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Biomedical subjects

L Wallentin

Publications and source records attributed to L Wallentin.

168 records · Page 10Linked to original sources

Metabolic and hormonal effects of post-menopausal oestrogen replacement treatment. I. Glucose, insulin and human growth hormone levels during oral glucose tolerance tests.

Glucose, insulin and growth hormone (GH) levels were measured during 3h oral glucose tolerance tests, performed in two groups of post-menopausal women. Nineteen subjects were given ethinyloestradiol (EOe) 0.05 mg daily and 20 received oestradiol valerinate (OeV) 2 mg daily. The tests were performed twice before treatment and after 1, 3 and 6 cycles of medication. EOe induced a slight but statistically significant deterioration of the glucose tolerance concomitant with a tendency to elevated insulin levels. The women taking OeV showed no significant alteration of the glucose or insulin levels. The GH concentrations were increased in both groups although the elevation was more pronounced in those taking EOe. The reduced carbohydrate tolerance was not believed to have been responsible for the raised GH levels.

Blood Glucose↗

Influence of fat ingestion on lecithin:cholesterol acyl transfer rate in plasma of normal persons.

Lecithin:cholesterol acyl transfer (LCAT) rate in plasma and lipid concentrations in total plasma and high density lipoproteins (HDL) were determined before and after oral fat loads in healthy human subjects. The changes of LCAT rate after fat loading were compared to the effect of chylomicrons or lipid emulsions added in vitro to fasting plasma. After the fat loads there was an increase of mean molar LCAT rate simultaneous with an increase of mean phospholipid (PL) and HDL-PL concentration but not simultaneous with the increase of mean triglyceride (TG) concentration. Individual changes of molar LCAT rate correlated positively with changes of PL, HDL-PL, and unesterified cholesterol (UC) concentration but not with changes of TG concentration in the separate plasma samples after the fat loads. If only the maximal changes in each subject in any sample at any time after the loads were taken into account, the maximal increase of molar LCAT rate correlated positively with the maximal increase of TG concentration. Molar LCAT rate was not influenced by addition of chylomicrons in vitro but increased after addition of a PL emulsion. It is suggested that LCAT rate is stimulated by an excess of PL in plasma and substrate lipoproteins. This excess of PL may be created in vivo temporarily during chylomicron catabolism. The stimulation of LCAT rate by fat ingestion emphasizes the importance of LCAT as a connecting link between triglyceride and cholesterol metabolism.

Acyltransferases↗

Evaluation of an in vitro assay of lecithin:cholesterol acyl transfer rate in plasma.

Crucial and previously criticized points in a slightly modified version of the Stokke-Norum assay of fractional lecithin:cholesterol acyl transfer (LACT) rate in plasma were studied. LCAT activity in the albumin added to the assay medium and negative influence of remaining organic solvent were important sources of error that it was necessary to eliminate. The assumption of equilibration of labeled cholesterol among lipoproteins in vitro was supported experimentally. Addition of isolated chylomicrons had no influence on initial LACT rate. Incubation time was decreased to 20 minutes to obtain a better estimate of initial LCAT rate in normals. Using gas-liquid chromatography to determine unesterified cholesterol concentration, the precision of measurement of molar LCAT rate was 5.2 per cent (coefficient of variation). Molar LCAT rate in healthy males 20-60 years of age was 56-130 mumol-1(-1)-h-1 (mean +/- 2 S.D.) and compared well with reports from other laboratories and in vivo measurements. At present this methodology is considered to be suitable for studies of LCAT and cholesterol turnover in different metabolic situations and clinical materials.

Acetone↗

Lecithin:cholesterol acyl transfer in plasma of normal persons in relation to lipid and lipoprotein concentration.

Information concerning variation in the lecithin:cholesterol acyl transfer (LCAT) rate in normal persons is scanty. We have therefore analyzed the LCAT rate and the lipid and lipoprotein concentrations in the plasma of healthy normolipidemic persons 20-60 years of age, 40 men and 40 women. 10 per decade and sex. Interindividual variation in molar LCAT rate was 57-130 mumol-u(-1)-h-1 (mean +/- 2 S.D.) with no sex difference. Intraindividual variation of molar LCAT rate studied in 8 women and 9 men was shown to be greater than expected from methodological error and was not explainable by the small changes in plasma lipid concentration during the observation period. In the women the molar LCAT rat was lower during the preovulatory phase of the menstrual cycle than during the postovulatory phase. There was positive correlations between the molar LCAT rate and most of the lipid parameters in plasma. By partial correlation analysis a positive correlation was shown between LCAT rate and triglyceride concentration irrespective of other lipid parameters. Keeping triglyceride concentration constant, there was a positive correlation between molar LCAT rate and total phospholipid, unesterified cholesterol, esterified cholesterol, or low-density lipoprotein (LDL) cholesterol concentration. No correlation was found between high-density lipoprotein (HDL) lipid concentration and LCAT rate. Thus in normal subjects there seems to be a direct relation between very low density lipoprotein and LDL lipid concentration and molar LCAT rate but no relation between HDL lipid concentration and LCAT rate.

Acyltransferases↗

Early statin treatment following acute myocardial infarction and 1-year survival.

CONTEXT: Randomized trials have established statin treatment as secondary prevention in coronary artery disease, but it is unclear whether early treatment with statins following acute myocardial infarction (AMI) influences survival. OBJECTIVE: To evaluate the association between statin treatment initiated before or at the time of hospital discharge and 1-year mortality after AMI. DESIGN AND SETTING: Prospective cohort study using data from the Swedish Register of Cardiac Intensive Care on patients admitted to the coronary care units of 58 Swedish hospitals in 1995-1998. One-year mortality data were obtained from the Swedish National Cause of Death Register. PATIENTS: Patients with first registry-recorded AMI who were younger than 80 years and who were discharged alive from the hospital, including 5528 who received statins at or before discharge and 14 071 who did not. MAIN OUTCOME MEASURE: Relative risk of 1-year mortality according to statin treatment. RESULTS: At 1 year, unadjusted mortality was 9.3% (1307 deaths) in the no-statin group and 4.0% (219 deaths) in the statin treatment group. In regression analysis adjusting for confounding factors and propensity score for statin use, early statin treatment was associated with a reduction in 1-year mortality (relative risk, 0.75; 95% confidence interval, 0.63-0.89; P =.001) in hospital survivors of AMI. This reduction in mortality was similar among all subgroups based on age, sex, baseline characteristics, previous disease manifestations, and medications. CONCLUSIONS: Early initiation of statin treatment in patients with AMI is associated with reduced 1-year mortality. These results emphasize the importance of implementing the results of randomized statin trials in unselected AMI patients.

Aged↗