Mechanism of supported Ru3Sn7 nanocluster-catalyzed selective hydrogenation of coconut oil to fatty alcohols

2018 ◽  
Vol 8 (5) ◽  
pp. 1322-1332 ◽  
Author(s):  
Zhicheng Luo ◽  
Qiming Bing ◽  
Jiechen Kong ◽  
Jing-yao Liu ◽  
Chen Zhao
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Selective Hydrogenation ◽  
Active Site ◽  
Coconut Oil ◽  
Fatty Alcohols ◽  
Hydrotreating Catalyst ◽  
Fatty Acid Hydrogenation

As a promising hydrotreating catalyst, it was previously reported that Ru⋯OSn (Ru electronically interacts with Sn oxides) on RuSn/SiO2 was the active site for fatty acid hydrogenation, but here in this work we found that Ru3Sn7 nanoclusters on RuSn/SiO2 were responsible for the selective hydrogenation of diverse fatty acids and coconut oil to fatty alcohols.

In Vitro Anticancer Activity of Virgin Coconut Oil and its Fractions in Liver and Oral Cancer Cells

2020 ◽  
Vol 19 (18) ◽  
pp. 2223-2230 ◽  
Author(s):  
Poonam Verma ◽  
Sanjukta Naik ◽  
Pranati Nanda ◽  
Silvi Banerjee ◽  
Satyanarayan Naik ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Oral Cancer ◽  
Anticancer Activity ◽  
Cancer Cells ◽  
Cell Line ◽  
Coconut Oil ◽  
Virgin Coconut Oil ◽  
Anticancer Efficacy ◽  
Oral Cancer Cells

Background: Coconut oil is an edible oil obtained from fresh, mature coconut kernels. Few studies have reported the anticancer role of coconut oil. The fatty acid component of coconut oil directly targets the liver by portal circulation and as chylomicron via lymph. However, the anti-cancer activity of coconut oil against liver cancer cells and oral cancer cells is yet to be tested. The active component of coconut oil, that is responsible for the anticancer activity is not well understood. In this study, three different coconut oils, Virgin Coconut Oil (VCO), Processed Coconut Oil (PCO) and Fractionated Coconut Oil (FCO), were used. Objective: Based on previous studies, it can be hypothesized that fatty acids in coconut oil may have anticancer potential and may trigger cell death in cancer cell lines. Methods: Each cell line was treated with different concentrations of Virgin Coconut Oil (VCO), Processed Coconut Oil (PCO) and Fractionated Coconut Oil (FCO). The treated cells were assayed by MTT after 72 hr of incubation. The fatty acid composition of different coconut oils was analyzed by gas chromatography. Result: Different concentrations of coconut oils were used to treat the cells. Interestingly, the anticancer efficacy of VCO, PCO and FCO was not uniform, rather the efficacy varied from cell line to cell line. Only 20% VCO showed significant anticancer activity in HepG2 cells in comparison to 80% PCO against the KB cell line. Remarkably, 20% of PCO and 5% of FCO showed potential growth inhibition in the KB cell line as compared to 80% PCO in HepG2 cells. Moreover, there was a difference in the efficacy of VCO, PCO and FCO, which might be due to their fatty acid composition. Comparing the anticancer efficacy of VCO, PCO and FCO in this study helped to predict which class of fatty acids and which fatty acid might be associated with the anticancer activity of VCO. Conclusion: This study shows that VCO, PCO and FCO have anticancer efficacy and may be used for the treatment of cancer, especially liver and oral cancer.

scholarly journals Differential Effects of Fatty Acid Saturation and Chain Length on NASH in Juvenile Iberian Pigs

2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 682-682 ◽  
Author(s):  
Kayla Dillard ◽  
Morgan Coffin ◽  
Gabriella Hernandez ◽  
Victoria Smith ◽  
Catherine Johnson ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Body Weight ◽  
Fatty Acid ◽  
Liver Injury ◽  
Olive Oil ◽  
Coconut Oil ◽  
Long Chain Fatty Acids ◽  
Medium Chain ◽  
Long Chain ◽  
Chain Fatty Acids

