Fatty Acids

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Is the Fatty Acids Profile in Blood a Good Predictor of Liver Changes? Correlation of Fatty Acids Profile with Fatty Acids Content in the Liver

Is the Fatty Acids Profile in Blood a Good Predictor of Liver Changes? Correlation of Fatty Acids Profile with Fatty Acids Content in the Liver

secretion from the liver [6]. The only reference method for the evaluation of fatty liver degree is histopathological testing via a liver biopsy. However, because the test is invasive, a complications exists. Thus, to diagnose NAFLD, ultrasonography is often performed combined with a panel of biochemical blood parameters. Unfortunately, this method does not provide a conclusive diagnosis, especially in the case of differentiating between NAFLD and NASH [7]. Excessive change in lipid pathways is also responsible for the progression from simple steatosis to NASH; therefore, liver and blood lipidomic signatures are good indicators of NAFLD progression [2,8]. The profile of fatty acids present in human blood is the result of lipids supplied with diet, lipolytic activity of adipose tissue, and fatty acid biosynthesis [9]. Studies have shown that lipids in plasma/serum are sensitive indicators of short-term changes connected with daily food intake, but erythrocytes/platelets can reflect long-term changes [10]. Therefore, the evaluation of metabolic changes should be estimated according to erythrocyte/platelet analysis [11]. Because the liver is the centre of lipid changes, fatty acids profiling should reflect the pathological changes within this organ. No data have yet reported a correlation between the profile of fatty acids, liver, and blood. Therefore, the aim of our study was to investigate the correlation between the fatty acids profile of blood pallets (containing erythrocytes and platelets) and the liver.
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Effect of monoglycerides and fatty acids on a ceramide bilayer

Effect of monoglycerides and fatty acids on a ceramide bilayer

components such as monoglycerides (MG) and free fatty acids (FA) are natural constituents of the stratum corneum arising from the partial hydrolysis of sebum triglycerides produced by the sebaceous glands. 17,18 Unsaturated oils such as monoolein, oleic and linoleic acids are widely used in pharmaceutical and cosmetic industries as drug penetration and solubility enhancers. 22–24,26–31 Stearic acid is used as the moisturizing ingredient in the novel body wash products 32,33 where it acts as a buffer against lipid extraction by cleanser surfactants. In vitro experiments 27,34 show that the effect of a fatty acid as a permeation enhancer depends on chain unsaturation: long saturated fatty acids do not enhance skin permeability, while unsaturated fatty acids mark- edly enhance skin permeation. However, atomistic understand- ing of how the oils get incorporated in the skin lipid layer from the topical application or how they affect the structure of the skin lipid matrix is missing. In this study we address these by a series of molecular dynamics simulations of ceramide bilayers as surrogates for the stratum corneum lipid layer along with carefully chosen natural oil components that mostly differ in numbers and positions of unsaturation of the tails.
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Effect of monoglycerides and fatty acids on a
ceramide bilayer

Effect of monoglycerides and fatty acids on a ceramide bilayer

components such as monoglycerides (MG) and free fatty acids (FA) are natural constituents of the stratum corneum arising from the partial hydrolysis of sebum triglycerides produced by the sebaceous glands. 17,18 Unsaturated oils such as monoolein, oleic and linoleic acids are widely used in pharmaceutical and cosmetic industries as drug penetration and solubility enhancers. 22–24,26–31 Stearic acid is used as the moisturizing ingredient in the novel body wash products 32,33 where it acts as a buffer against lipid extraction by cleanser surfactants. In vitro experiments 27,34 show that the effect of a fatty acid as a permeation enhancer depends on chain unsaturation: long saturated fatty acids do not enhance skin permeability, while unsaturated fatty acids mark- edly enhance skin permeation. However, atomistic understand- ing of how the oils get incorporated in the skin lipid layer from the topical application or how they affect the structure of the skin lipid matrix is missing. In this study we address these by a series of molecular dynamics simulations of ceramide bilayers as surrogates for the stratum corneum lipid layer along with carefully chosen natural oil components that mostly differ in numbers and positions of unsaturation of the tails.
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EFFECT OF GROWTH HORMONE ON PLASMA FATTY ACIDS

EFFECT OF GROWTH HORMONE ON PLASMA FATTY ACIDS

Fasting values of plasma unesterified fatty acids were raised in man by human and simian growth hormone and in the dog by human, simian, porcine and bovine growth hormone.. Glucose, gluc[r]

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Ventromedial Hypothalamic Lesions and the Mobilization of Fatty Acids

