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Biomedical subjects

G Mühlfellner

Publications and source records attributed to G Mühlfellner.

15 recordsLinked to original sources
PubMed1979

Effect of polyenyl phosphatidyl choline on clofibrate-induced increase in LDL cholesterol.

In a double-blind, randomised, cross-over trial clofibrate and a combination of polyenyl phosphatidyl choline (PPC) plus clofibrate were tested in 67 patients with hyperlipoproteinemia. Each treatment lasted for 4 weeks and was separated by a 4 week placebo period. The daily doses were clofibrate 1.2 g and PPC 1.8 g + clofibrate 1.2 g. respectively. The results revealed that polypenyl phosphatidyl choline prevented the elevation of LDL-cholesterol induced by clofibrate treatment, and that the lipid-lowering potency of the combination did not differ significantly from that of clofibrate. Since elevation of LDL-cholesterol is considered to increase the risk of coronary heart disease, the combination appears to offer a therapeutic advantage. Despite the significance of this clinical observation, a final decision may only be obtained from a prospective, long term investigation in patients with coronary heart diseases and hyperlipoproteinemia.

Adult↗
PubMed1978

Plasma lipids, triglyceride/fatty acid pattern, and plasma insulin in fasted healthy volunteers during continuous ingestion of ethanol. Influence of lipolysis inhibited by nicotinic acid.

Healthy fasted volunteers were subjected to an acute oral ethanol load over 12 h after a diet of 3 days with high linolenic acid content. Free fatty acids, triglycerides, glycerol, phospholipids, cholesterol and insulin, as well as the fatty acid pattern of triglycerides in the plasma, were determined during the test. The test was repeated with nicotinic acid added. The lipid values obtained and the comparisons of fatty acid composition both indicate that the predominant role of peripheral lipolysis in the genesis of acute ethanol-induced hypertriglyceridemia, in spite of the possibility of enhanced synthesis of palmitic acid in the liver.

Adipose Tissue↗
PubMed1978

[Coronary artery reserve in patients with hyperlipoproteinemias (author's transl)].

The coronary reserve was measured in 119 patients with different types of primary hyperlipoproteinemia. Cardiovascular diseased with clinical manifestation were excluded. 90 patients of same age with normal serum lipids served as controls. The groups did not differ in other risk factors as blood pressure or overweight (the latter excluded in hyperlipoproteinemia type IV). The controls showed decreased coronary reserve in 8%, type IIa patients in 36%, IIb patients in 18% and type IV patients in 23%. The frequency of restriction in coronary flow increased with age: in hyperlipoproteinemic patients of 50 years and more it was found in nearly 40%. Further interesting results were the significantly higher systolic and diastolic blood pressures reached during exercise in our hyperlipoproteinemic patients.

Adolescent↗
PubMed1977

[Beta-sitosterin in the treatment of essential type II hyperlipoproteinemias].

The effect of Beta-Sitosterol (Sitosterin Delalande) on plasma lipids in 20 pretreated patients with type IIa and IIb familial hyperlipoproteinemia is reported. 6-18 g of the drug were given for a time of two to twelve months. In 11 patients the plasma cholesterol level decreased between 10 and 30%. Since Beta-Sitosterol has no effect on plasma triglycerides, an additional hypertriglyceridemia must be taken care of and treated if necessary. Beta-Sitosterol can be called an effective substance in the treatment of hypercholesterinemia. In addition the diet cure becomes easier.

Adult↗
PubMed1977

Studies on the metabolic defect in Broad-beta disease (hyperlipoproteinaemia type III).

The apoprotein composition of the main lipoprotein fractions (VLDL, LDL-1, LDL-2 and HDL) was studied initially in 15 patients with Broad-beta disease. Analytical isoelectric focusing of urea-soluble apo-VLDL and apo LSL-1 demonstrated a variant pattern of the polymorphic Apoprotein E with a deficient Apo E-III band in all patients. The Apo E-III deficiency pattern was seen in only six out of 304 hyperlipidaemic controls. These six Apo E-III deficient controls had characteristic signs of Broad-beta disease, and thus represented patients not previously recognized as having the disorder. The Apo E focusing patterns were constant on repeated examinations and were stable under different metabolic conditions. The data show that Apo E-III deficiency in VLDL is a specific qualitative marker for Broad-beta disease, allowing an unequivocal diagnosis that had not been possible previously. Indirect evidence suggests that Apo E-III deficiency is the basic lipoprotein abnormality underlying the familial dyslipoproteinaemia.

Adult↗
PubMed1976

[Changes of triglycerid-fatty acids in healthy volunteers during acute ethanol ingestion with and without blocking peripheral lipolysis (author's transl)].

This investigation decided to answer the question of the origin of fatty acids for the increased synthesis of triglycerides in acute ethanol-induced hyperlipoproteinemia. Healthy persons ingested 0.5 g of ethanol/kg body weight initially and 0,15 g of ethanol/kg and hour for 12 hours. The fatty acids of plasma triglycerides were determined before and after ingestion of ethanol in persons fasting and nourished isocaloricaly, with and without blocking peripheral lipolysis by nicotinic acid and with addition of glucose. The fasting persons triglycerides fatty acids increased to 165.7 % of the initial value after 12 hours of ethanol ingestion, with a preferential increase in palmitic-, oleic- and stearic acid. When lipolysis in adipose tissue was blocked by 0.5 g of nicotinic adic/hour the triglyceride-fatty acids reached only 116.2% after 12 hours, with a decrease in oleic acid, which is present in adipose tissue to a higher degree than in plasma triglycerides. When nourished isocaloricaly, the enhancement of plasma triglyceride-fatty acids could not be suppressed by nicotinic acid. The changes in concentration and pattern of triglyceride-fatty acids announce that the fatty acids used for increased synthesis of triglycerides in fasting persons come from adipose tissue preferentially. In contrast ethanol-ingested hyperlipoproteinemia during ingestion of a food which cannot be suppressed by nicotinic acid, seems to orginate from fatty acids of the food and for de novo synthesis of fatty acids in the liver.

Adipose Tissue↗
PubMed1976

[Beta-sitosterin in unsuccessfully pretreated patients with hypercholesteremia. Simultaneously, a contribution to dose dependence].

To 9 patients with hyperlipoproteinemia type II and treated with different hypolipidemic drugs without success, sitosterol was given for a period of 4 to 16 months. The effective dose was 10.56 to 21.12g beta-sitosterol corresponding to 12 to 24g granulate. One patient developed a serious diarrhoe and dropped out. 4 patients showed an impressive decrease of serum cholesterol levels.

Adult↗