Abstract Objectives Non-alcoholic fatty liver disease (NAFLD) represents the major cause of pediatric chronic liver pathology in the United States. The objective of this study was to compare the relative effect of inclusion of isocaloric amounts of saturated medium-chain fatty acids (hydrogenated coconut oil), saturated long-chain fatty acids (lard) and unsaturated long-chain fatty acids (olive oil) on endpoints of NAFLD and insulin resistance. Methods Thirty-eight 15-d-old Iberian pigs were fed 1 of 4 diets containing (g/kg body weight × d) 1) control (CON; n = 8): 0 g fructose, 10.5 g fat, and 187 kcal metabolizable energy (ME), 2) lard (LAR; n = 10): 21.6 g fructose, 17.1 g fat (100% lard) and 299 kcal ME, 3) hydrogenated coconut oil (COCO; n = 10): 21.6 g fructose, 16.9 g fat (42.5% lard and 57.5% coconut oil) and 299 kcal ME, and 4) olive oil (OLV, n = 10): 21.6 g fructose, 17.1 g fat (43.5% lard and 56.5% olive oil) and 299 kcal ME, for 9 consecutive weeks. Body weight was recorded every 3 d. Serum markers of liver injury and dyslipidemia were measured on d 60 at 2 h post feeding, with all other serum measures assessed on d 70. Liver tissue was collected on d 70 for histology, triacylglyceride (TG) quantification, and metabolomics analysis. Results Tissue histology indicated the presence of steatosis in LAR, COCO and OLV compared with CON (P ≤ 0.001), with a further increase in in non-alcoholic steatohepatitis (NASH) in OLV and COCO compared with LAR (P ≤ 0.01). Alanine and aspartate aminotransferases were higher in COCO and OLV (P ≤ 0.01) than CON. All treatment groups had lower liver concentrations of methyl donor's choline and betaine versus CON, while bile acids were differentially changed (P ≤ 0.05). COCO had higher levels of TGs with less carbons (Total carbons < 52) than all other groups (P ≤ 0.05). Several long-chain acylcarnitines involved in fat oxidation were higher in OLV versus all other groups (P ≤ 0.05). Conclusions Inclusion of fats enriched in medium-chain saturated and long-chain unsaturated fatty acids in a high-fructose high-fat diet increased liver injury, compared with fats with a long-chain saturated fatty acid profile. Further research is required to investigate the mechanisms causing this difference in physiological response to these dietary fat sources. Funding Sources ARI, AcornSeekers.

scholarly journals Impact of Selected Cosmetic Ingredients on Common Microorganisms of Healthy Human Skin

Cosmetics ◽  
2019 ◽  
Vol 6 (3) ◽  
pp. 45 ◽  
Author(s):  
Dorota Dobler ◽  
Thomas Schmidts ◽  
Sören Wildenhain ◽  
Ilona Seewald ◽  
Michael Merzhäuser ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Human Skin ◽  
Chain Length ◽  
Skin Diseases ◽  
Free Acid ◽  
Fatty Alcohols ◽  
Fatty Acid Esters ◽  
Bacterial Strains ◽  
Acid Esters

Human skin is a complex ecosystem and is host to a large number of microorganisms. When the bacterial ecosystem is balanced and differentiated, skin remains healthy. However, the use of cosmetics can change this balance and promote the appearance of skin diseases. The skin’s microorganisms can utilize some cosmetic components, which either promote their growth, or produce metabolites that influence the skin environment. In this study, we tested the ability of the Malassezia species and some bacterial strains to assimilate substances frequently used in dermal formulations. The growth capability of microorganisms was determined and their lipase activity was analyzed. The growth of all Malassezia spp. in the presence of free acids, free acid esters, and fatty alcohols with a fatty chain length above 12 carbon atoms was observed. No growth was observed in the presence of fatty alcohol ethers, secondary fatty alcohols, paraffin- and silicon-based substances, polymers, polyethylene glycols, quaternary ammonium salts, hydroxy fatty acid esters, or fatty acids and fatty acid esters with a fatty chain length shorter than 12 carbon atoms. The hydrolysis of esters by Malassezia lipases was detected using High Performance Thin Layer Chromatography (HPTLC). The production of free fatty acids as well as fatty alcohols was observed. The growth promotion or inhibition of bacterial strains was only found in the presence of a few ingredients. Based on these results, formulations containing microbiome inert ingredients were developed.

