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Biomedical subjects

T Kuusi

Publications and source records attributed to T Kuusi.

At least 55 records · Page 3Linked to original sources
PubMed1987

Desogestrel- and levonorgestrel-containing oral contraceptives have different effects on urinary excretion of prostacyclin metabolites and serum high density lipoproteins.

Prostacyclin synthesis is stimulated in vitro by high density lipoproteins (HDL), which themselves are differently affected by desogestrel (DG)- and levonorgestrel (LN)- containing oral contraceptives. In this study we measured the urinary excretion of the metabolites of prostacyclin [6-keto-prostaglandin F 1 alpha(6-keto) and 2,3-dinor-6-keto-prostaglandin F1 alpha (dinor)] and of thromboxane A2 [thromboxane B2 (TxB2)] as well as serum HDL- and HDL2 cholesterol concentrations before and during DG and LN administration alone or in combination with ethinyl estradiol (EE) in 26 women. Before the trial, urinary dinor excretion correlated with serum total HDL cholesterol (r = 0.499; P less than 0.01) and HDL2 cholesterol levels (r = 0.668; P less than 0.001; n = 26). Administration of DG (150 micrograms/day; 14 women) or LN (150 micrograms/day; 12 women) for 2 weeks caused no changes in the excretion of these prostanoids, but LN administration decreased serum HDL cholesterol levels. After that, the women underwent a monophasic regimen of 150 micrograms DG or LN plus 30 micrograms EE for 3 months and thereafter polyphasic regimens of the same steroids for a further 3 months. The DG-containing pills increased urinary dinor excretion by 25-40%, but caused no changes in 6-keto and TxB2 excretion, as measured on days 19-21 of the cycles. LN-containing pills reduced urinary 6-keto excretion by 22% at the end of polyphasic treatment, but caused no changes in dinor and TxB2 output. DG plus EE, but not LN plus EE, increased serum total HDL and HDL2 cholesterol concentrations by a maximum of 25%. Thus, a DG plus EE combination may stimulate PGI2 synthesis by increasing the levels of HDL/HDL2. Theoretically, this stimulation protects against occlusive vascular disorders.

6-Ketoprostaglandin F1 alpha↗
PubMed1987

Aprotinin and Na2CaEDTA in experimental hemorrhagic pancreatitis in pigs.

We have analyzed the effects of aprotinin and Na2CaEDTA on phospholipase A2 activity and on the outcome of experimental pancreatitis in pigs. Hemorrhagic pancreatitis was induced in 29 piglets by infusing Na-taurocholate and trypsin into the pancreatic duct with simultaneous intravenous injection of secretin. Twelve animals serving as controls had no specific treatment. Nine animals were treated with aprotinin and eight pigs with Na2CaEDTA. Ten of the control animals died within 24 h of the induction of pancreatitis, and two of them lived for a week. In the aprotinin group three piglets died within 24 h and two died during the next day; four animals lived for a week. In the Na2CaEDTA group five animals died within 24 h and one the next day; two animals lived for a week. In all the animals serum phospholipase A2 activity increased significantly (p less than 0.01), there being no differences between the groups. In those animals that lived for a week the phospholipase A2 activities decreased on the 2nd day. This decrease was seen in both treated groups. Aprotinin prolonged the survival time of the animals. This prolongation was statistically significant (p less than 0.05, chi-square test, logrank test). Na2CaEDTA did not improve the prognosis of the animals. Neither of the drugs given influenced the serum phospholipase A2 activities during the first hours of the disease.

Amylases↗
PubMed1987

Normalization of lipoprotein lipase and hepatic lipase by gemfibrozil results in correction of lipoprotein abnormalities in chronic renal failure.

Eighteen patients with chronic renal failure (serum creatinine 173-756 mumol/l) and hyperlipidemia were treated with gemfibrozil (1200 mg/day). The drug caused a significant improvement of the dyslipidemia within one week and the effect was progressive during the 28 weeks of treatment. Very-low-density lipoprotein triglycerides and very-low-density lipoprotein cholesterol decreased by about 50% and high-density lipoprotein cholesterol increased by 30%. The lipoprotein changes occurred simultaneously with a significant activation to normal levels of postheparin plasma lipoprotein and hepatic lipases. Opposite effects were observed when gemfibrozil was discontinued and the patients were given placebo. No major harmful effects were observed.

Adult↗
PubMed1986

High density lipoproteins in postprandial lipemia. Relation to sex and lipoprotein lipase activity.

