Publications by authors named "Nikkila E"

We investigated the modulating effect of serum total triglycerides on the lipid composition of various lipoproteins, and on the response to gemfibrozil treatment. This placebo controlled study was conducted blind in 60 participants of the Helsinki Heart Study. An inverse relationship was observed between cholesterol content in all lipoprotein fractions and serum total triglyceride level.

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Acute infections provoke insulin resistance. These experiments were designed to study the severity, duration, and mechanisms of insulin resistance caused by acute infections. First, we studied eight patients [mean age, 29 +/- 11 (+/- SD) yr; body mass index, 23 +/- 2 kg/m2] with acute viral or bacterial infections during the acute stage of their infection and 1-3 months after recovery.

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We studied the clinical effectiveness and mechanism underlying the glucose-lowering effect of evening insulin therapy. Nocturnal profiles of blood glucose, plasma free fatty acid (FFA), glycerol, and lactate and overnight glucose kinetics [( 3-3H] glucose infusion) were measured in 15 non-insulin-dependent diabetic (NIDDM) patients with a relative body weight of 128 +/-4% who were poorly controlled with oral therapy alone. The patients were studied before and 2 wk and 3 mo after bedtime insulin (23 +/- 3 IU) was given in addition to oral therapy.

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Several studies have indicated that genetic polymorphism of apolipoprotein (apo) E is related to coronary artery disease (CAD). We therefore determined the apo E phenotype in 91 consecutive Finnish men with angiographically confirmed CAD. The apo E phenotype distribution differed significantly from that observed in the Finnish population (p less than 0.

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The short-term effects of moderate alcohol consumption on energy balance, serum lipids, and lipoproteins were studied in eight healthy middle-aged men (age 30 to 47 years and body mass index 23.1 to 27.7 w/h2).

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The lipid and lipoprotein profile was examined in male patients with acute myocardial infarction (AMI) at the time of infarction (group A) and in male patients who had survived AMI 2-3 years before the study (group B), and compared to that of healthy controls. The myocardial infarction (MI) patients exhibited similar total cholesterol and LDL-cholesterol levels as the controls. However, the LDL mass concentration was higher in patients than in controls (P less than 0.

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Our earlier studies have shown that heavy alcohol intake increases the serum concentration of HDL2. The present study aimed to test which HDL subfraction is affected by moderate alcohol intake, and to examine the time- and dose-dependency of alcohol-induced changes in serum lipoproteins. Therefore, 30 or 60 g day-1 of alcohol were given to 10 healthy male volunteers during two 3-week periods separated by an abstinence period of 3 weeks.

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To study the effects of acute infections on serum lipids and lipoproteins we measured the concentration and composition of different lipoproteins, apoproteins A-I, A-II, and B, and the activities of plasma postheparin lipolytic enzymes, lipoprotein lipase (LPL) and hepatic lipase (HL) during acute and convalescence phase and after complete recovery in 72 infectious patients (33 with viral infection and 39 with bacterial infection). The mass concentrations of both low density lipoprotein (LDL) (P less than .001) and high density lipoprotein (HDL)2 (P less than .

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To study the effects of short term low dose prednisone administration on serum lipids and lipoproteins we measured the concentration and composition of serum lipoproteins; serum apoproteins (apo) A-I, A-II, and B; and plasma lipolytic enzymes before and during prednisone administration (30 mg/day for 7 days) in eight normal men. We also measured insulin binding to adipocytes. Serum high density lipoprotein (HDL) cholesterol increased significantly after 2 days of prednisone administration; the maximal increase was 27% (P less than 0.

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The production and catabolism of very low density lipoprotein triglycerides (VLDL-TG) were determined in 11 index patients with primary hypertriglyceridemia and in their 70 first-degree relatives. In the probands the mean value for VLDL-TG production rate was twice normal, and the mean fractional catabolic rate (FCR) was reduced to 50% from normal. A similar kinetic pattern was also observed in most hypertriglyceridemic relatives.

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The activity of lipoprotein lipase (LPL) was measured in adipose tissue (AT-LPL) and postheparin plasma (PH-LPL) of 13 obese patients (aged 11 to 31 years) who had surgery for craniopharyngioma 1 to 13 years earlier. AT-LPL activity (mean +/- SEM) was higher in them than in subjects matched with respect to age, sex, and relative body weight (4.6 +/- 1.

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To study the effects of rigorous insulin therapy on serum lipoproteins in patients with noninsulin-dependent diabetes not controlled with oral agents only, we measured serum lipoproteins, apoproteins, lipolytic enzymes, and glucose disposal using an insulin clamp technique before and after 4 weeks of insulin therapy. Lipoproteins were isolated by ultracentrifugation and high density lipoprotein (HDL) subfractions, by rate-zonal density gradient ultracentrifugation. The group included 11 women and eight men (age 58 +/- 1 years and RBW 125 +/- 4%).