Ventromedial Hypothalamic Lesions and the Mobilization of Fatty Acids

We have explored the effects of ventromedial hypothalamic lesions on the mobilization of free fatty acids in rats exposed to several stresses. The rise in free fatty acids and glycerol in response to norepinephrine had the same time-course and dose-response characteristics in the sham-operated and lesioned animals, indicating comparable degrees of peripheral responsiveness to this hormone. Forced swimming significantly lowered insulin and increased glycerol and free fatty acids more in control than in ventromedial hypothalamic- lesioned rats. During fasting, the rise in glycerol and free fatty acids was smaller in the lesioned rats, but the fall in insulin was greater. Exposure to cold raised fatty acids and glycerol more in the control than in the sham-operated animals, but had no significant effect on plasma insulin or glucose concentration. Injection of 2-deoxyglucose was done on lesioned or control rats with intact or removed adrenal medullas. The rise in free fatty acids and glycerol was less in the lesioned rats than in the controls, and was not affected by adrenodemedullation. The rise in glucose, however, was completely blocked in the adrenodemedullated rats. Changes in insulin were small and not statistically significant. The reduced mobilization of fatty acids from adipose tissue depots after ventromedial hypothalamic injury is consistent with the hypothesis that the ventromedial hypothalamic region serves to modulate activation of the sympathetic nervous […]
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Long chain fatty acids of peptococci and peptostreptococci

Long chain fatty acids of peptococci and peptostreptococci

This study presents an analysis of the long- streptococcus micros, Peptostreptococcus productus, chain fatty acids LCFAs extracted from the Peptostreptococcus parvulus, Peptococcus asacc[r]

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The effect of skin fatty acids on Staphylococcus aureus

The effect of skin fatty acids on Staphylococcus aureus

There was broad (but not exact) correlation between the effects of C-6-H on gene expression and protein level revealing a pleiotropic alteration in cellular physiology and virulence. Despite multiple changes in gene expression as a result of C-6-H exposure, no single resistance mechanism could be identified, which might suggest the contribution of several factors. Our data, however, support the hypoth- esis that the key regulator of virulence determinant produc- tion, SaeR, is affected by C-6-H and results in the reduced expression of several toxins. This would make sense as skin fatty acids are key markers for an environment in which S. aureus will colonise as part of the commensal flora. Expression of components able to disrupt the host will destroy this niche and potentiate other defences, thus plac- ing the organism at risk.
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Significance of Fatty Acids in Pregnancy-Induced Immunosuppression

Significance of Fatty Acids in Pregnancy-Induced Immunosuppression

Although there is little doubt as to the importance of PUFA in both the activation and the maintenance of NADPH oxidase in human PMN, the possibility that changes in the fatty acid content may have more far-reaching effects upon PMN func- tion cannot be disregarded. It has recently been established that compounds that readily affect membrane fluidity in PMN also affect oxidase activity (16, 25). Furthermore, since the fluidity of membranes is known to be influenced by the degree of saturation or unsaturation and/or hydrocarbon chain length of fatty acids, it seems reasonable to assume that the pregnan- cy-induced fatty acid changes that we have reported will alter PMN membrane fluidity. The fluidity of the plasma membrane may affect oxidase activity in a number of ways: (i) by the manner in which the multicomponent NADPH oxidase is ar- ranged within the lipid bilayer or (ii) by the extent of expres- sion and affinity of membrane-bound receptors. This latter explanation seems unlikely, since LTB 4 generation was re-
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Role of free fatty acids in endothelial dysfunction

Role of free fatty acids in endothelial dysfunction

FFAs may contribute to inflammatory states that lead to enhance endothelial permeability [122]. One of the major pathways leading to FFAs-induced ED is the acti- vation of NF-κB, reported in many studies [123]. Intake of trans fatty acids (TFAs), consumed through foods made from partially hydrogenated vegetable oils, can ac- tivate the NF-κB pathway, leading to increased endothe- lial superoxide production and reduced NO production [124]. The NF-κB pathway is a major player mediating the deleterious effects of SFAs on human coronary ar- tery ECs [125]. Surprisingly, FFAs of PUFA such as LA also may play a role in inducing inflammatory responses by increasing the levels of TNF-α, MCP-1, vascular cell adhesion molecule 1 (VCAM-1), and intercellular adhe- sion molecule 1 (ICAM-1) through the activation of NF- κB and activator protein 1 (AP-1) [126], and affect the release of NO [113]. Interestingly, a study has shown that IKK-β, which is an activator of NF-κB, can also di- minish NO production [127] (Fig. 1). Moreover, a role of the FFAs in inducement of the NLRP3 inflammasome has been shown that could lead to an increase in the endothelial permeability [122]. In microvascular endo- thelial cells (MVECs), using palmitate, the authors have showed that it could activate the NLRP3 inflammasome with a resulting reduction in endothelial tight junction proteins - zonula occludens-1 and -2 (ZO-1 and ZO-2). Further exploring of the mechanisms, it had been found that FFAs mediated such effects by triggering the pro- duction of HMGB1 which might explain the early onset of endothelial injury during obesity.
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Method of Converting Free Fatty Acids to Fatty Acid Methyl Esters

