Increasing Dietary α-Linolenic Acid Enhances Tissue Levels of Long-Chain n-3 PUFA when Linoleic Acid Intake Is Low in Hamsters

Abstract

Background/Aims: We tested whether feeding hamsters diets varying in α-linolenic acid (ALA) content and low in linoleic acid (LA) could increase the tissue levels of eicosapentaenoic acid (EPA), docosapentaenoic acid (DPA), and docosahexaenoic acid (DHA) to the same extent as a fish oil-supplemented diet. Methods: For 5 weeks, 60 hamsters were fed 1 of the following 5 diets containing 2% of total dietary energy (TE) as LA and either 0.5% (diet A), 1% (diets B and E), 2% (diet C), or 4% (diet D) ALA of TE, so that the ratio of LA/ALA was 4:1, 2:1, 1:1, or 1:2. Diet E was supplemented with fish oil at the level of 0.2% of total energy intake. At the end of the study, overnight-fasted hamsters were sacrificed, and blood and tissues were collected. Results: Tissue levels of ALA, EPA, DPA, and DHA rose in proportion to the increase in the dietary ALA level (p < 0.01); however, the levels of DHA reached a plateau at ALA intakes above 1% (p < 0.01). These changes were accompanied by decreases in arachidonic acid with or without increases in LA levels (p < 0.01). Hamsters fed diet D had similar or higher EPA, DPA, and DHA tissue levels to those fed diet E (p < 0.01). Conclusions: In hamsters, diets containing 4% energy as ALA and 2% energy as LA can increase the tissue levels of EPA, DPA, and DHA to the same extent as feeding 0.2% energy as fish oil.

Attenuation of colonic inflammation by partial replacement of dietary linoleic acid with α-linolenic acid in a rat model of inflammatory bowel disease

“…This is influenced by several factors including sex, genetic factors, physiological status and dietary factors ( 33 ) . High intake of LA and hence a high LA:ALA ratio could inhibit the conversion of ALA, which is supported by several animal studies ( 34 – 36 ) . However, recent human studies using a tracer isotope technique demonstrated that the conversion of ALA to LC n -3 PUFA is determined by the absolute levels of LA and ALA and not the ratio ( 37 ) .…”

Dietary omega-3 and omega-6 polyunsaturated fatty acids modulate hepatic pathology

“…Studies have suggested that humans evolved on a diet containing approximately a 1:1 ratio of ω-6:ω-3 PUFA[7]; however, current western diets has a high ω-6:ω-3 ratio. [8] A diet high in ω-6 PUFAs, such as linoleic acid (LA), results in decreased tissue levels of ω-3 long-chain (Lc) PUFAs, including eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA)[9], and a heightened risk of chronic inflammatory disease processes. [10] In contrast, a diet containing a low ω-6:ω-3 PUFA ratio, or one that is supplemented with Lc ω-3 PUFAs, reduces risk factors for chronic inflammatory diseases, including cardiovascular disease,[11, 12] cancer,[13, 14] and obesity.…”

Eicosapentaenoic and docosahexaenoic acids as inflammation-modulating and lipid homeostasis influencing nutraceuticals: A review

“…Moreover, DHA accumulation in ALA-fed animals is a tissue-selective process (Barceló -Goblijn & Murphy, 2009). In hamsters, diets containing 4% energy as ALA and 2% energy as linoleic acid (LA) can increase the tissue levels of EPA and DHA to the same extent as feeding 0.2% energy as fish oil (Aziz et al, 2010). As far as humans are concerned, regarding dietary PUFA n-3, only DHA accumulates in the membrane phospholipids (Jump, 2004), and the plasma DHA pool is far greater than that of EPA; therefore a small increment in the plasma DHA pool as a consequence of ALA conversion is usually hard to detect (Brenna, Salem, Sinclair, & Cunnane, 2009).…”