EPA, GLA, and AA effects on rats

Title: Arachidonic Acid Offsets the Effects on Mouse Brain and Behavior of a Diet with a Low (n-6):(n-3) Ratio and Very High Levels of Docosahexaenoic Acid

Author: 

P. E. Wainwright*,⁴, 

H.-C. Xing*, 

L. Mutsaers*, 

D. McCutcheon*, and 

D. Kyle†

Date:

Dec 2003

Link; http://jn.nutrition.org/content/127/1/184.short

Summary:

PUFAs are an important part of membrane phospholipids in microglia (immune system glial cell), neurons, and immune cells. EPA, GLA, and AA play different and big roles in membrane fluidity, lipid peroxidation, eicosanoid production, receptor and channel functions, and gene expressions. This can be altered when the phospholipid content of these membranes are changed.

Interleukins were injected into rats, causing inflammatory-sickness response and stress/anxiety. It did the latter by increasing the concentration of corticosterone.

Ethyl-EPA supplemented in the diet reduced the stress/anxiety behavior of rats in a maze. It did this by reducing the concentration of serum corticosterone.

Another group of rats were supplemented with an omega 6 fatty acid, Ethyl GLA (Ethyl-gamma-linolenic acid). It did not effect stress behaviors or corticosterone concentration. However, both Ethyl EPA and Ethyl GLA reduced prostaglandin secretion and increased secretion of anti-inflammatory cytokines. Therefore, they both reduced the inflammatory-sickness.

Another group was supplemented with AA, the omega-6 fatty acid Arachidonic Acid. It increased anxiety behavior, increased the basal inflammatory response, and raised corticosterone concentrations. However, it did not enhance the effects caused by the injected interleukine.

AA, an omega-6 fatty acid, can be converted to pro-inflammatory eicosanoids. They can induce the inflammatory response. Though GLA is the precursor of AA, it inhibits inflammation. EPA, one of the precursors, of DHA reduces proinflammatory cytokines by reducing membrane AA synthesis. However, having an optimal ratio of n-3 and n6 fatty acids is important for normal signal transduction.