Twelve subjects (6 women, 6 men) were given 120 g fat orally for 2 h to study its effect on serum high density lipoproteins (HDL), HDL subfractions and apoproteins A-I and A-II. In addition, we measured the fasting activity of adipose tissue lipoprotein lipase (LPL). The HDL2 mass concentration increased significantly in women (216 +/- 10 vs 232 +/- 12 mg/dl, P less than 0.01) but not in men (114 +/- 10 vs 119 +/- 11 mg/dl, NS). The changes of the HDL2 mass in women were due to significant increases of phospholipids, and both apoproteins A-I and A-II. In men, only HDL2 phospholipids rose slightly. The HDL2 cholesterol remained unchanged postprandially. Both fasting and maximal postprandial concentrations of HDL2 correlated positively with adipose tissue LPL activity (r = +0.63, P less than 0.05 and r = +0.61, P less than 0.05). The concentration of HDL3 remained unchanged postprandially but compositional changes were observed. Thus, the HDL3 phospholipids increased slightly in both sexes whereas the HDL3 cholesteryl esters fell significantly. The postprandial changes of HDL2 and HDL3 phospholipids were evident in both zonal ultracentrifugation and equilibrium ultracentrifugation. In addition, 5 women received intragastric fat infusions with or without extra soya phospholipids, lecithin. The HDL2 mass concentration increased after both infusions. In 4 of the 5 subjects the overall increment of the HDL2 phospholipids was larger after the phospholipid-rich emulsion than after phospholipid-poor one. This difference was obvious in zonal profile of HDL subfractions which revealed also a slight increase of HDL3 phospholipids after both infusions. In conclusion, the response of HDL2 to fat meal is more pronounced in women than in men and it seems to be dependent on fasting LPL activity which is higher in women than in men. Further, the alterations in postprandial composition of HDL subfractions can be modified by the composition of fat meal.

Adipose Tissue↗
PubMed1986

Long-term ethanol ingestion causes an increase of phospholipase A2 activity in acute experimental pancreatitis in rats.

Alcohol is recognized as one etiological factor in pancreatitis and according to recent studies, phospholipase A2 (PLA2) may be an important factor in the pathogenesis of this disease. However, the effect of chronic ethanol ingestion on PLA2 activity has not been studied in pancreatitis. To clarify the possible relation of these two factors 48 male Wistar rats received 15% (v/v) ethanol in drinking water for 12 weeks and 48 rats served as controls drinking tap water. Blood samples were collected from the control animals by puncturing the abdominal aorta. Experimental pancreatitis was induced by intraductal retrograde infusion of normal rat bile and blood samples collected 24 hr after the infusion. PLA2 activities in the plasma were measured by using the substrate with a 3H-labeled fatty acid in position 2. PLA2 activities in the control group were 11.2 +/- 1.3 (mean +/- SE) nmole/ml/min and 21.7 +/- 3.5 twenty-four hours later (P less than 0.05). In alcoholic rats the activities were 11.1 +/- 1.4 and 54.0 +/- 10.3, respectively (P less than 0.003). The increase of the activities was greater in alcoholic rats and the difference between the groups statistically significant (P less than 0.025). The mortality rate was 4.2% among the control animals and 29.2% in the alcoholic groups (P less than 0.026). The results of this study suggest that chronic alcohol ingestion makes the pancreas vulnerable to severe pancreatitis with high mortality. This is associated with significantly increased activities of PLA2.

Alcoholism↗
PubMed1986

Variation of postheparin plasma hepatic lipase by menstrual cycle.

The effect of cyclic hormonal changes on the lipolytic enzymes in postheparin plasma was studied in 24 young women. The activity of hepatic lipase was significantly suppressed in the luteal phase of the menstrual cycle in 14 women with "normal" (greater than 3.2 micrograms/L) progesterone levels, which was attributed to the preceding midcycle peak of estrogen secretion. Ten subjects with "deficient" luteal phase levels of progesterone exhibited no significant fluctuations in hepatic lipase activity. No cyclic variation occurred in postheparin plasma lipoprotein lipase activity. Significant but inconstant variations also occurred in some lipoprotein fractions, including a reduction in LDL cholesterol in the luteal phase. However, the changes in lipoproteins were not related to lipolytic enzyme activities, nor could they be attributed to hormonal changes with any certainty.

Adult↗
PubMed1986

Postheparin plasma lipoprotein and hepatic lipase activities in hyperinsulinemic infants of diabetic mothers and in large-for-date infants at birth.