Lipids of the intestinal mucosa of normal and essential fatty acid deficient rats

1970 ◽  
Vol 48 (9) ◽  
pp. 631-639 ◽  
Author(s):  
M. Yurkowski ◽  
B. L. Walker
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Free Fatty Acids ◽  
Essential Fatty Acid ◽  
Corn Oil ◽  
Essential Fatty Acids ◽  
Coconut Oil ◽  
Fatty Acid Deficiency ◽  
Arachidonic Acids ◽  
Layer Chromatography

Mucosal lipids were isolated from the proximal, middle, and distal intestinal sections of rats fed diets containing either 10% corn oil or 10% hydrogenated coconut oil, the latter diet being deficient in essential fatty acids. By a combination of column and thin-layer chromatography, the lipids were fractionated and the major components found to consist of triglycerides, free fatty acids, cholesterol, phosphatidylcholine, and phosphatidylethanolamine. Several minor constituents were present. Triglycerides and free fatty acids were generally present in higher concentrations in animals fed corn oil, and the concentration of mucosal triglycerides decreased towards the distal end of the intestine whereas free fatty acids increased in this group. Essential fatty acid deficiency resulted in lower levels of linoleic and arachidonic acids and higher levels of palmitoleic, oleic, and eicosatrienoic acids in the mucosal lipids. Mono- and di-enoic fatty acids tended to decrease in concentration from the proximal to the distal end of the intestine; the polyunsaturated acids and, to some extent, the saturated acids, were lowest in the proximal section of the intestine.

scholarly journals Artificial rearing of pigs

1973 ◽  
Vol 29 (3) ◽  
pp. 447-455 ◽  
Author(s):  
R. Braude ◽  
M. J. Newport
Keyword(s):  
Fatty Acids ◽  
Small Intestine ◽  
Fatty Acid Composition ◽  
Fatty Acid ◽  
Acid Composition ◽  
Beef Tallow ◽  
Coconut Oil ◽  
Live Weight ◽  
Distal Portion ◽  
Soya Bean

1. The butterfat in a whole-milk diet was replaced by either beef tallow, coconut oil or soya-bean oil. The diets contained 280 g fat and 720 g dried skim milk per kg and were supplemented with vitamins A, D, E and K.2. These diets were offered as a milk, containing 200 g solids/Kg, to pigs weaned at 2 d of age during a 26 d experiment. The pigs were fed at hourly intervals to a scale based on live weight (scale E).3. The performance of the pigs and the apparent digestibility of the dietary fats indicated that soya-bean oil was equal to butterfat. Butterfat was slightly superior to coconut oil and markedly superior to beef tallow.4. The amount and composition of the fatty acids were studied in the proximal, mid and distal portions of the small intestine. When the beef tallow diet was given there was an increased amount of total fatty acids in the digesta of the small intestine, mainly in the distal portion. The digesta contained the smallest quantity of fatty acids when the soya-bean oil diet was given. The fatty acid composition of the digesta indicated that the short- and medium chain fatty acids from all the diets were well utilized, but an increasing proportion of stearic acid occurred in the distal portion of the small intestine. The interpretation of changes in fatty acid composition in the digesta in relation to absorption is discussed.

scholarly journals Two Lipid Signals Guide Fruiting Body Development of Myxococcus xanthus

mBio ◽  
2014 ◽  
Vol 5 (1) ◽  
Author(s):  
Swapna Bhat ◽  
Tilman Ahrendt ◽  
Christina Dauth ◽  
Helge B. Bode ◽  
Lawrence J. Shimkets
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Fruiting Body ◽  
Myxococcus Xanthus ◽  
Chain Fatty Acid ◽  
Fatty Alcohols ◽  
Lipid Bodies ◽  
Wild Type ◽  
Bioactive Lipids ◽  
Content Type

