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Journal Article

Citation

Vrbaski SR, Petrović GT, Ristić VI, Ristić MS. J. Stud. Alcohol 1988; 49(4): 369-374.

Affiliation

Department of Human Nutrition, Institute for Medical Research, Beograd, Yugoslavia.

Copyright

(Copyright © 1988, Rutgers Center of Alcohol Studies)

DOI

unavailable

PMID

3172786

Abstract

A previous study was undertaken to determine the influence of the combined effects of ethanol consumption and a low-protein diet on brain membrane (phospholipids and gangliosides) and myelin (monogalactosyl glycolipids) lipids. Male Wistar rats chronically consuming ethanol were fed isoenergetic diets containing 22% protein (controls) or 6% protein (protein-deprived) from 60 to 240 days of age. Protein malnutrition initiated at 60 days of age affected phosphatidylglycerol, sphingophospholipid, monosialoganglioside GM1 and cerebroside containing nervonic fatty acid by 240 days of age. Among the effects of ethanol was an increase of the relative proportion of lipid galactose in monogalactosyl glycolipids and of N-acetylneuraminic acid in the trisialoganglioside GT1b, while there was decrease of the lipid phosphorus in the investigated phospholipids and of the disialoganglioside GD1a. The low-protein diet generally interfered with ethanol effects except for monosialo GM3, GM2 and GM1 gangliosides. The present study was carried out to investigate whether the ethanol-induced effect on these brain lipids could be elevated when we switched these animals to diets with 21 or 34% protein during the following 90 days. It was found that increasing protein intake and cessation of drinking ethanol returned the investigated brain phospholipids, monogalactosyl glycolipids and gangliosides to control values.


Language: en

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