To study postheparin plasma lipase activities in nonfed newborn infants immediately after birth and to investigate the possible influence of fetal hyperinsulinemia on lipoprotein lipase activity, we measured lipoprotein and hepatic lipase activities in 55 macrosomic newborn infants: group I consisted of 21 infants born to mothers with insulin-dependent diabetes. The infants were hyperinsulinemic at birth and had hypoglycemia and poor lipolysis at the age of 2 h. Group II consisted of 18 infants born to mothers with gestational diabetes. Group III consisted of 16 large-for-date infants born to nondiabetic mothers. The mean postheparin plasma lipoprotein lipase activities at 2 h of age were similar (mean 36 mumol free fatty acids/ml/h; SEM 15) in groups I-III. Lipoprotein lipase activity correlated negatively with cord-serum triglycerides (range 0.13-1.2 mmol/liter) but did not correlate with serum insulin (range 5.4-524 microU/ml) or C-peptide (range 0.6-21.0 micrograms/liter). Hepatic lipase activity was somewhat higher in group I (mean 68 mumol free fatty acids/ml/h; SEM 23) than in groups II and III (mean 55 mumol free fatty acids/ml/h; SEM 14). Hemoglobin Alc was the only important factor explaining the difference in hepatic lipase activities between groups. Lipoproteins and apolipoproteins A-I, A-II, and B were similar in all three groups. We conclude that in large-for-date infants lipoprotein lipase is active at birth without exogenous fat induction, and that these infants are capable of hydrolyzing fat, their main source of energy, immediately after birth. In addition, we conclude that postheparin plasma lipoprotein lipase activity is not affected by fetal hyperinsulinemia.

Apolipoprotein A-I↗
PubMed1986

Postheparin plasma lipoprotein and hepatic lipase activities in hyperinsulinemic infants of diabetic mothers and in large-for-date infants at birth.

To study postheparin plasma lipase activities in nonfed newborn infants immediately after birth and to investigate the possible influence of fetal hyperinsulinemia on lipoprotein lipase activity, we measured lipoprotein and hepatic lipase activities in 55 macrosomic newborn infants: group I consisted of 21 infants born to mothers with insulin-dependent diabetes. The infants were hyperinsulinemic at birth and had hypoglycemia and poor lipolysis at the age of 2 h. Group II consisted of 18 infants born to mothers with gestational diabetes. Group III consisted of 16 large-for-date infants born to nondiabetic mothers. The mean postheparin plasma lipoprotein lipase activities at 2 h of age were similar (mean 36 mumol free fatty acids/ml/h; SEM 15) in groups I-III. Lipoprotein lipase activity correlated negatively with cord-serum triglycerides (range 0.13-1.2 mmol/liter) but did not correlate with serum insulin (range 5.4-524 microU/ml) or C-peptide (range 0.6-21.0 micrograms/liter). Hepatic lipase activity was somewhat higher in group I (mean 68 mumol free fatty acids/ml/h; SEM 23) than in groups II and III (mean 55 mumol free fatty acids/ml/h; SEM 14). Hemoglobin Alc was the only important factor explaining the difference in hepatic lipase activities between groups. Lipoproteins and apolipoproteins A-I, A-II, and B were similar in all three groups. We conclude that in large-for-date infants lipoprotein lipase is active at birth without exogenous fat induction, and that these infants are capable of hydrolyzing fat, their main source of energy, immediately after birth. In addition, we conclude that postheparin plasma lipoprotein lipase activity is not affected by fetal hyperinsulinemia.

Birth Weight↗
PubMed1986

Apolipoprotein E polymorphism in the Finnish population: gene frequencies and relation to lipoprotein concentrations.

ApoE phenotypes were determined in 615 unrelated Finnish individuals. The apoE gene frequencies observed (epsilon 2, 0.041; epsilon 3, 0.733; epsilon 4, 0.227) differ significantly from those in other populations. The frequency of the allele epsilon 2 was lower and that of epsilon 4 higher than in all other studied populations. Plasma lipids and apolipoproteins A-I, A-II and B were recorded in 207 of the typed subjects. By comparison with the most frequent homozygous apoE 3/3 phenotype, it was found that total cholesterol, LDL-cholesterol, and apoB concentrations were all markedly higher in apoE 4/4 and to a lesser degree in apoE 4/3 phenotypic groups. On the other hand, these lipid and apolipoprotein levels tended to be lower in E-2 heterozygotes. These data confirm and extend, in a different ethnic group, previous results of an effect of apoE genes on plasma lipoprotein concentrations. The data suggest that the apoE gene locus may be one factor responsible for the high LDL cholesterol concentrations in the Finnish population.

Alleles↗
PubMed1985

Very low density lipoprotein triglyceride kinetics during hepatic lipase suppression by estrogen. Studies on the physiological role of hepatic endothelial lipase.

