مقاله انگلیسی رایگان در مورد رژیم غذایی دارای کمبود اسید چرب و اثر آن بر بافت موش – الزویر 2020

1- Introduction

2- Materials and methods

3- Results

4- Discussion

References

Abstract

No data are available on whether a diet deficient of the essential fatty acids is able to modulate tissue levels of endocannabinoids and congeners. Male rats fed for 12 weeks a diet deficient of essential fatty acids, palmitic and oleic acids (EFAD), replaced with saturated fatty acids (SAFA), showed lowered n-3 and n-6 PUFAs levels in plasma, liver and adipose tissue, with concomitant steep increase of oleic and mead acids, while in hypothalamus no changes in PUFA concentration were detected and only palmitoleic acid was found increased. We found a reduction of anandamide and palmitoylethanolamide in liver and brain, while oleoylethanolamide increased significantly in liver and adipose tissue, associated to a 50 % body weight decrease. Changes in N-acylethanolamide profile may contribute to body weight reduction distinctive of EFA deficiency.

Introduction

Several lines of evidence show that dietary fatty acids may influence endocannabinoids (ECs) and their congeners tissue profiles in vitro [1] and in vivo [2]. Most of the studies aimed at evaluating whether changes in arachidonic acid (ARA, 20:4n-6) tissue phospholipids (PL) content were able to modulate the main ECs anandamide (AEA) and 2-arachidonoylglycerol (2-AG) [3]. Two major strategies have been described in the literature, reduction of ARA by increasing dietary n-3 long chain polyunsaturated fatty acids (n-3 LCPUFAs), i.e. eicosapentaenoic acid (EPA, 20:5n-3) and docosahexaenoic acid (DHA, 22:6n-3) [4], or increasing it by feeding ARA precursor, linoleic acid (LA, 18:2n-6) [5]. In humans, it has been shown that increasing dietary EPA and DHA was able to decrease 2-AG [6] or AEA [7]; however, other nutritional strategies to increase tissue n-3 LCPUFAs, as demonstrated with intake of cheese enriched in alpha-linolenic (ALA, 18:3n-3), conjugated linoleic (CLA, 18:2c9t11) and vaccenic (VA, 18:1t11) acids, were able to significantly decrease plasma levels of AEA in hypercholesterolemic patients [8]. On the other hand, no data are available on whether a diet deficient in n-3 and in n-6 fatty acids replaced by saturated fatty acids (SAFA) is able to modify EC and congeners tissue profile. It is well known that intake of an essential fatty acid deficient (EFAD) diet is characterized by growth retardation and weight loss [9], even though the mechanism of action is not quite well understood. ARA possesses essential functions, particularly in cellular signalling via its role of precursors for numerous derivatives such as prostaglandins, leukotrienes, hepoxilins and other eicosanoids including ECs which strongly influence body composition homeostasis [10]. Symptoms of n-6 fatty acid deficiency involves, initially, scaly skin, decreased growth and increased transepidermal water loss, all symptoms that seem to be attributable to an essential structural role of LA in O-acylated ceramides of the epidermal water permeability barrier [11]. A dietary intake of around 1 en% of LA should be enough to prevent these symptoms in animals and in humans [12]. An early symptom of n-3 fatty acids deficiency is delayed brain development due to their essential role for proper brain function, probably via their incorporation into specific cellular PL [13]. Humans in the Western world ingest far less n-3 fatty acids (around 1–3 g⁄d, mainly ALA and, to a lesser extent, EPA and DHA) than n-6 fatty acids (10–20 g/d, mainly LA). The dietary intake of EPA and DHA varies greatly between individuals and between geographical populations and is mainly related to the dietary intake of seafood. It is well evident that EPA and DHA can inhibit the in vitro production of ARA-derived eicosanoids [14], but the in vivo formation seems to be much less influenced by dietary intake of EPA and DHA [14].