As my readers know, one of the main inflammatory effects of PUFA is due to their conversion into downstream metabolites by enzymes such as COX and LOX. The study below demonstrates that both omega-6 and omega-3 PUFA actually promote the expression of COX, thus increasing the their own downstream conversion into inflammatory mediators. In other words, not only are omega-6 and omega-3 PUFA precursors to inflammatory mediators, PUFA promotes that process directly, thus ensuring that any dietary PUFA consumed will certainly generate an inflammatory reaction. Finally, as in the case of the recently posted studies on PUFA promoting platelet aggregation, serotonin release and inhibiting protein synthesis (all negative effects) saturated fatty acids (SFA) were without effects – i.e. SFA did not increase the expression of inflammatory pathways.
https://pubmed.ncbi.nlm.nih.gov/17459764/
“…We examined in HaCaT keratinocyte cell line whether eicosapentaenoic acid (EPA) a n-3 PUFA, gamma-linoleic acid (GLA) a n-6 PUFA, and arachidic acid a saturated fatty acid, modulate expression of cyclooxygenase-2 (COX-2), an enzyme pivotal to skin inflammation and reparation. We demonstrate that only treatment of HaCaT with GLA and EPA or a PPARgamma ligand (roziglitazone), induced COX-2 expression (protein and mRNA). Moreover stimulation of COX-2 promoter activity was increased by those PUFAs or rosiglitazone. The inhibitory effects of GW9662 and T0070907 (PPARgamma antagonists), on COX-2 expression and on stimulation of COX-2 promoter activity by EPA and GLA suggest that PPARgamma is implicated in COX-2 induction. Finally, PLA2 inhibitor methyl arachidonyl fluorophosphonate blocked the PUFA effects on COX-2 induction, promoter activity and arachidonic acid mobilization suggesting involvement of AA metabolites in PPAR activation. These findings demonstrate that n-3 and n-6 PUFA increased PPARgamma activity is necessary for the COX-2 induction in HaCaT human keratinocyte cells.”
