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Biomedical subjects

A G Olsson

Publications and source records attributed to A G Olsson.

At least 19 recordsLinked to original sources
PubMed1992

Plasma lipid and lipoprotein effects of transdermal administration of estradiol and estradiol/norethisterone acetate.

To evaluate the effect of transdermal sequential treatment with estradiol and estradiol/norethisterone acetate on lipoprotein metabolism, 25 postmenopausal women received treatment for 12 cycles of 4 weeks each (2 weeks estradiol 50 micrograms/day and 2 weeks a combined patch delivering norethisterone acetate 0.25 mg/day and estradiol 50 micrograms/day). Blood samples for lipoprotein analyses were drawn before treatment and in estrogen and combined phases in cycles 3 and 12. Plasma total cholesterol, low (LDL) and high (HDL) density lipoprotein were all significantly reduced in both estrogen and combined phases. Eighteen of the women continued the treatment for 36 cycles. In this group the HDL-cholesterol had returned to baseline values in combined phase in cycle 24. Plasma cholesterol and LDL-cholesterol values remained significantly reduced throughout the whole study compared to the pre-trial values. The present study by transdermal sequential hormonal treatment results in a lipid and lipoprotein pattern with reduced total cholesterol and LDL cholesterol in postmenopausal women.

Administration, Cutaneous↗
PubMed1979

Separation of two serum very low density lipoprotein fractions using starch block electrophoresis.

A quantitative electrophoretic method has been developed in order to differentiate very low density (VLDL) pre-beta lipoproteins from late pre-beta lipoproteins using starch as a supporting medium. It was possible to obtain a bimodal distribution of lipoprotein lipids from VLDL which on agarose gel electrophoresis had a pre-beta band and a late pre-beta band. Optimal conditions were: ammonium carbonate buffer, mu = 0.025, dialysis prior to electrophoresis. Agarose gel electrophoresis demonstrated that the fast and slow components obtained on starch block electrophoresis corresponded to the pre-beta and late pre-beta band respectively. With increasing migration towards the anode the ratio of cholesterol to triglycerides decreased continuously. It is suggested that the fast triglyceride rich component represent newly secreted VLDL species and the slower component mainly postlipolytic particles. The pre-beta band on agarose gel electrophoresis might represent more newly secreted VLDL than the late pre-beta band. However, it cannot be excluded that part of late pre-beta lipoproteins may be secreted de novo.

Blood Proteins↗
PubMed1979

Dissociation of the effects of nicotinic acid on vasodilatation and lipolysis by a prostaglandin synthesis inhibitor, indomethacin, in man.

The effects of nicotinic acid on plasma free fatty acid (FFA) concentration and forearm blood flow were studied in seven healthy fasting volunteers with and without pretreatment by indomethacin to see if some effects of nicotinic acid are mediated by release of endogenous prostaglandin. 1 g of nicotinic acid per os decreased plasma FFA concentration to a lowest value of 1/4 of initial level and increased forearm blood flow four times. When the same dose of nicotinic acid was given after pretreatment with indomethacin, the blood flow increase was only 1/3 of that without indomethacin. Indomethacin did not alter the rapid initial decrease in plasma FFA, although the period of low FFA concentration was shortened and the rebound to supranormal concentration was abolished. Thus the vasodilatory effect of nicotinic acid seems to be mediated by release of endogenous prostaglandin while the inhibition of lipolysis by the drug is mainly produced by other mechanisms.

Adult↗
PubMed1978

Acute effects of cholestyramine on serum lipoprotein concentrations in type II hyperlipoproteinaemia.

Twelve subjects with primary type IIA hyperlipoproteinaemia were treated with cholestyramine under metabolic ward conditions in order to study the timing of effects of different serum lipoprotein classes. After 1 day's treatment changes occurred in all 3 classes, i.e., very low (VLDL), low (LDL) and high (HDL) density lipoprotein classes. VLDL increased abruptly and remained constant during treatment. The ratio of cholesterol/triglycerides decreased suggesting the formation of larger particles. LDL cholesterol decreased continuously suggesting a different mechanism behind this effect than that on VLDL. LDL triglyceride remained constant indicating a relative increase of LDL1. HDL cholesterol decreased while HDL triglycerides increased. All changes made the lipoprotein pattern more "type IV-like". The findings were in agreement with an increased formation of VLDL and an increased flux of lipoprotein through the cascade VLDL-IDL-LDL1-LDL2.

Aged↗
PubMed1978

Dose-response study of bezafibrate on serum lipoprotein concentrations in hyperlipoproteinanemia.

