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Biomedical subjects

C Cortese

Publications and source records attributed to C Cortese.

At least 73 records · Page 4Linked to original sources
PubMed1985

Plasma apolipoprotein B metabolism in familial type III dysbetalipoproteinaemia.

Lipoprotein metabolism was studied in eleven patients with Type III hyperlipoproteinaemia, one with normolipidaemic dysbetalipoproteinaemia and eight controls. Apolipoprotein B kinetics in very low density, intermediate density and low density lipoproteins (VLDL, IDL and LDL) was investigated. Fractional catabolic rates (FCRs) of VLDL-apo B and IDL-apo B were lower (P less than 0.005 and P less than 0.001) in the patients: 0.064 +/- 0.018 and 0.059 +/- 0.006 h-1 respectively, (mean +/- SEM), compared with 0.219 +/- 0.035 and 0.243 +/- 0.028 h-1. Synthetic rates (SRs) of IDL-apo B varied widely from 1.5 mg kg-1 day-1 in the subject with normolipidaemic dysbetalipoproteinaemia to 2.8-25.2 mg kg-1 day-1 in Type III. The mean time for conversion of IDL-apo B to LDL-apo B was prolonged, 18.7 h compared with 3.8 h in the controls (P less than 0.001). LDL-apo B pool size and SR were lower in the patients (P less than 0.05 for both). Two patients treated with gemfibrozil showed reduced hyperlipidaemia and decreased SR of VLDL-apo B and IDL-apo B. Dysbetalipoproteinaemia is associated with pronounced impairment of IDL and VLDL-remnant catabolism, lipoprotein levels reflecting an interaction between this defect and SR of these lipoproteins.

Adult↗
PubMed1984

Metabolic study of variation in plasma cholesterol level in normal men.

Variation in plasma cholesterol in normal populations underlies a 2-5 fold range of risk of coronary heart disease. The metabolic basis of this variation was studied in a healthy population recruited from a general-practice list. Compared with men in the modal decile of plasma cholesterol, those in the top decile maintained their high levels by overproduction of low-density lipoprotein (LDL). Men in the bottom decile of plasma cholesterol had low levels of LDL, resulting chiefly from a greater rate of fractional catabolism of this lipoprotein; and blood mononuclear cells from men in the bottom decile catabolised LDL more rapidly in vitro than did cells from other men. Intake of dietary lipids by men in the top, modal, and bottom deciles did not differ significantly. Different mechanisms appear to underlie high and low levels of plasma cholesterol in a normal population.

Adult↗
PubMed1984

A multifactorial diet in the management of hyperlipidaemia.

To augment the effectiveness of conventional lipid-lowering treatment, a diet has been evolved combining modified fat content with an increase in vegetable-derived fibre and protein. This was evaluated in 37 hyperlipidaemic and normal ambulant subjects in whom plasma lipid and lipoprotein responses were measured for 4.7-11 months. Mean reductions in plasma cholesterol, triglyceride and low density lipoprotein cholesterol levels were 22, 24 and 25% respectively; there was no significant change in the cholesterol concentrations in high density lipoprotein or in its HDL2 subclass. The effectiveness of the diet in reducing hyperlipidaemia, its influence in optimizing the distribution of cholesterol between plasma lipoprotein classes, and its nutrient composition suggest that it is an advance on existing lipid-lowering dietary patterns.

Adult↗
PubMed1984

Studies of lipoprotein metabolism in a patient with fish-eye disease.

In the rare familial disorder fish-eye disease, hypertriglyceridaemia is associated with elevated levels of very-low-density lipoprotein (VLDL) and enrichment of low-density lipoprotein (LDL) with triglyceride. The kinetic basis of the dyslipoproteinaemia was investigated by studying the metabolism of the apolipoprotein-B moeity of VLDL, intermediate-density lipoprotein (IDL) and LDL in a 68-year-old woman with this condition. The major kinetic abnormality was a pronounced reduction in the rate of fractional conversion of VLDL-B to IDL-B and of IDL-B to LDL-B, suggesting that the dyslipoproteinaemia represents accumulation in plasma of partly degraded products of VLDL metabolism. This kinetic disorder has features in common with type-III hyperlipoproteinaemia. In studies in vitro no defect in the enzyme, activator or substrate components of the lipoprotein lipase or hepatic lipase systems was observed.

