Die Wirkung des Äthylalkohols auf die Plasmalipide isocalorisch ernährter Versuchspersonen

Mühlfellner, G; Mühlfellner, O; Kaffarnik, H

doi:10.1007/bf02048763

Cited by 7 publications

(1 citation statement)

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“…We have described earlier certain changes in plasma lipids of healthy persons after the intake of a measure of ethanol close to the upper limit of daily drinkable amounts. Our experiments were carried out on fasting persons I16) and on those being kept on an isocaloric diet (26). The results tended towards the direction that, under acute alcohol load, the fatty acids necessary for an increased triglyceride synthesis originate, in the main, from a peripheral lipolysis.…”

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confidence: 94%

Alteration of plasma lipids and intermediates of lipid metabolism in healthy fasting volunteers by ethanol and fructose

Schneider

Tesdorfpf²,

Kaffarnik³

et al. 1976

Res. Exp. Med.

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After healthy persons, aged between 20 and 35 years, had consumed either ethanol or ethanol and fructose, triglycerides, free glycerol, FFA, phospholipids and total cholesterol were determined. After a basic dosage of 0.5 g ethanol/kg body weight, each person received a maeintenance dosage of 0.1 g ethanol/kg body weight and hour. Control experiments were carried out on persons receiving only fructose and on fasting persons who consumed no ethanol. After 8 hrs, triglycerides rose in the ethanol group by 107 %, in the ethanol-fructose group by 63 %. FFA exhibited in both ethanol and ethanol-fructose groups an initial decrease, with a secondary increase in the ethanol group. The initial decrease was greater in the ethanol-fructose group. A significant rise in free glycerol by 419 % was observed 30 min after the intake of combined ethanol/fructose. Free glycerol rose under ethanol alone by 144%. The ohospholipids exhibited a slight rise in the ethanol group; no significant changes occured in the cholesterol. The blood ethanol level was lower under ethanol-fructose than under ethanol alone. The addition of fructose diminishes the ethanol-induced hypertriglyceridemia. Our investigations give further proof that, under short-term ethanol load, the fatty acids necessary for the increased triglyceride synthesis in the liver, originate predominantly from a peripheral lipolysis, and that changes in liver metabolism depending on the oxidation of ethanol are not of less importance for the development of the acute ethanol-induced hyperlipidemia.

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confidence: 94%