Incorporation of fatty acids from fish oil and olive oil into colonic mucosal lipids and effects upon eicosanoid synthesis in inflammatory bowel disease.

Abstract

The incorporation of the fatty acids in fish and olive oil into the colonic mucosa of patients with inflammatory bowel disease was examined during 12 weeks' dietary supplementation with the oils, and the influence on colonic mucosal prostaglandin and thromboxane generation was measured. With a dietary supplement of 18 g fish oil daily, concentrations of the major polyunsaturated fatty acids in fish oil, eicosapentaenoic acid and docosahexaenoic acid, were significantly raised in mucosal lipids. The first time these were measured, after three weeks' supplementation, the mean increases in eicosapentaenoic and docosahexaenoic acid were seven fold and 1.5 fold respectively, and these increases were maintained during the 12 week study. Arachidonic acid values fell throughout the study and this reduction was significant at 12 weeks. Mucosal prostaglandin E2 (PGE2), thromboxane B2, and 6-keto prostaglandin F,,, synthesis were suppressed, and this reached significance (p<005) at three and 12 weeks for PGE2 and at 12 weeks for thromboxane B2.

Change in the fatty acid pattern of erythrocyte membrane phospholipids after oral supplementation of specific fatty acids in patients with gastrointestinal diseases

“…The goal of specific fatty acid supplementation in patients with maldigestion and malabsorption is the incorporation of n-3 PUFA into membrane phospholipids to ameliorate gastrointestinal barrier function and to minimize oxidative stress and pro-inflammation in the gastrointestinal tract (Hillier et al, 1991;Belluzzi et al, 1996;Calder, 2008). Timely supplementation avoids the shift in membrane fatty acid pattern demonstrated in healthy subjects and patients with Crohn's disease without diagnosed malabsorption (Belluzzi et al, 1996;Cao et al, 2006).…”

“…It has been suggested that a change in membrane fatty acid patterns due to oral supplementation of a specific fatty acid composition decreases AA concentrations of tissue and cell membrane phospholipids as a result of a reduced ratio of n-6 to n-3 PUFA (Hillier et al, 1991;Cao et al, 2006). The concomitant medium-chain triglyceride component is supposed to prevent a diminished incorporation of long-chain PUFA into the phospholipids of the erythrocyte membrane (Periago et al, 1990).…”

A randomized double blind comparison of short-term duodenally administrated whale and seal blubber oils in patients with inflammatory bowel disease and joint pain

“…The AA to EPA ratio is rate limiting for eicosanoid production [3]. In IBD-patients, short-term (14-day) oral administration of SO and cod liver oil reduced plasma levels of leukotriene B4 (LTB 4 ) [24], and decreased levels of PGE 2 in colonic mucosa [47] and blood mononuclear cells [48] have been seen after long-term oral fish oil supplementation. Indeed reduced synthesis of nociceptive PGE 2 due to COX-inhibition is a generally accepted mechanism by which fish oil as well as NSAIDs/COX-2 inhibitors ameliorate inflammatory pain [26,4].…”

n−3 Polyunsaturated fatty acids, inflammation, and inflammatory diseases

“…Certainly, dietary fish oil has beneficial effects in animal models of colitis (130,131). Long-chain nҀ3 PUFAs are incorporated into gut mucosal tissue of patients with inflammatory bowel disease who supplement their diet with fish oil (132)(133)(134), and there are reports that this results in antiinflammatory effects, such as decreased LTB 4 production by neutrophils (134 -136) and colonic mucosa (136,137), decreased PGE 2 and thromboxane B 2 production by colonic mucosa (133), and decreased production of PGE 2 by blood mononuclear cells (138). Small open-label or pilot studies reported clinical benefit of fish oil supplementation in ulcerative colitis (135,139).…”