The effect of bezafibrate in the dosages 450, 900 and 1350 mg daily on serum lipoprotein concentrations were studied in 20 subjects with primary hyperlipoproteinaemia (16 of type IV, 2 of type II B, 1 of type III). Except for LDL cholesterol maximum effects were obtained with 450 mg daily. Total serum cholesterol and triglycerides (TG) fell significantly. Mean very low density lipoprotein (VLDL) TG fell by 54%. The maximum effect on low density lipoprotein was obtained with 900 mg daily. The effect was highly dependent on initial concentrations, decreases being observed above 4 mmoles/l and increases below that concentration. High density lipoprotein cholesterol increased by 31% (P less than 0.01) independently of the VLDL decrease. Three subjects suffered gastrointestinal side-effects on 1350 mg daily. Only benign reversible changes were noted on non-lipid measurements. Bezafibrate is a well-tolerated drug with a good VLDL TG lowering effect. It is particularly effective in increasing HDL cholesterol concentrations.

Cholesterol↗
PubMed1978

One-year study of the effect of bezafibrate on serum lipoprotein concentrations in hyperlipoproteinaemia.

The effect of bezafibrate (2-(4-[2-(4-chlorobenzamido)-ethyl]-phenoxy)-2-methylporopionic acid) (450 mg daily) on serum lipoprotein concentrations was studied for 1 year in 14 subjects with hyperlipoproteinaemia (3 of type II A, 2 of type II B, 2 of type III and 7 of type IV). After 2 months serum cholesterol decreased from 7.12--6.08 mmoles/l (15% P less than 0.01), triglycerides from 2.52--1.96 mmoles/l (22%, P less than 0.01), very low density lipoprotein triglycerides from 1.48--0.86 mmoles/l (42%, P less than 0.01) and low density lipoprotein cholesterol from 5.00--3.81 mmoles/l (24%, P less than 0.01). While triglyceride concentrations of serum and lipoproteins remained constant for 1 year, serum and LDL cholesterol concentrations increased slightly after 6 and 12 months. The former rise was partly due also to a rise of the possibly beneficial high density lipoprotein cholesterol from 1.27--1.68 mmoles/l (32%, P less than 0.01) after 6 months, making the effect on total cholesterol less pronounced. Subjective side-effects were nausea in one patient. No severe biochemical side-effects were noted.

Cholesterol↗
PubMed1978

Acute effect of dietary therapy of type IV hyperlipoproteinaemia on the serum and lipoprotein concentrations and relative composition.

In a detailed study the acute effect of diet and hospital admission on the plasma and lipoprotein lipid concentrations and composition was studied in 28 patients with type IV hyperlipoproteinaemia. Within 6 days there were significant falls in the mean serum cholesterol and triglycerides, very low density lipoprotein (VLDL) cholesterol and triglycerides and in high density lipoprotein triglycerides. These changes were accompanied by a significant rise in the mean low density lipoprotein (LDL) cholesterol concentrations. Using multiple regession models highly significant predictions of the change in VLDL triglyceride (R2 = 0.71) and LDL cholesterol (R2 = 0.47) were obtained utilising the pre-treatment lipoprotein levels as independant variables. Since elevated LDL cholesterol concentations are associated with atherosclerotic disease such models may have important therapeutic applications.

Cholesterol↗
PubMed1978

Conversion of the electrophoretic pattern of type IV hyperlipidaemia to type III by intravenous heparin.

Heparin was given i.v. to subjects with type IV hyperlipoproteinaemia who had only ordinary pre-beta lipoproteins and no late pre-beta lipoproteins (LP-beta) in their very low density lipoproteins (VLDL, d less than 1.006) upon agarose gel lipoprotein electrophoresis. Within 15 min the electrophoretic pattern of VLDL had changed completely. The normal pre-beta lipoproteins had disappeared and a discrete LP-beta lipoprotein had appeared. This new electrophoretic pattern, induced 15 min after heparin, is similar to that diagnostic of type III hyperlipoproteinaemia. It is suggested that the LP-beta lipoproteins represent an end stage in the catabolism of VLDL.

Cholesterol↗
PubMed1978

The relation between carbohydrate extraction by the forearm and arterial free fatty acid concentration in man. I. Forearm work with nicotinic acid infusion.

To see if the magnitude of carbohydrate extraction by working skeletal muscle in man is inversely correlated with the arterial free fatty acid (FFA) concentration as in the heart, eighteen healthy men were studied during dynamic forearm work with and without nicotinic acid. The extraction or release of glucose, lactate and pyruvate was determined by the simultaneous sampling of blood from the brachial artery (a) and a deep vein (dv) of the active forearm. Nicotinic acid decreased the arterial FFA concentration from 498 +/- 53 to 134 +/- 12 mumol per litre plasma and this caused a decrease in calculated extraction of FFA. However, it did not affect the extraction of glucose, which was of a magnitude similar to one third of the oxidative metabolism in both situations. One of the possible reasons of this difference compared to the human heart muscle is that the exercising skeletal muscle may utilize stored substrate to a greater extent, which makes possible shifts in substrate utilized for oxidation without changes in substrate extraction. Another reason may be that FFA utilization covers a far smaller proportion of oxidative metabolism in skeletal than in heart muscle already before nicotinic acid.

Adult↗