Aged↗
PubMed1983

Hypocholesterolaemia and non-cardiovascular disease: metabolic studies on subjects with low plasma cholesterol concentrations.

Some epidemiological studies have suggested an inverse relation between serum cholesterol concentration and mortality from cancer. Two hypotheses that might explain such a relation were investigated. To assay potentially deleterious effects of hypocholesterolaemia on cell membranes the lipid content and fluidity of blood mononuclear cells were measured in healthy male volunteers with a wide range of serum cholesterol concentration (3.2-10.0 mmol/l (124-387 mg/100 ml)). Fluidity, unesterified cholesterol content, and the ratio of cholesterol to phospholipid were unrelated to serum cholesterol and to low density lipoprotein cholesterol concentrations. Similar measurements were made on fibroblasts and mononuclear cells incubated with a range of concentrations of low density lipoprotein; fluidity was altered only at extremely low concentrations, suggesting that changes in cell membranes are unlikely to occur at serum cholesterol concentrations attainable by dietary or drug treatment of hyperlipidaemia. In the same population direct relations were confirmed between low density lipoprotein concentration and plasma concentrations of retinol and beta carotene. This is compatible with the suggestion that an association between low cholesterol concentration and cancer may be secondary to a relation between low retinoid concentrations and cancer.

Adult↗
PubMed1983

Lack of correlation between the maximum low-density lipoprotein (LDL) receptor activity of blood lymphocytes and plasma LDL concentration in normal men.

1. Measurements were made of the maximal low-density lipoprotein (LDL) receptor activities of blood lymphocytes from 81 healthy men with a wide range of plasma LDL cholesterol concentrations (1.45-7.55 mmol/l). 2. Receptor activity was quantified by measuring the degradation of 125I-labelled LDL (10 micrograms of protein/ml) to trichloroacetic acid-soluble material during a 6 h incubation, after derepression of the lymphocytes for 72 h in lipoprotein-deficient medium. 3. No significant correlation existed between LDL receptor activity in vitro and plasma LDL cholesterol concentration in vivo (r = -0.08).

Adult↗
PubMed1983

Modes of action of lipid-lowering diets in man: studies of apolipoprotein B kinetics in relation to fat consumption and dietary fatty acid composition.

The mechanisms by which dietary fat influences fasting plasma lipid concentrations have been investigated in hyperlipidaemic subjects. The synthetic and fractional catabolic (FCR) rates of the apoprotein B (apo B) of very-low density (VLDL) and low-density (LDL) lipoproteins were measured using radioiodinated autologous lipoproteins. Reductions of LDL concentration in eight subjects during low-fat (25% of energy) diets were largely explained by diminished synthesis (-20%, P less than 0.02), and possibly also by an increased FCR (+15%, P = 0.05) of LDL, compared with observations made during a high-fat (45% of energy) diet of similar fatty acid composition. VLDL apo B synthesis and FCR were not significantly altered. When a diet rich in polyunsaturated fatty acids was exchanged for one high in saturated fatty acids (fat providing 45% of energy on both occasions) in four subjects, the synthetic rates of both VLDL apo B (-31%, P less than 0.02) and LDL apo B (-23%, P less than 0.10) were reduced while their FCRs were unchanged.

Adult↗
PubMed1982

Myelomatosis with type III hyperlipoproteinemia: clinical and metabolic studies.