The exact role of the heparin-releasable hepatic endothelial lipase has remained controversial. It has been suggested that it acts in concert with lipoprotein lipase in the step-wise delipidation of triglyceride-rich lipoproteins. On the other hand, there is evidence indicating that high density lipoprotein2 is the preferred substrate for hepatic lipase. Here, it is shown that a moderate (27%) suppression of hepatic lipase activity by estrogen did not impair removal of 3H-labeled very low density lipoproteins (VLDL) triglycerides, suggesting that this enzyme is not a major regulator of VLDL catabolism under physiological circumstances.

Endothelium↗
PubMed1985

Effects of two progestins with different androgenic properties on hepatic endothelial lipase and high density lipoprotein2.

Thirty postmenopausal women were randomly treated with desogestrel (DG) or levonorgestrel (LN) 125 micrograms/day for 3 weeks. Desogestrel reduced the serum total and free (non-protein bound) testosterone concentrations. It caused a small decrease in the sex hormone binding globulin capacity (SHBG) but did not influence the free testosterone index (testosterone/SHBG ratio). Levonorgestrel, on the other hand, did not influence the free testosterone concentration, but caused a significant increase in the free testosterone index. Levonorgestrel reduced the HDL and particularly the HDL2 cholesterol concentrations (mean change from 1.75 to 1.45 mmol/l for HDL and from 0.73 to 0.50 mmol/l for HDL2, P less than 0.001). It also caused a reduction in the VLDL triglyceride (P less than 0.05) but not the total serum triglyceride concentration. Desogestrel did not cause any significant changes in HDL or HDL2 cholesterol concentrations, but it reduced the VLDL triglyceride (P less than 0.01) and total serum (P less than 0.05) triglyceride concentrations. Neither of the two progestins influenced the postheparin plasma lipoprotein lipase (LPL) activity or the serum cholesterol esterification rate by lecithin:cholesterol acyltransferase (LCAT). It is therefore possible that both steroids decreased the hepatic output of triglycerides, which may be clinically important since both progestins are used in combination with ethinylestradiol (EE) which increases the hepatic TG synthesis. The failure of desogestrel to change HDL levels is consistent with earlier data on the lack of effects on HDL by non-androgenic progestins. Levonorgestrel increased the mean activity of postheparin plasma hepatic lipase (HL) from 23.3 to 28.0 mumol X h-1 X ml-1 (P less than 0.05). In contrast, this activity was not influenced by desogestrel. The magnitude of the changes in postheparin plasma HL activity and the free testosterone index (testosterone/SHBG ratio) showed significant positive correlation (+ 0.41, P less than 0.05). On the other hand, the changes in the HDL2 cholesterol and the postheparin plasma HL activity were inversely interrelated (r = 0.52, P less than 0.01). These relationships are consistent with the idea that the effects of different progestins on the HDL cholesterol are mediated by the sex steroid sensitive hepatic endothelial lipase.

Androgens↗
PubMed1985

Sequence of alcohol-induced initial changes in plasma lipoproteins (VLDL and HDL) and lipolytic enzymes in humans.

The sequence of alterations in the concentration and composition of different plasma lipoproteins following alcohol intake is not known. We therefore monitored the concentrations of cholesterol, triglycerides, phospholipids, and proteins in the major lipoprotein fractions (VLDL, LDL, HDL2, and HDL3) in ten nonalcoholic healthy male volunteers who were given 5.5 g of alcohol per kilogram of body weight during 21/2 days (a weekend). In addition, lipoprotein lipase activity was measured in post-heparin plasma and in adipose tissue and hepatic lipase activity was measured in post-heparin plasma before and after the experiment. in a separate control experiment, the same subjects received meals and liquids without alcohol. Blood alcohol levels remained below 1.5 g/L. Alcohol caused a progressive increase in the fasting VLDL triglyceride and phospholipid concentrations, both of which were doubled during the experiment (P less than 0.001). In contrast, the VLDL cholesterol levels remained unchanged until the third morning, when there was a slight increase. The LDL triglyceride and phospholipid concentrations also rose without simultaneous changes in the LDL cholesterol concentration. Consistent with these changes, the HDL cholesterol concentration showed no response to alcohol during the experiment, but the HDL phospholipid level rose from 76 to 99 mg/dL (P less than 0.001). This was reflected as an increase in the HDL2 concentration from 124 to 158 mg/dL (P less than 0.01), whereas no change occurred in the HDL3 level. The increment of HDL2 concentration was due to a rise of its triglycerides, phospholipids, and apoproteins A-I and A-II but not to a rise of cholesterol.(ABSTRACT TRUNCATED AT 250 WORDS)

Adipose Tissue↗
PubMed1985

Dietary fat and blood pressure: an intervention study on the effects of a low-fat diet with two levels of polyunsaturated fat.