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Twenty six preterm infants were studied at the age of 2, 7, and 26 days. The activities of lipoprotein and hepatic lipase in plasma taken 15 minutes after a heparin bolus of 100 IU/kg had been given and the concentrations of carnitine in serum and urine were measured. The mean gestational age was 31 weeks (range 26-35 weeks) and birth weight 1580 g (range 840-2280 g).

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Two separate studies were carried out with acipimox, a new antilipolytic agent with long-lasting activity. First, in a randomized, double-blind, cross-over study a dose of 750 mg/day of acipimox versus placebo was employed for 60 days in 11 patients with type IV hyperlipoproteinemia. Mean plasma triglyceride levels were reduced after acipimox compared to placebo (434 +/- 60 vs 777 +/- 224 mg/dl, P less than 0.

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We studied the effects of testosterone substitution on serum concentrations of lipids, lipoproteins, apoproteins and on the activity of hepatic lipase (HL) and lipoprotein lipase (LPL) in postheparin plasma and on the activity of LPL in adipose tissue (AT-LPL) in 13 male hypopituitary patients. The activities of LPL and HL in postheparin plasma were markedly increased by 1 week after a testosterone enanthate injection (P less than 0.001).

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Serum lipoproteins and postheparin plasma lipoprotein lipase and hepatic lipase (HL) activities were determined in 23 hypothyroid women treated with graded doses of thyroxine (T4) (50, 100, and 150 micrograms/day), each given for 3 weeks. Since the sex hormone-binding globulin (SHBG) and thereby serum sex steroid concentrations are sensitive to thyroid status, we also measured serum testosterone, estradiol, and SHBG at each time. Stepwise T4 treatment resulted in gradual improvement in thyroid status.

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A basic difference between dietary and drug therapy of hypercholesterolemia is that dietary therapy can be used as part of a population strategy, whereas the decision to use drugs is always made on an individual basis. In each case, the decision to treat must be based on the assumption that more good than harm is caused to the patient. This is a difficult situation for the physician.

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Hypocholesterolaemic agents are powerful modifiers of the plasma lipoprotein pattern. In addition to lowering plasma low density lipoprotein (LDL) cholesterol, such drugs may elevate, decrease or have no effect on high density lipoprotein (HDL) cholesterol. Bile acid binding resins and 3-hydroxy-3-methylglutaryl Coenzyme A (HMG-CoA) reductase inhibitors cause a reduction in hepatic cholesterol content resulting in stimulation of LDL receptor activity.

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The effect of a ten-day caloric restriction period and of subsequent refeeding on adipose tissue lipoprotein lipase (LPL) activity was studied in 14 moderately obese women. The enzyme assays were made from subcutaneous fat taken from three separate regions (gluteal, femoral, and abdominal) after overnight fasting and from one region also after a standard meal. There was a close correlation between the activities measured from the different subcutaneous sites.

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Two DNA polymorphisms adjacent to the apolipoprotein A-I/C-III and insulin genes have been suggested to be associated with hypertriglyceridemia and increased risk of coronary heart disease. Using cloned apolipoprotein A-I and insulin gene probes, we determined the genotypes of 39 subjects from six different kindreds with familial clustering of hypertriglyceridemia, 20 additional unrelated subjects with hypertriglyceridemia, 39 patients with angiographically confirmed coronary heart disease (CHD) and 61 normolipemic control subjects. The S2 allele bearing an additional SstI restriction site in the apo A-I/C-III complex was found in 16% of healthy controls, 23% of patients with CHD and 62% (P less than 0.

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Cyproterone acetate (CPA) was administered to 13 menstruating women from day 14 to day 27 of the cycle at a dose of 5 mg/day. Serum lipoprotein lipid levels and postheparin plasma lipase activity were determined on day 27 of the cycle before treatment and during two treatment cycles. No significant changes were observed in hepatic lipase activity or in very-low-density (VLDL) or low density lipoprotein (LDL) concentrations.

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The influence of sex steroids on the serum lipoprotein pattern was recognized more than 30 years ago, and it still remains among the areas of major interest. This is because of the compatible sex difference in plasma lipoprotein pattern and in coronary heart disease risk. Recent discoveries of the role of hepatic lipase in lipoprotein metabolism have elucidated mechanisms behind sex steroid-induced changes in lipoproteins.

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The effects of alcohol intake on serum lipids and lipoproteins depend on the dose and mode of alcohol intake, individual susceptibility, genetic variables, and dietary factors. Therefore the changes of lipoprotein pattern are different among moderate and heavy drinkers. Moderate intake of alcohol increases the concentrations of apolipoproteins (apo) AI, apo AII, and high-density lipoprotein subfraction (HDL3) in plasma without any effects on other lipoproteins.

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