lipid moiety was less than 4% when the I/protein ratio of the product was kept at or below 1 : 1. Decay of the radiolabelled LDL in rats was monoexponential.

Animals↗
PubMed1976

Low density lipoprotein metabolism in a family of familial hypercholesterolemic patients.

A low-density lipoprotein turnover study was performed on six heteroxygous familial hypercholesterolemic subjects and five control subjects. The diagnosis of the condition was clear-cut on biochemical, clinical, and genetic grounds. Kinetic analysis of the plasma decay curves gave the following mean values: (1) The plasma concentration of low density lipoprotein apoprotein (apoLDL) in the affected subjects was 247 mg/dl, a 2.5-fold increase over control values (98 mg/dl). (2) The calculated fractional catabolic rate of the intravascular apoLDL pool in the dyslipo-proteniemics was reduced with respect to control data (16.4%/day versus 31.2%/day), and the half-life of the apolipoprotein was correspondingly increased (6.07 days versus 3.63 days). (3) The absolute catabolic rate of the apoLDL was 15.6 mg/kg/day in contrast to the lower value of 11.6 mg/kg/day in the control group. (4) A strong negative correlation was observed between the plasma apoLDL concentration and the fractional catabolic rate (r = 0.96). We conclude from our data that increased apoLDL synthesis coupled with a defective or saturated catabolic mechanism is implicated in the pathogenesis of familial hypercholesterolemia.

Adult↗