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Effects of dietary corn oil and salmon oil on lipids and prostaglandin E 2 in rat gastric mucosa
Author(s) -
Grataroli Renée,
Léonardi Jeannie,
Charbonnier Monique,
Lafont Raymond,
Lafont Huguette,
Nalbone Gilles
Publication year - 1988
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/bf02535665
Subject(s) - corn oil , fish oil , arachidonic acid , gastric mucosa , prostaglandin , polyunsaturated fatty acid , phospholipase a2 , prostaglandin e2 , food science , chemistry , lipidology , clinical chemistry , biology , medicine , fatty acid , endocrinology , biochemistry , stomach , fish <actinopterygii> , enzyme , fishery
Three groups of male rats were fed either a corn oilenriched diet (17%, w/w), a salmon oil‐enriched diet (12.5%) supplemented with corn oil (4.5%) or a low‐fat diet (4.4%) for eight wk to investigate the possible relationships between dietary fatty acids and lipid composition, and prostaglandin E 2 level and phospholipase A 2 activity in the rat gastric mucosa. High‐fat diets induced no important variation in total protein, phospholipid and cholesterol contents of gastric mucosa. Compared with a low‐fat diet, corn oil produced a higher n−6/n−3 ratio in mucosal lipids, whereas this ratio was markedly lowered by a fish oil diet. In comparison with the low‐fat diet, the production of prostaglandin E 2 (PGE 2 ) in gastric mucosa of rats fed salmon oil was significantly, decreased by a factor of 2.8. In the corn oil group, PGE 2 production tended to decrease, but not significantly. In comparison with the low‐fat diet, both specific and total gastric mucosal phospholipase A 2 activities were increased (+18 and 23%, respectively) in the salmon oil group; they were unchanged in the corn oil group. It is suggested that the decrease of gastric PGE 2 in rats fed fish oil is not provoked by a decrease in phospholipase A 2 activity but may be the result of the substitution of arachidonic acid by n−3 PUFA or activation of PGE 2 catabolism.