The effects of inflammation and dietary alpha-linolenic acid on the metabolism of linoleic and alpha-linolenic acid

How linoleic (18:2ω6) and α-linolenic acid (18:3ω3) are metabolized during inflammation and whether dietary 18:3ω3 can influence this process is not known. The goal of this body of work was therefore to study the metabolism of 18:2ω6 and 18:3ω3 in inflammatory models with differing intakes of dietary 18:3ω3.; In one study pigs were weaned into environments that resulted in either a low or high antigen exposure and consumed either a control or high 18:3ω3 diet. Pigs exposed to higher levels of antigens had higher β-oxidation and a lower carcass content of 18:2ω6 and 18:3ω3 relative pigs exposed to lower levels of antigen. A high dietary 18:3ω3 intake in pigs exposed to higher levels of antigens decreased the β-oxidation and increased the carcass content of 18:2ω6 and 18:3ω3. In a subsequent study it was shown that the immunization of pigs exposed to low levels of antigens decreased 18:2ω6 and 18:3ω3 in the triglycerides and phospholipids of the inflamed muscle. This model also induced an elevated response from the innate, cellular and humoral immune systems. This immunization model was then used in combination with a control or high 18:3ω3 intake and again a high 18:3ω3 diet interacted with the decreased 18:2ω6 and 18:3ω3 in the triglycerides and phospholipids of the inflamed muscle. The high dietary 18:3ω3 intake also decreased the innate and increased the cellular and humoral immune responses to the immunization. Finally in rats it was shown that a ω6 polyunsaturated fatty acid deficient diet interacted (increased the β-oxidation) with the metabolism of 18:3ω3.; In conclusion 18:2ω6 and 18:3ω3 are extensively metabolized during inflammation and a high 18:3ω3 diet interacts with their metabolism possibly by influencing the innate, humoral and cellular immune response.