Method of Converting Free Fatty Acids to Fatty Acid Methyl Esters

A method for converting free fatty acids in acid oil or acid fat into fatty acid methyl esters is disclosed. The method involves adding a small amount of methanol and an acid catalyst to the acid oil or acid fat and subjecting the mixture to conditions that allow the fatty acid methyl esters to form. A lipid phase containing the fatty acid methyl esters and triglycerides can from and be separated from the rest of the reaction mixture. The lipid phase can then be subjected to conditions suitable for converting the triglycerides into fatty acid methyl esters. The method of present invention is especially useful for a process of generating biodiesel using a starting material of vegetable and animal oils and fats that contain a relatively high level of free fatty acids.
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Fatty Acids, Triacylglycerol and Sn -2 Fatty Acids Distributions Variations in Seed Oil from Camellia Cultivars

Fatty Acids, Triacylglycerol and Sn -2 Fatty Acids Distributions Variations in Seed Oil from Camellia Cultivars

Beside of ECN40,there has no significant difference between EFC and ECC for ECN, the average ECN40 was 0.02% for ECC, but it was 0.42% for EFC(cultivars DZ1, 6.83%), Comprehensive LLLn values in Tables 4, significant differences should not be attributed to the cultivars but the experiment error caused. Meantime the distribution information of ECN also showed that the distribution of ECC was more uniform than that of EFC. The contents of ECN42, ECN44 and ECN46 of camellia seed oil in present work were lower than that of rapeseed oil, corn oil, soybean oil, sunflower oil, grape seed oil, rice bran oil, peanut oil and cottonseed oil, but ECN50 was higher than that of reports [42], results in this work further indicated the contents of saturated fatty acids distribution in sn-1/3 is higher than that of reports [32]. To the best of the authors’ knowledge, this is the first literature data for comparison of the ECN of camellia seed oil from different cultivars.
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Combined effect of unsaturated fatty acids and saturated fatty acids on the metabolic syndrome: tehran lipid and glucose study

Combined effect of unsaturated fatty acids and saturated fatty acids on the metabolic syndrome: tehran lipid and glucose study

Some limitations should be considered, one being the use of UASD FCT to determine the intakes of PUFA, MUFA and SFA, because of not having a complete Iran- ian FCT. Given the cross-sectional design, we could not determine causality between interaction of different type of fatty acids and the MetS and its components. Future studies using longitudinal data are needed to determine these effects. In addition, this study included only healthy adults, and our findings cannot be extrapolated to other populations.

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Trans fatty acids and coronary artery disease

Trans fatty acids and coronary artery disease

Humans do not produce TFA and all comes from the diet. Two sources of TFA are found; in products derived from ruminant animals, such as milk and meat, and in foods that contain artificially manufactured hydrogenated vegetable oil. Both are derived from hydrogenation of unsaturated fats. In the case of ruminant TFA, the bacteria in the ruminant animal’s gut hydrogenate the fatty acids.

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Do fatty acids affect fetal programming?

Do fatty acids affect fetal programming?

During pregnancy, metabolic changes occur in lipid me- tabolism and the circulating levels of triglycerides, choles- terol, fatty acids, and phospholipids. These changes with insulin resistance and estrogen stimulation contribute to hyperlipidemia, hyperphagia, lipogenesis, and increases in fat mass and body weight in the 1st and 2nd trimesters. Maternal fat accumulation also causes changes in fetal metabolism, growth, and development. On the other hand, in the 3rd trimester, catabolic lipase activity arises as a re- sult of an increase in lipolytic activity in adipose tissue and a decrease in adipose tissue lipoprotein lipase activity. These changes in catabolic status result in increases in triglyceride, phospholipid, and cholesterol levels. The increase in cholesterol and free fatty acids results in negative effects on fetal metabolism, and it also alters the synthesis of cell membranes and steroid hormones [31]. Thus, changes in nutrients that pass through the placenta can affect fetal metabolism, growth, and devel- opment [32, 33].
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ESSENTIAL FATTY ACIDS IN PREMATURE INFANT FEEDING

