Blocking delta destaurase 5 will inhibit the formation of Archnidonic acid the omega six raw material for the eisosanoid pathways.
It may aslo push the omega six to DGLA conversion via the series one pathway which is reported as producing less inflamatory agents that the series two pathways.
This presumably acounts for its reported anti inflamatory properties.
But does it also block the 5 pathway for omegas threes long chain fabrication in the body (DHA and EPA)? (AMENDMENT I have just found a trial which suggests it does not which makes it a really interesting dietary adjunct) [Trial see below)
Also if excess omega six souces is a factor in inflamtion in a persons body the consequences in blocking the elongation pathways. The body has been supplied with the omega six and has to do something with it - burn it in exercise or for energy - store it in fat - and if there is too much of it in the circulation trials suggest things start going wrong with inapproriate oxidation leading heart conditions.
All of which might lead on to the conclusion that the easiest long term option is not getting to much in the first place.
RB
http://www.ncbi.nlm.nih.gov/entrez/q...t_uids=1291640
1: J Nutr Sci Vitaminol (Tokyo). 1992 Aug;38(4):353-63. Links
Effects of sesamin and curcumin on delta 5-desaturation and chain elongation of polyunsaturated fatty acid metabolism in primary cultured rat hepatocytes.
* Fujiyama-Fujiwara Y,
* Umeda R,
* Igarashi O.
Institute of Environmental Science for Human Life, Ochanomizu University, Tokyo, Japan.
Effects of sesamin and curcumin on delta 5-desaturation and chain elongation of polyunsaturated fatty acid (PUFA) were studied in rat primary cultured hepatocytes. When sesamin was added to culture medium containing 20:4 (n-3), rat hepatocytes after 24 h of incubation produced 20:5 (n-3) from 20:4 (n-3), whereas when incubated with 20:3 (n-6), the metabolite by delta 5-desaturation did not accumulate, and consequently, the ratio of 20:3 (n-6)/20:4 (n-6) increased with the amount of sesamin added. Curcumin was more effective than sesamin in this respect. Both sesamin and curcumin interfered with chain elongation of PUFAs. An addition of 18:3 (n-6) or 18:4 (n-3) increased the cellular concentrations of 20:3 (n-6) or 20:4 (n-3), respectively, but the simultaneous addition of sesamin or curcumin inhibited the chain elongation of C18 acids (the fatty acids with 18 carbons) into corresponding C20 and C18 acids. Similarly, the elongation from C20 of n-3 and n-6 families to C22 was also inhibited with sesamin and curcumin. These results suggested that: 1) sesamin and curcumin inhibited delta 5-desaturation of n-6 fatty acid, but not n-3 fatty acid in rat hepatocytes; 2) curcumin was more effective than sesamin; 3) chain elongation was also inhibited by sesamin and curcumin.
PMID: 1291640 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov/entrez/q...t_uids=9610840
1: Prostaglandins Leukot Essent Fatty Acids. 1998 Mar;58(3):185-91. Links
Dietary alpha-linolenic acid increases TNF-alpha, and decreases IL-6, IL-10 in response to LPS: effects of sesamin on the delta-5 desaturation of omega6 and omega3 fatty acids in mice.
* Chavali SR,
* Zhong WW,
* Forse RA.
Department of Surgery, Harvard Institute of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA 02215, USA.
Sesamin (a non-fat portion of sesame seed oil) inhibits delta-5 desaturase activity resulting in an accumulation of dihomo-gamma-linolenic acid (DGLA) which can displace arachidonic acid (AA) and decrease the formation of pro-inflammatory mediators. We investigated the effects of consumption of diets containing 0.25wt% sesamin and 15 wt% safflower oil (SO) (providing 12% of the added fat as linoleic acid) or a 15 wt% 2:1 mixture of linseed oil and SO (LOSO) (providing 6% alpha-linolenic acid and 6% linoleic acid) for 3 weeks on the liver membrane fatty acid composition and on the production of prostaglandin (PG) E2, TNF-alpha, IL-6 and IL10 in mice. Consumption of sesamin-supplemented SO and LOSO diets resulted in a significant increase in the levels of 20:3omega6 (DGLA), suggesting that sesamin inhibited delta-5 desaturation of omega6 fatty acids. In animals fed LOSO diets, the levels of alpha-linolenic acid, eicosapentaenoic acid (EPA) and of docosahexaenoic acid (DHA) were elevated with a concomitant decrease of arachidonic acid (AA) in the liver membrane phospholipids. Further, in animals fed LOSO diets with or without sesamin, an increase in the circulating levels of TNF-alpha was associated with a concomitant decrease in PGE2. Despite a lack of differences in the levels of AA, the PGE2 levels were significantly lower in mice fed sesamin-supplemented SO compared to those fed SO alone. Thus, these data suggest that irrespective of the availability of a specific fatty acid as a substrate, through regulating the PGE2 synthesis, the production of TNF-alpha could be modulated.
PMID: 9610840 [PubMed - indexed for MEDLINE]