The role of dietary fat in human blood pressure control was studied among 84 middle-aged subjects (mainly couples) in two semirural communities in North Karelia, Finland. The families were randomly allocated into two groups that, after a baseline period of 2 weeks, changed their diet for a 12-week intervention period so that the proportion of energy derived from fats was similarly reduced in both groups, from 38 to 24%, but the polyunsaturated/saturated fatty acid (P/S) ratio was increased--from 0.2 to 0.9 in group I and to 0.4 in group II. After the intervention period, both groups switched back to their usual diet for a period of 5 weeks. During the intervention period, total serum cholesterol was reduced by 16% in group I and 14% in group II. Mean body weight and urinary sodium, potassium, calcium, and magnesium excretion changes were small or nonexistent. Mean systolic blood pressure decreased 4 mm Hg in group I (P less than 0.01) and 3 mm Hg in group II (P less than 0.01), and mean diastolic blood pressure decreased 5 mm Hg (P less than 0.001) and 4 mm Hg (P less than 0.01), respectively. The reductions were reversed during the switch-back period (P less than 0.01). These results confirm previous findings of the blood-pressure-reducing effect of a low-fat/high-P/S diet. Although a number of possible confounding factors can be ruled out, the dietary constituent accounting for the blood pressure change cannot be ascertained definitely. The results showed no significant further blood pressure reduction with more than a moderately increased P/S ratio when the saturated fat intake was markedly reduced.

Adult↗
PubMed1985

Phosphoglucomutase (PGM1) subtypes in a Finnish population determined by isoelectric focusing in agarose gel.

The red cell enzyme phosphoglucomutase first locus (PGM1) phenotypes of 639 adult Finns were determined by isoelectric focusing in agarose gel. All the ten commonly occurring phenotypes were detected and the frequencies of the four alleles at the PGM1 locus were as follows: PGMa11 = 0.5313, PGMa21 = 0.1800, PGMa31 = 0.2199 and PGMa41 = 0.0689. The PGM1 phenotypes of 221 mothers with 228 offspring were in accordance with autosomal codominant inheritance.

Alleles↗
PubMed1985

Immunonephelometric measurement of human plasma apolipoproteins A-I and A-II: an assay performed by consecutive addition of the two antisera to a single specimen.

A consecutive immunonephelometric assay for human apolipoproteins (apo) A-I and A-II is described and validated. Apo A-II is first measured from guanidine-HCl-treated samples using a monospecific antiserum raised in sheep against purified apo A-II. This is followed by addition of anti apo A-I serum to the same tubes and recording of the light scattering after 90 min. The results of 125 serum samples were compared with those obtained by the radial immunodiffusion method, and thereby, correlation coefficients of 0.98 and 0.91 could be calculated for apo A-I and apo A-II concentrations, respectively. The within-assay variations of apo A-I and apo A-II methods were 3.28% and 2.40%, respectively, the corresponding inter-assay variations were 7.76% and 8.90%.

Antigen-Antibody Complex↗
PubMed1985

Concentration and composition of serum lipoproteins during a low-fat diet at two levels of polyunsaturated fat.

A 12-week dietary intervention was carried out among 40 families from North Karelia, a county in Finland with an exceptionally high rate of coronary heart disease and high serum cholesterol values. The proportion of dietary energy derived from fat was reduced during the 12-week intervention period from about 39% to 23% in all families. The families were randomly allocated into two groups. Twenty families consumed a diet with a polyunsaturated to saturated fat (P/S) ratio of 0.9 (group I), while the other 20 families had a diet with a P/S ratio of 0.4 (group II). Total serum cholesterol decreased by 16% and 9% in men of groups I and II, respectively, and by 16% in women of both groups. These changes were due to a decrease in both low density lipoprotein (LDL) and high density lipoprotein (HDL) cholesterol. LDL cholesterol and phospholipid reached minimum values after 6 weeks on both intervention diets, but LDL protein responded more slowly. Thus, after 6 weeks LDL had an altered composition containing less cholesterol and phospholipids and more protein and triglycerides than during the baseline diet. During the intervention, the linoleic acid content in the serum cholesteryl ester fraction increased, and the magnitude of this change correlated negatively with the changes in total and LDL cholesterol. The decrease in HDL cholesterol during the two intervention diets was due to a fall in the HDL2 cholesterol (29% and 24% in men, and 26% and 25% in women in groups I and II, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