ESSENTIAL FATTY ACIDS IN PREMATURE INFANT FEEDING

The levels in serum for total fatty acids, cholesterol, dienoic, tnienoic, and tetraenoie acids and the partial calorie efficiency cal-. culations for the premature infants in the[r]

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Fatty acids, inflammation and intestinal health in pigs

Fatty acids, inflammation and intestinal health in pigs

Fatty acids are a major energy source, important compo- nents of the cell membrane, metabolic substrates in many biochemical pathways, cell-signaling molecules, and play a critical role as immune modulators [6–8]. Research has shown that fatty acids, especially n-3 polyunsaturated fatty acids (PUFA), exert beneficial effects on inflammatory bowel diseases in animal models and clinical trials [6, 7]. The protective role of these fatty acids in the intestine is closely related to their inhibitory effects on the over-release of intestinal inflammatory mediators, especially pro- inflammatory cytokines [6–8]. Recently, the studies in pig nutrition also support potential therapeutic roles for the specific fatty acid [short chain and medium chain fatty acids, and long chain PUFA including n-3 PUFA, arachi- donic acid (ARA) and conjugated linoleic acids (CLA)] in intestinal inflammation [9–11]. In this article, we mainly focus on the effect of inflammation on GI structure and function, and the role of specific fatty acids on intestinal health of pigs, especially under inflammatory conditions.
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Crosstalk between zinc and fatty acids in plasma

Crosstalk between zinc and fatty acids in plasma

Albumin is the major carrier of free fatty acids (FFAs) in plasma [59], and harbours seven binding sites that are common to FFAs with a range of chain-lengths (C10-C18) across its three domains (Fig. 1a) [60,61]. In vitro, saturated, mono- and poly-unsaturated FFAs, with chain lengths ranging from C6 to C24, can be bound [62]. FFA affinities of albumins from different species are similar, although the effects of FFA binding on protein properties may vary, and drawing conclusions for an albumin from one particular mammalian species using data for another has been discouraged [62]. Binding constants are chain-length dependent (K D ≈ 1.5–35 nM for the strongest sites), with C18:1 (oleic
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Allosteric modulation of zinc speciation by fatty acids

Allosteric modulation of zinc speciation by fatty acids

This demonstrated, albeit in vitro, that elevated plasma fatty acids can directly in fl uence the ACB assay. Furthermore, since this “ modi fi cation ” is non-covalent, it explains the rapid (within hours) return to normal IMA levels once the ischemic event is over. Given the long half-live of al- bumin, any covalent modi fi cations are unlikely to be cleared as quickly, whereas clearance of plasma fatty acid occurs on a comparable time scale [36]. However, it is important to note that the suggested molecular mechanism does not exclude other mechanisms that in fl uence albumin cobalt-binding such as reduced pH as a consequence of acidosis.
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Amino acids and fatty acids in Turbinaria conoides

Amino acids and fatty acids in Turbinaria conoides

Sample was collected from the sea coast of Mandapam, Tamil Nadu, India in the form of dry sample. Algal sample were cleaned at epiphytes and necrotic parts were removed. Sample was rinsed with sterile water to remove any associated debris. Sample was kept under sunshade for 7 days. After drying the powder was then used the primary estimation of amino acids and fatty acids. This powder was stored in cold conditions in an airtight container and analysis was carried out within three months of processing.

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The role of fatty acids in insulin resistance

The role of fatty acids in insulin resistance

In many ways insulin resistance appears to start in the hypothalamus. The hypothalamus acts to match energy intake to energy expenditure to prevent excess accumu- lation of stored energy [23]. In particular, satiety signals from the gut are matched to adiposity (primarily-leptin) and blood (primarily-insulin) hormonal signals to control food intake [24, 25]. Unfortunately, either excess calories or saturated fats (especially palmitic acid) can cause in- flammation in the hypothalamus, leading to resistance to the satiety signaling of both insulin and leptin [26–28]. As a result, satiety is attenuated and hunger increases. The hypothalamus also contains GPR120 binding proteins that are specific for long-chain omega-3 fatty acids such as EPA and DHA [29]. Thus the presence of adequate levels of these omega-3 fatty acids in the diet can decrease in- flammation within the hypothalamus [30]. In fact, intra- cerebroventricular (icv) injections of omega-3 fatty acids Table 1 Potential inflammatory pathways leading to increased insulin resistance
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