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The Role Of The Free Fatty Acid, Lauric Acid, I... [2021]

Plasma free fatty acids levels are increased in subjects with obesity and type 2 diabetes, playing detrimental roles in the pathogenesis of atherosclerosis and cardiovascular diseases. Increasing evidence showing that dysfunction of the vascular endothelium, the inner lining of the blood vessels, is the key player in the pathogenesis of atherosclerosis. In this review, we aimed to summarize the roles and the underlying mechanisms using the evidence collected from clinical and experimental studies about free fatty acid-mediated endothelial dysfunction. Because of the multifaceted roles of plasma free fatty acids in mediating endothelial dysfunction, elevated free fatty acid level is now considered as an important link in the onset of endothelial dysfunction due to metabolic syndromes such as diabetes and obesity. Free fatty acid-mediated endothelial dysfunction involves several mechanisms including impaired insulin signaling and nitric oxide production, oxidative stress, inflammation and the activation of the renin-angiotensin system and apoptosis in the endothelial cells. Therefore, targeting the signaling pathways involved in free fatty acid-induced endothelial dysfunction could serve as a preventive approach to protect against the occurrence of endothelial dysfunction and the subsequent complications such as atherosclerosis.

The Role of the Free Fatty Acid, Lauric Acid, i...


Beta-hydroxy fatty acids are a major component of lipid A moiety of lipopolysaccharide. We aimed to investigate the role of free beta-hydroxy fatty acids on inflammation, as well as to evaluate their effects on cytokine release from human blood cells, and whether they exist in plasma of patients with chronic inflammatory diseases with/without insulin resistance. Peripheral venous blood was incubated with beta-hydroxy lauric and beta-hydroxy myristic acids (each 100 ng, 1 microg, 10 microg/mL) up to 24 hours. Cytokines were measured from culture media and plasma. Free fatty acids and biochemical parameters were also measured from patients' plasma. Only beta-hydroxy lauric acid significantly stimulated interleukin-6 production at 10 microg/mL compared to control (533.9 +/- 218.1 versus 438.3 +/- 219.6 pg/mL, P

Both sll0180 and slr2131 genes that encode the Sll0180 and Slr2131 proteins, respectively, were removed from Synechocystis sp. PCC 6803 and SD277, a high fatty acid-producing Synechocystis-based strain, to test the hypothesis that Sll0180 and Slr2131 contribute to the efflux of chemicals out of Synechocystis sp. PCC 6803 and SD277. The mutant Synechocystis sp. PCC 6803 and SD277 strains with either sll0180 or slr2131 removed from the chromosome had significantly decreased half maximal inhibitory concentrations to various antibiotics. The free fatty acid (FFA) concentration of the SD277 mutant strains increased intracellularly yet decreased extracellularly indicating that Sll0180 and Slr2131 have a role in FFA efflux. E. coli wild-type gene acrA (a homolog to sll0180) was added on a plasmid to the respective mutant strains lacking the sll0180 gene. Similarly, the E. coli wild-type gene acrB (a homolog to slr2131) was added to the respective mutant strains lacking the slr2131 gene. The tolerance to chloramphenicol of each mutant strain containing the wild-type E. coli gene was restored when compared to the parent stains. The extracellular FFA concentration of SD277 Δslr2131 with E. coli acrB increased significantly compared to both SD277 and SD277 Δslr2131.

Lauric acid, as a component of triglycerides, comprises about half of the fatty-acid content in coconut milk, coconut oil, laurel oil, and palm kernel oil (not to be confused with palm oil),[10][11] Otherwise, it is relatively uncommon. It is also found in human breast milk (6.2% of total fat), cow's milk (2.9%), and goat's milk (3.1%).[10]

The endothelium acts as the barrier that prevents circulating lipids such as lipoproteins and fatty acids into the arterial wall; it also regulates normal functioning in the circulatory system by balancing vasodilation and vasoconstriction, modulating the several responses and signals. Plasma lipids can interact with endothelium via different mechanisms and produce different phenotypes. Increased plasma-free fatty acids (FFAs) levels are associated with the pathogenesis of atherosclerosis and cardiovascular diseases (CVD). Because of the multi-dimensional roles of plasma FFAs in mediating endothelial dysfunction, increased FFA level is now considered an essential link in the onset of endothelial dysfunction in CVD. FFA-mediated endothelial dysfunction involves several mechanisms, including dysregulated production of nitric oxide and cytokines, metaflammation, oxidative stress, inflammation, activation of the renin-angiotensin system, and apoptosis. Therefore, modulation of FFA-mediated pathways involved in endothelial dysfunction may prevent the complications associated with CVD risk. This review presents details as to how endothelium is affected by FFAs involving several metabolic pathways.

