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N Zöllner

Publications and source records attributed to N Zöllner.

At least 127 records · Page 7Linked to original sources
PubMed1986

Dietary linolenic acid in man--an overview.

Small amounts of linolenic acid are ubiquitous in human food but only a few foodstuffs contain sizable amounts, namely some plant oils, butter and fish; in marine fish, linolenic acid is accomplished by eicosapaentaenoic acid, highly exceeding linolenic acid in quantity. Of the linolenic acid ingested, some is incorporated into phospholipids and cholesteryl esters, very little is elongated and eventually converted to prostaglandins; probably most linolenic acid is used as fuel. Polyunsaturated fatty acids of the (n-3)-series should no longer be considered to be similar with respect to their metabolic fate and their effects. In particular, results from experiments with "eskimo diets" may not be applied to considerations of linolenic acid. There may be a small dietary requirement for linolenic acid, possibly only for growing children; yet it is prudent to recommend diets which are not devoid of linolenic acid, especially in formula diets or parenteral nutrition. Some experiments suggest that high doses of linolenic acid exert untoward effects by inhibiting prostaglandin synthesis of the 1- and 2-series. The ratio between linoleic and linolenic acid in relevant experiments was such that only excessive use of linseed oil could produce them under conventional dietary conditions. Still it must be considered prudent to keep the linolenic acid content of foods well below that of linoleic acid.

Dietary Fats, Unsaturated↗
PubMed1986

Regulation of lipogenesis in mitogen-stimulated human lymphocytes by thyroid hormones.

The hormonal regulation of precursor incorporation into cellular lipids has been investigated in human lymphocytes stimulated with phytohemeagglutinine. Addition of thyroxine (5 micrograms/ml) for 72 h increased incorporation of [14C]acetate into the triacylglycerol fraction to 290% above the hormone-free control values. Incorporation into the cholesterol fraction was elevated up to 188% under the same conditions. Triiodothyronine was less effective than thyroxine: maximal effects were 153% of the control for triacylglycerols and 142% for cholesterol. Similar results were obtained when [14C]palmitic acid was used as a precursor for triacylglycerol synthesis. Effects of insulin on the parameters described were less pronounced than those obtained with thyroid hormones. Cellular triacylglycerol and protein contents were not elevated significantly by thyroid hormone addition. Further, incorporation of labelled thymidine, uridine, and leucine into acid-precipitable products was not elevated by triiodothyronine above mitogen-stimulated levels. It is concluded, that rapidly dividing lymphocytes provide a suitable system for studies concerning human lipid metabolism.

Acetates↗
PubMed1986

Effect of alpha-linolenic acid in the human diet on linoleic acid metabolism and prostaglandin biosynthesis.

The effect of dietary alpha-linolenic acid intake on linoleic acid metabolism and prostaglandin (PG) biosynthesis was investigated in two groups of six healthy females (25-32 yr). They were given isocaloric formula diets (FD) containing linoleic acid at a constant intake (4% of calories), with different amounts of alpha-linolenic acid: 0% (FD4/0), 4% (FD4/4), 8% (FD4/8) (group I) and 12% (FD4/12) or 16% (FD4/16) (group II); the diets were given for 2 weeks each. Comparing diet FD4/0 to FD4/16, enrichment of alpha-linolenic acid was greatest in cholesteryl esters (+6.8% in plasma, +7.1% in low density lipoproteins (LDL), +5.9% in high density lipoproteins (HDL)), less in phosphatidylcholine (+2.5% in plasma, +2.9% in LDL, +2.7% in HDL), and least in platelet lipids (+0.7%). The accumulation of alpha-linolenic acid was compensated by a decrease of oleic acid. Eicosapentaenoic acid (EPA), which was excluded from the diet, increased in all plasma lipids with augmented alpha-linolenic acid intake, indicating a chain elongation and desaturation of alpha-linolenic acid to EPA. However, even at the end of FD4/16, EPA was less than 2% of total fatty acids in all plasma lipids. Plasma linoleic acid levels were constant during all dietary regimes, according to the constant dietary intake of this fatty acid. No replacement of linoleic acid by alpha-linolenic acid could be observed. The percentage of arachidonic acid in all lipids was unaffected by alpha-linolenic acid intake. As arachidonic acid was not provided by the diet, it can be concluded that alpha-linolenic acid does not inhibit chain elongation and desaturation of linoleic acid to arachidonic acid in man.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1985

Osmotic fragility of drug carrier erythrocytes.

Erythrocytes have been proposed as biogradable cellular carriers for drugs. Potentials of this therapeutic approach are organ-specific targeting, protection and prolonged in vivo function of the encapsulated drugs. Previous studies demonstrated the advantage of a hypo-osmotic dialysis procedure for macromolecule loading resulting in cells that are closely similar to normal erythrocytes. Osmotic fragility of unloaded and loaded "carrier" erythrocytes was studied both in respect of shelf-life and in vivo survival. Sudden haemolysis which is characteristic for normal erythrocytes was never obtained with carrier erythrocytes. Haemolysis appeared at all osmotic pressures and increased stepwise indicating the existence of various cell populations. However, the majority of cells were haemolysed at lower values of the osmotic fragility curve. Osmotic fragility was highly increased when cytotoxic chemotherapeutics were encapsulated, and these cells appeared as spherocytes using scanning electron microscopy. Osmotic fragility proved to be a simple but reliable method for the in vitro evaluation of carrier erythrocytes and the effect of the encapsulated substances.

