RAT GASTRIC HYDROPHOBIC BARRIER - MODULATION OF PHOSPHATIDYLCHOLINE MOLECULAR-SPECIES BY DIETARY LIPIDS

Citation
W. Bernhard et al., RAT GASTRIC HYDROPHOBIC BARRIER - MODULATION OF PHOSPHATIDYLCHOLINE MOLECULAR-SPECIES BY DIETARY LIPIDS, Lipids, 31(5), 1996, pp. 507-511
Citations number
26
Categorie Soggetti
Biology
Journal title
LipidsACNP
ISSN journal
00244201
Volume
31
Issue
5
Year of publication
1996
Pages
507 - 511
Database
ISI
SICI code
0024-4201(1996)31:5<507:RGHB-M>2.0.ZU;2-N
Abstract
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 P C16:0/18:2, but not PC16:0/16:0, are predominantly released into gastr ic mucus. We investigated whether these molecular species in mucus are modified by dietary fat. Rats were fed (for three weeks) a diet suppl emented 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 a nd PC18:0/20:4. Cod liver oil and palm oil increased PC16:0/18:1, wher eas sunflower oil decreased PC16:0/18:1. Palm oil additionally decreas ed 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 compri sed 37.6 +/- 3.3 and 33.1 +/- 1.4 mol% in controls. PC16:0/16:0 was lo wer 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 a nd PC16:0/18:2 are modified by dietary fat in tissue. In gastric secre tions, however, PC16:0/18:1 and PC16:0/18:2 are kept constant and toge ther 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 die tary treatment. Additionally, cod liver oil decreases the content of P C16:0/20:4 and PC18:0/20:4 in gastric mucosa, thereby possibly decreas ing the formation of eicosanoids.