arachidonic acid https://greenmedinfo.com/category/keywords/arachidonic-acid en Dietary interventions to increase the dihomo-gamma-linoleic acid to arachidonic acid ratio may not necessarily decrease PGE2 synthesis in tissues where COX-1 enzymes predominate over COX-2. https://greenmedinfo.com/article/dietary-interventions-increase-dihomo-gamma-linoleic-acid-arachidonic-acid-rat PMID:  Biochem J. 2002 Jul 15 ;365(Pt 2):489-96. PMID: 11939906 Abstract Title:  Differential metabolism of dihomo-gamma-linolenic acid and arachidonic acid by cyclo-oxygenase-1 and cyclo-oxygenase-2: implications for cellular synthesis of prostaglandin E1 and prostaglandin E2. Abstract:  Prostaglandin (PG) E(1) has been shown to possess anti-inflammatory properties and to modulate vascular reactivity. These activities are sometimes distinct from those of PGE(2), suggesting that endogenously produced PGE(1) may have some beneficial therapeutic effects compared with PGE(2). Increasing the endogenous formation of PGE(1) requires optimization of two separate processes, namely, enrichment of cellular lipids with dihomo-gamma-linolenic acid (20:3 n-6; DGLA) and effective cyclo-oxygenase-dependent oxygenation of substrate DGLA relative to arachidonic acid (AA; 20:4 n-6). DGLA and AA had similar affinities (K(m) values) and maximal reaction rates (V(max)) for cyclo-oxygenase-2 (COX-2), whereas AA was metabolized preferentially by cyclo-oxygenase-1 (COX-1). To overcome the kinetic preference of COX-1 for AA, CP-24879, a mixed Delta(5)/Delta(6) desaturase inhibitor, was used to enhance preferential accumulation of DGLA over AA in cells cultured in the presence of precursor gamma-linolenic acid (18:3 n-6). This protocol was tested in two cell lines and both yielded a DGLA/AA ratio of approx. 2.8 in the total cellular lipids. From the enzyme kinetic data, it was calculated that this ratio should offset the preference of COX-1 for AA over DGLA. PGE(1) synthesis in the DGLA-enriched cells was increased concurrent with a decline in PGE(2) formation. Nevertheless, PGE(1) synthesis was still substantially lower than that of PGE(2). It appears that employing a dietary or a combined dietary/pharmacological paradigm to augment the cellular ratio of DGLA/AA is not an effective route to enhance endogenous synthesis of PGE(1) over PGE(2), at least in cells/tissues where COX-1 predominates over COX-2. <p><a href="https://greenmedinfo.com/article/dietary-interventions-increase-dihomo-gamma-linoleic-acid-arachidonic-acid-rat" target="_blank">read more</a></p> https://greenmedinfo.com/article/dietary-interventions-increase-dihomo-gamma-linoleic-acid-arachidonic-acid-rat#comments Dietary Modification: Alteration of Dietary Fat Types and/or Ratios Prostaglandin PGE2 downregulation Anti-Inflammatory Agents arachidonic acid Cyclooxygenase Inhibitors Essential Fatty Acids Gamma-Linoleic Acid GLA Inflammation omega-6 fatty acids Prostaglandin E2 In Vitro Study Thu, 25 Jul 2019 17:32:52 +0000 greenmedinfo 191869 at https://greenmedinfo.com Insulin induces the expression of delta-5 desaturase (FADS1) in a dose-dependent manner which may explain insulin's regulation of dihomo-gamma-linoleic acid to inflammatory arachidonic acid. https://greenmedinfo.com/article/insulin-induces-expression-delta-5-desaturase-fads1-dose-dependent-manner-whic PMID:  Scand J Clin Lab Invest. 2011 Jul ;71(4):330-9. Epub 2011 Mar 17. PMID: 21413848 Abstract Title:  Insulin induces fatty acid desaturase expression in human monocytes. Abstract:  Increasing evidence suggests that fatty acid desaturases, rate-limiting enzymes in unsaturated fatty acid biosynthesis, are important factors in the pathogenesis of lipid-induced insulin resistance. The conversion of dihomogamma linolenic acid (DGLA) into arachidonic acid (AA) in human plasma phospholipids has been shown to be regulated by insulin, suggesting a role for insulin in fatty acid desaturase 1 regulation. However insulin&#039;s role in monocyte inflammation associated with obesity and lifestyle disease development is uncertain. We therefore investigated if insulin is able to induce expression of stearoyl-CoA desaturase (SCD,Δ9 desaturase), fatty acid desaturase 1 (FADS1, Δ5 desaturase), and fatty acid desaturase 2 (FADS2, Δ6 desaturase), as well as the sterol regulatory element binding transcription factor 1-c (SREBP-1c) in monocytes. Here, for the first time, we demonstrate that THP-1 monocytes are insulin-responsive in inducing expression of SCD, FADS1, and FADS2 in a time- and dose-dependent manner. Understanding secondary consequences of postprandial hyperinsulinemia may open up new strategies for prevention and/or treatment of obesity-related metabolic complications. <p><a href="https://greenmedinfo.com/article/insulin-induces-expression-delta-5-desaturase-fads1-dose-dependent-manner-whic" target="_blank">read more</a></p> https://greenmedinfo.com/article/insulin-induces-expression-delta-5-desaturase-fads1-dose-dependent-manner-whic#comments Endocrine Disruptor: Insulin Resistance Inflammatory Insulin arachidonic acid Dose Response High Sugar Diet hyperinsulinemia Inflammation Insulin Resistance In Vitro Study Thu, 25 Jul 2019 16:39:59 +0000 greenmedinfo 191864 at https://greenmedinfo.com Sesame lignans inhibit delta-5 desaturase activity, increasing dihomo-gamma-linoleic acid levels and decreasing prostaglandin E2 synthesis. https://greenmedinfo.com/article/sesame-lignans-inhibit-delta-5-desaturase-activity-increasing-dihomo-gamma-lin PMID:  Prostaglandins Leukot Essent Fatty Acids. 1998 Mar ;58(3):185-91. PMID: 9610840 Abstract Title:  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. Abstract:  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. <p><a href="https://greenmedinfo.com/article/sesame-lignans-inhibit-delta-5-desaturase-activity-increasing-dihomo-gamma-lin" target="_blank">read more</a></p> https://greenmedinfo.com/article/sesame-lignans-inhibit-delta-5-desaturase-activity-increasing-dihomo-gamma-lin#comments Lignans Prostaglandin PGE2 downregulation Anti-Inflammatory Agents arachidonic acid Gamma-Linoleic Acid GLA Inflammation Prostaglandin E2 Animal Study Thu, 25 Jul 2019 16:04:41 +0000 greenmedinfo 191861 at https://greenmedinfo.com