Various studies have concluded that PA substantially contributes to the development of atherosclerosis [55]. Both in vivo and in vitro studies have demonstrated the mechanisms by which PA contributes to the pathogenesis of CVDs. PA promotes inflammatory responses and cellular senescence in cardiac fibroblasts. PA achieves senescence in these cells by activating toll-like receptor 4 (TLR4) and NLRP3 inflammasome, increasing mitochondrial ROS levels [56]. PA also induces apoptosis of the vascular smooth muscle cells by inducing the TLR4 pathway and generating ROS [57]. Both PA and SA downregulated eNOS in porcine aortic endothelial cells. Although PUFAs have a protective role against endothelium dysfunction [58], their elevated FFAs adversely affect the endothelium by decreasing NO release and increasing ET-1 levels. Linoleic acid,18:2n-6 (LA) negatively regulates eNOS phosphorylation and affects the intracellular NO levels in ECV304 cells [59].

Many clinical studies showed protective effects of OA on flow-mediated dilation and other endothelial markers; however, they did not focus on FFA-induced endothelium dysfunction [60,61,62]. Studies demonstrated that n-3 long-chain polyunsaturated fatty acids (LCPUFAs) such as docosahexaenoic acid, 22:6n-3 (DHA), eicosapentaenoic acid,20:5n-3 (EPA), and polyphenols were beneficial in FFA-induced endothelium dysfunction [59, 63,64,65]. The mitochondria-related AMPK/eNOS pathway alleviates endothelium dysfunction and atherosclerosis in mice fed with a high-fat diet [66]. L-carnitine, an essential factor for fatty acid transport/oxidation in the mitochondria, attenuates FFA-induced obesity-related endothelium dysfunction in human subjects [67].

Dietary polyunsaturated fatty acids (PUFAs) commonly consumed by humans encompass two major groups: the n-3 and n-6 families of fatty acids. Linoleic acid, 18:2n-6 (LA) and alpha-linolenic acid,18:3n-3 (ALA) are the dietary essential fatty acids (EFAs) [82]. LA and ALA are not interchangeable but can be further elongated and desaturated by the same enzyme systems to produce n-6 and n-3 LCPUFAs in the body. Some common n-3 PUFAs include ALA, EPA and DHA, and common n-6 ones include LA and arachidonic acid,20:4n-6 (ARA). LCPUFAs are the precursors for eicosanoid biosynthesis and various signaling compounds with relevant roles in human health and disease. Whereas dietary LA and ALA are primarily from vegetable oils, preformed LCPUFAs may also be consumed in animal-origin foods. The importance of LCPUFAs has been related to their structural action, their specific interaction with membrane proteins, and their ability to serve as precursors of second messengers. LCPUFAs (20 carbon) are substrates for cyclooxygenase (prostaglandin-endoperoxide synthase) and lipoxygenases and produce various compounds collectively called eicosanoids. These compounds have diverse biological functions in cell growth and development, inflammation, and the cardiovascular system. The biological response elicited after eicosanoid release is dependent on the net balance of eicosanoids derived from n-6 and n-3 LCPUFAs. ARA is the most predominant precursor fatty acid of the highly biologically active eicosanoids of the 2 series in the Western diet. Also, the endogenous formation of cyclooxygenase and non-cyclooxygenase metabolites of fatty acids has been implicated in gene expression. Because each type of EFA can interfere with the other's metabolism, an excess of n-6 fatty acids will reduce the metabolism of ALA, possibly leading to a deficit of n-3 LCPUFA metabolites. Therefore, a proper balance between the n-6 and n-3 fatty acids in the diet is essential to maintain optimum health.

(a) The food additive consists of one or any mixture of the following straight-chain monobasic carboxylic acids and their associated fatty acids manufactured from fats and oils derived from edible sources: Capric acid, caprylic acid, lauric acid, myristic acid, oleic acid, palmitic acid, and stearic acid.

In this study, it was aimed to investigate the effects of the addition of caprylic (octanoic, C8:0), capric (decanoic, C10:0) and lauric (dodecanoic, C12:0) acids from medium-chain free fatty acids to broiler diets. A total of 120 one-dayold male broiler chicks (Ross 308) were used and the study was conducted on 4 main groups of broilers; one control and three trials. The birds in the control group was fed an unadulterated basal diet and those in the experimental groups were fed with 0.2% of caprylic, capric and lauric acids (in addition to a basal diet) respectively. In the study, there was no significant difference between the groups in terms of mean live weight gain, feed consumption, feed conversion rate, serum glucose, total cholesterol, total protein and albumin (P>0.05). However, the triglyceride levels were detected to be significantly lower in the experimental groups (P 041b061a72


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