ABSTRACTMyxococcus xanthusproduces several extracellular signals that guide fruiting body morphogenesis and spore differentiation. Mutants defective in producing a signal may be rescued by codevelopment with wild-type cells or cell fractions containing the signal. In this paper, we identify two molecules that rescue development of the E signal-deficient mutant LS1191 at physiological concentrations,iso15:0 branched-chain fatty acid (FA) and 1-iso15:0-alkyl-2,3-di-iso15:0-acyl glycerol (TG1), a development-specific monoalkyl-diacylglycerol. The physiological concentrations of the bioactive lipids were determined by mass spectrometry from developing wild-type cells using chemically synthesized standards. Synthetic TG1 restored fruiting body morphogenesis and sporulation and activated the expression of the developmentally regulated gene with locus tagMXAN_2146at physiological concentrations, unlike its nearly identical tri-iso15:0 triacylglycerol (TAG) counterpart, which has an ester linkage instead of an ether linkage.iso15:0 FA restored development at physiological concentrations, unlike palmitic acid, a straight-chain fatty acid. The addition of either lipid stimulates cell shortening, with an 87% decline in membrane surface area, concomitantly with the production of lipid bodies at each cell pole and in the center of the cell. We suggest that cells produce triacylglycerol from membrane phospholipids. Bioactive lipids may be released byprogrammedcelldeath (PCD), which claims up to 80% of developing cells, since cells undergoing PCD produce lipid bodies before lysing.IMPORTANCELike mammalian adipose tissue, many of theM. xanthuslipid body lipids are triacylglycerols (TAGs), containing ester-linked fatty acids. In both systems, ester-linked fatty acids are retrieved from TAGs with lipases and consumed by the fatty acid degradation cycle. Both mammals andM. xanthusalso produce lipids containing ether-linked fatty alcohols with alkyl or vinyl linkages, such as plasmalogens. Alkyl and vinyl linkages are not hydrolyzed by lipases, and no clear role has emerged for lipids bearing them. For example, plasmalogen deficiency in mice has detrimental consequences to spermatocyte development, myelination, axonal survival, eye development, and long-term survival, though the precise reasons remain elusive. Lipids containing alkyl- and vinyl-linked fatty alcohols are development-specific products inM. xanthus. Here, we show that one of them rescues the development of E signal-producing mutants at physiological concentrations.

scholarly journals Structure and mechanism of Staphylococcus aureus oleate hydratase (OhyA)

2020 ◽  
pp. jbc.RA120.016818
Author(s):  
Christopher D. Radka ◽  
Justin L. Batte ◽  
Matthew W. Frank ◽  
Brandon M. Young ◽  
Charles O. Rock
Keyword(s):  
Fatty Acids ◽  
Staphylococcus Aureus ◽  
Fatty Acid ◽  
Active Site ◽  
Catalytic Mechanism ◽  
Unsaturated Fatty Acids ◽  
Binary And Ternary Complexes ◽  
Hydronium Ion ◽  
Multiple Structures ◽  
Fad Binding

FAD-dependent bacterial oleate hydratases (OhyA) catalyze the addition of water to isolated fatty acid carbon-carbon double bonds.  Staphylococcus aureus uses OhyA to counteract the host innate immune response by inactivating antimicrobial unsaturated fatty acids.  Mechanistic information explaining how OhyAs catalyze regio- and stereospecific hydration is required to understand their biological functions and the potential for engineering new products.  In this study, we deduced the catalytic mechanism of OhyA from multiple structures of S. aureus OhyA in binary and ternary complexes with combinations of ligands along with biochemical analyses of relevant mutants.  The substrate-free state shows Arg81 is the gatekeeper that controls fatty acid entrance to the active site.  FAD binding engages the catalytic loop to simultaneously rotate Glu82 into its active conformation and Arg81 out of the hydrophobic substrate tunnel, allowing the fatty acid to rotate into the active site.  FAD binding also dehydrates the active site, leaving a single water molecule connected to Glu82.  This active site water is a hydronium ion based on the analysis of its hydrogen bond network in the OhyA•PEG400•FAD complex. We conclude that OhyA accelerates acid-catalyzed alkene hydration by positioning the fatty acid double bond to attack the active site hydronium ion, followed by the addition of water to the transient carbocation intermediate.  Structural transitions within S. aureus OhyA channel oleate to the active site, curl oleate around the substrate water, and stabilize the hydroxylated product to inactivate antimicrobial fatty acids.

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