Erythrocyte Aging↗
PubMed1985

Prostaglandin formation and platelet aggregation during fasting and linoleic acid intake.

Prostaglandin formation, estimated by the determination of tetranorprostanedioic acid (TNPDA) in the urine, and platelet aggregation were investigated in seven healthy volunteers each day during fasting, and in three of them additionally during intake of carbohydrates (328kcal/day) or safflor oil (328 kcal, 20 g linoleic acid). Monitoring TNPDA in 8-h fractions of the urine showed a reduction during the night (23.00-07.00) by 70% on the average. During Days 1 and 2 of fasting the amount of TNPDA in 24-h urine was the same as under a conventional diet. On Day 3, TNPDA decreased in all experimental subjects to 162 micrograms/day on the average and was not changed by carbohydrate intake. A linoleic acid intake of 20 g/day increased TNPDA in 24-h urine to pre-experimental levels measured under free diet. Platelet aggregation did not change during the experiment. No relationship between prostaglandin formation and lipolysis in man was found.

Adult↗
PubMed1985

[The effect of linoleic acid intake on its concentration and resultant products in individual plasma lipids in humans].

Dietary linoleic acid enrichment in different plasma lipids was investigated in six healthy females. They were given formula diets (FD) containing no arachidonic acid, and providing a linoleic acid supply of 0% (FD0), 4% (FD4) or 20% (FD20) of total energy intake. At the end of each two weeks FD period fatty acid distribution was determined in cholesterol esters (CE) and in lecithin of LDL and HDL. The increase of linoleic acid in CE was twice that found in the lecithin of LDL and HDL. Comparing FD0 and FD20 the increase of linoleic acid in CE of LDL and HDL was 34%, and in lecithin 15%. Simultaneously oleic acid was lowered in CE (-17%) and in lecithin (-8%) of LDL and HDL. Comparing FD0 and FD20 arachidonic acid, which derives from linoleic acid, was lowered with increased linoleic acid intake in LDL-CE (-5%) and in HDL-lecithin (-8%), while no effect was found in LDL-lecithin. Our results demonstrate that dietary linoleic acid enrichment occurs preferentially in CE of LDL and HDL, but does not lead to an increase of arachidonic acid in plasma lipids. However, a decrease was found for arachidonic acid in HDL-lecithin, while in LDL-lecithin no effect could be observed. From this it is concluded that incorporation and metabolism of linoleic acid in different plasma lipids is not identical, although lipid exchange and lipid transfer have been shown for most lipoprotein fractions.

Adult↗
PubMed1985

Unsaturated 1-O-alkyl-2-acetyl-sn-glycero-3-phosphocholines (unsaturated platelet-activating factor): aggregation of human platelets after incubation with indomethacin, creatinephosphate/creatinephosphokinase, xylocain and hirudine, and serotonin release after incubation with indomethacin.

Unsaturated platelet-activating factor (PAF) aggregates thrombocytes of healthy female volunteers and releases within 1 min up to 30.95% of the platelet serotonin. Indomethacin does not inhibit the aggregation but reduces the release of serotonin induced by unsaturated PAF in citrated platelet-rich plasma (PRP). Creatinephosphate combined with creatinephosphokinase (CP/CPK) inhibits the second phase, whereas xylocain inhibits the first and second phase of aggregation induced by unsaturated PAF. Hirudine shows no influence on the aggregation induced by unsaturated PAF.

Blood Platelets↗
PubMed1985

Effect of plasma exchange with and without concomitant drug treatment on lipids and lipoproteins in patients with familial hypercholesterolemia confirmed by tissue culture.

Repeated plasma exchange is an effective treatment for young patients with familial hypercholesterolemia. We treated 2 homozygous and 1 heterozygous patient with very high cholesterol levels with continuous plasma exchange using human albumin solution as exchange medium. The treatment was repeated every 2 weeks in 2 patients and weekly in the third. Treatment periods of plasma exchange alone and of plasma exchange with concomitant drug therapy were compared. For drug treatment beta-pyridylcarbinol, the alcohol corresponding to nicotinic acid (0.9 g/day equivalent to 3 g of nicotinic acid) and cholestyramine (16 g/day) were used. Plasma exchange alone resulted in a decrease of all lipids by 55% and of apolipoproteins by 50-60% as compared to the plasma levels before exchange. Subsequently all lipoproteins rose again to reach pre-exchange levels within about 2 weeks. There was no difference between the homozygous and the heterozygous patients. Beta-pyridylcarbinol or cholestyramine given concomitantly did not alter the post-exchange increase of total, LDL, HDL cholesterol nor of the corresponding apolipoproteins except of apolipoprotein B.

Adult↗
PubMed1984

[Sonographic observation of the course of aneurysms of the abdominal aorta].

Forty-two patients with an abdominal aortic aneurysm that had not been treated surgically were repeatedly examined by ultrasonography. The average observation time of all patients was 3.1 years. The total observation period including follow-up times of all patients adds up to 129 "patient years". Within this time none of the 35 asymptomatic abdominal aneurysms with transversal diameters of maximally 5 cm ruptured. Three patients of seven with larger and symptomatic aneurysms died in consequence of a rupture. Small asymptomatic abdominal aortic aneurysms seem to have a better prognosis than previously supposed. The question whether all abdominal aneurysms should be operated on needs reconsideration, especially in the elderly.

Aged↗