Dietary oat bran and probiotic interaction in polyunsaturated fatty acid and oxylipin metabolism

Abstract

Background and Rationale: Polyunsaturated fatty acids (PUFA) are essential in human diet. The PUFAs becomes oxidized in vivo to release mediators that can be toxic or bioactive. A good balance of omega-6 to omega-3 PUFA is required in human to prevent chronic diseases. However, this is deranged by the high fat diet (HFD) in the modern diet leading to heart diseases such as atherosclerosis. Oat bran diet is widely recommended for maintaining healthy heart. It is rich in PUFA and also a good source of prebiotic soluble fibres. Moreover, diet enriched with probiotics is also suggested to be cardio-protective. Objectives: Indicates the purpose of the study: It is proposed, supplementation of pro- and prebiotics can regulate the balance of PUFA and its mediators in HFD. Mythology: Describe pertinent experimental procedures: C57BL/6N mice were fed with HFD with or without probiotic, and Apolipoprotein E-/- female mice were fed with HFD or HFD with 30% oat bran (HFD+Oat). PUFA and its mediators were analysed in the oat bran, and the heart and liver tissues using LC-MS/MS. Results: Summarize the results of the research: Probiotic had did not improve liver PUFA and its mediator profile of C57BL/6N mice. In ApoE-/- mice, the levels of arachidonic (AA), a-linolenic (ALA) and docosahexaenoic acids elevated in liver tissue whereas only AA and ALA increased in heart tissue after HFD+Oat compared to HFD. HFD dysregulated the mediators (HETEs, PGF2a, IsoPs, HDHA, NeuroPs, NeuroFs) in the liver tissues while the addition of oat to HFD dysregulated the mediators (HETEs, dihomo-IsoPs, dihomo-IsoFs, HDHA, NeuroFs) in the heart tissues of ApoE-/- mice. Notably, mediators related to pro-inflammation (HETEs, PGF2a) levels were elevated and those that are anti-inflammatory (HDHA, NeuroPs) were reduced. Conclusions: State the main conclusions: The oat bran modified PUFA metabolism in the liver and consequently heart tissues of ApoE-/- mice. As a result, its mediators were also altered, where elevation of pro-inflammatory ones may not be advantageous in the development of atherosclerosis.