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Rat gastric hydrophobic barrier: Modulation of phosphatidylcholine molecular species by dietary lipids
Author(s) -
Bernhard W.,
Postle A. D.,
Linck M.,
Sewing K. Fr.
Publication year - 1996
Publication title -
lipids
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.601
H-Index - 120
eISSN - 1558-9307
pISSN - 0024-4201
DOI - 10.1007/bf02522644
Subject(s) - phosphatidylcholine , mucus , sunflower oil , clinical chemistry , food science , corn oil , chemistry , cod liver oil , lipidology , medicine , biochemistry , biology , endocrinology , phospholipid , ecology , membrane
Phospholipids protect the gastric mucosa by forming a proton‐repellent hydrophobic layer on its luminal surface. We have recently shown that two molecular species of phosphatidylcholine (PC), PC16:0/18:1, and PC16:0/18:2, but not PC16:0/16:0, are predominantly released into gastric mucus. We investigated whether these molecular species in mucus are modified by dietary fat. Rats were fed (for three weeks) a diet supplemented with either 10% cod liver, palm, or sunflower oil, or 10% corn starch as a control. In tissue, cod liver oil decreased PC16:0/20:4 and PC18:0/20:4. Cod liver oil and palm oil increased PC16:0/18:1, whereas sunflower oil decreased PC16:0/18:1. Palm oil additionally decreased PC16:0/18:2, whereas the other diets had no effect on PC16:0/18:2. In mucus, however, PC16:0/18:1 and PC16:0/18:2 were not significantly altered by any diet. They were increased over tissue values and comprised 37.6±3.3 and 33.1±1.4 mol% in controls. PC16:0/16:0 was lower in mucus than in mucosa and even decreased by cod liver oil (1.2±0.2 vs. 2.7±0.3 mol%; P <0.01). We conclude that PC16:0/18:1 and PC16:0/18:2 are modified by dietary fat in tissue. In gastric secretions, however, PC16:0/18:1 and PC16:0/18:2 are kept constant and together comprise 70 mol% of the released PC species, whereas PC16:0/16:0 does not play a role for the gastric hydrophobic barrier under any dietary treatment. Additionally, cod liver oil decreases the content of PC16:0/20:4 and PC18:0/20:4 in gastric mucosa, thereby possibly decreasing the formation of eicosanoids.