We investigated the metabolism of intermediate-density lipoproteins (IDL [1.006 to 1.019 g per milliliter]) and low-density lipoproteins (LDL [1.019 to 1.063 g per milliliter]) in two men with Type III hyperlipoproteinemia associated with myelomatosis. In vivo kinetic studies using radiolabeled autologous lipoproteins demonstrated a greatly reduced fractional catabolic rate of IDL, relative to control values (patients vs. normal, 0.006 and 0.025 per hour vs. 0.20 +/- 0.08 per hour [mean +/- S.E.M]) and a greatly prolonged IDL-to-LDL conversion time (45 and 17 hours vs. 5.4 +/- 1.6 hours). In studies in vitro, LDL from both patients failed to bind to the LDL receptor of normal blood lymphocytes, whereas LDL from subjects with familial Type III hyperlipoproteinemia bound normally to the receptor. In one patient immunoglobulin was shown to be associated with IDL and LDL. Thus, hyperlipoproteinemia reflected an impaired metabolism of IDL, probably secondary to the binding of immunoglobulin to the lipoproteins. A similar impairment of receptor-mediated LDL catabolism did not elevate the plasma LDL concentration because of the low IDL-to-LDL conversion rate.

Apoproteins↗
PubMed1982

The effects of probucol on plasma lipoproteins in polygenic and familial hypercholesterolaemia.

During treatment with probucol at the dose of 1 g per day, the mean reduction in low density lipoprotein (LDL) cholesterol concentration was 11.2% in polygenic hypercholesterolaemia (n = 9) and 9.4% in heterozygous familial hypercholesterolaemia (n = 6). However, there was marked heterogeneity of response: in seven of the patients with polygenic hypercholesterolaemia who had in common moderate elevation of LDL cholesterol (5.3-6.4 mmol/1), the reduction ranged from 13 to 40% (mean, 23%). In two of this group the change in LDL concentration was associated with a decrease in LDL apolipoprotein B synthetic rate. Of the patients with familial hypercholesterolaemia one showed a 33% reduction in LDL cholesterol, and one a 13% reduction. Total high density lipoprotein (HDL) cholesterol concentration tended to decrease during treatment. This reflected a reduction of the cholesterol concentration in the HDL3 subclass; HDL2 cholesterol remaining unchanged. Plasma triglyceride and very low density lipoprotein cholesterol were unaffected by probucol. The drug was well tolerated with only one patient complaining of severe diarrhoea, and two of mild and transient diarrhoea. No clinically significant changes occurred in serial resting electrocardiograms. Thus, probucol appears to be a useful drug for the treatment of most patients with polygenic hypercholesterolaemia, and of some patients with heterozygous familial hypercholesterolaemia.

Adolescent↗
PubMed1982

Heritability of the low density lipoprotein receptor activity of human blood mononuclear cells: studies in normolipidaemic adult male twins.

1. The concordance of low density lipoprotein (LDL) receptor activity of blood mononuclear cells was examined in 26 pairs of monozygotic and 17 pairs of dizygotic normolipidaemic young adult male twins. 2. Receptor activity was quantified as the degradation of 125I-labelled LDL during a 6 h incubation, after derepression of the cells for 72 h in lipoprotein-deficient medium. 3. The total variance of receptor activity was similar in the two groups of twins. In contrast, within-pair variance was five times greater in dizygotic twins than in monozygotic twins (P less than 0.001). 4. Estimates of heritability, mostly based on the intra-class correlation coefficients (monozygotic, r = 0.83; dizygotic, r = 0.39), ranged from 0.72 to 1.05. 5. These results suggest that the maximal LDL receptor activity of peripheral cells in normolipidaemic subjects is largely genetically determined.

Adolescent↗
PubMed1981

Splanchnic metabolism of plasma apolipoprotein B: studies of artery-hepatic vein differences of mass and radiolabel in fasted human subjects.

The metabolism of apoprotein B-containing plasma lipoproteins by human splanchnic tissues has been studied in 29 men undergoing coronary angiography. Before catheterization autologous radio-iodinated lipoproteins were infused into a peripheral vein: 10 subjects received (125)I-labeled Sf 12-60 lipoproteins; 12 received (125)I-labeled Sf 12-60 plus (131)I-labeled Sf 100-400 lipoproteins; and 7 received (125)I-labeled Sf 12-60 plus (131)I-labeled Sf 0-12 lipoproteins. Paired arterial and hepatic vein blood samples were subsequently collected for replicate measurements of apoprotein B (apo B) mass, radioactivity and specific activity in each lipoprotein class. Splanchnic plasma flow was measured with indocyanine green. All studies were conducted after a 14-h overnight fast. Newly synthesized apo B was shown to be secreted by splanchnic tissues as a component of Sf 100-400 lipoproteins, with no detectable uptake of apo B from this class. Sf 12-60 apo B was extracted by the splanchnic bed, with no detectable secretion. After continuous intravenous infusion of (125)I-labeled Sf 12-60 for five or more hours, 41-67% (mean 55%) of extracted Sf 12-60 apo B radioactivity reappeared in hepatic vein Sf 0-12 apo B. There was no detectable splanchnic catabolism of Sf 0-12 apo B. The rates of Sf 100-400 apo B secretion, calculated as the product of artery-hepatic vein concentration difference and splanchnic plasma flow, were greater than the previously reported rates of very low density lipoprotein apo B turnover in fed subjects obtained by kinetic analysis of plasma specific radioactivity decay curves, suggesting that there may be a diurnal variation in hepatic apo B synthesis. They also exceeded the splanchnic extraction rates of Sf 12-60 apo B, suggesting there was some extrasplanchnic catabolism of the apo B of Sf > 60 lipoproteins.

Adult↗
PubMedDate not supplied

Noninvasive ultrasound evaluation of pressure gradients in aortic root of homozygotes for familial hypercholesterolemia.

The aim of this study was to measure noninvasively by Doppler ultrasound the blood flow velocity at the level of the aortic root in patients with homozygous familial hypercholesterolemia (FH) to detect abnormal pressure gradients. Seven patients with homozygous FH and seven healthy controls matched for age and sex were included in the study. Continuous-wave Doppler (2 MHz) was used to measure the highest detectable velocity from the aortic root; the probe was positioned in the suprasternal notch. When an abnormal velocity was detected, the corresponding pressure drop was calculated from the formula: Delta P = 4Vmax2. Each FH patient had an abnormal aortic velocity consistent with a pressure gradient across the valvular area. All the controls had normal aortic velocities (p less than 0.01). The measurement of the pressure drop across the aortic valvular area in FH patients gives an estimate of the lesions produced by cholesterol deposition in a crucial area of the cardiovascular system near the origin of coronary arteries. The noninvasivity of this method makes it an excellent method for obtaining parameters for follow-up and clinical trials.

Adolescent↗
PubMedDate not supplied

Influence of plasma lipoproteins on platelet aggregation in a normal male population.

Aggregation tests were performed on platelet-rich plasma from healthy male volunteers to determine the minimum concentration of adenosine diphosphate (ADP), epinephrine, collagen, or thrombin required to induce secondary aggregation. Platelets were also analyzed for cholesterol and phospholipid, and in some cases their membrane fluidity was determined by fluorescence depolarization of the probe, diphenylhexatriene. Concentrations of the major lipoprotein fractions in the plasma were measured and related to the sensitivity of platelets to the four agonists. Low density lipoprotein (LDL) and total cholesterol concentrations, but not high density lipoproteins (HDL) or very low density lipoproteins (VLDL), were positively correlated with sensitivity to aggregation by epinephrine, but not by other agonists. By arrangement of the lipoprotein concentration into quintiles, the effect of LDL was most striking in the lower two quintiles, where the sensitivity to adrenaline and ADP were much diminished. The middle and upper two quintiles showed a similar sensitivity. Lower platelet cholesterol/phospholipid ratios were also associated with a reduced sensitivity to epinephrine or ADP, but only at the lower end of the range. Membrane microviscosity was correlated negatively with collagen sensitivity and with VLDL cholesterol concentrations, but positively with HDL cholesterol concentrations. Platelet behavior appears, therefore, to be influenced by lipoprotein concentrations within the range found in a healthy population.

Adenosine Diphosphate↗