Academic literature on the topic 'Exogenous fatty acid'
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Journal articles on the topic "Exogenous fatty acid"
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Song, Jae-Eun, Tiago C. Alves, Bernardo Stutz, Matija Šestan-Peša, Nicole Kilian, Sungho Jin, Sabrina Diano, Richard G. Kibbey, and Tamas L. Horvath. "Mitochondrial Fission Governed by Drp1 Regulates Exogenous Fatty Acid Usage and Storage in Hela Cells." Metabolites 11, no. 5 (May 18, 2021): 322. http://dx.doi.org/10.3390/metabo11050322.
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In the presence of high abundance of exogenous fatty acids, cells either store fatty acids in lipid droplets or oxidize them in mitochondria. In this study, we aimed to explore a novel and direct role of mitochondrial fission in lipid homeostasis in HeLa cells. We observed the association between mitochondrial morphology and lipid droplet accumulation in response to high exogenous fatty acids. We inhibited mitochondrial fission by silencing dynamin-related protein 1(DRP1) and observed the shift in fatty acid storage-usage balance. Inhibition of mitochondrial fission resulted in an increase in fatty acid content of lipid droplets and a decrease in mitochondrial fatty acid oxidation. Next, we overexpressed carnitine palmitoyltransferase-1 (CPT1), a key mitochondrial protein in fatty acid oxidation, to further examine the relationship between mitochondrial fatty acid usage and mitochondrial morphology. Mitochondrial fission plays a role in distributing exogenous fatty acids. CPT1A controlled the respiratory rate of mitochondrial fatty acid oxidation but did not cause a shift in the distribution of fatty acids between mitochondria and lipid droplets. Our data reveals a novel function for mitochondrial fission in balancing exogenous fatty acids between usage and storage, assigning a role for mitochondrial dynamics in control of intracellular fuel utilization and partitioning.
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Peters-Golden, M., and C. Shelly. "Inhibitory effect of exogenous arachidonic acid on alveolar macrophage 5-lipoxygenase metabolism. Role of ATP depletion." Journal of Immunology 140, no. 6 (March 15, 1988): 1958–66. http://dx.doi.org/10.4049/jimmunol.140.6.1958.
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Abstract Although a variety of agonists have the capacity to stimulate the release of endogenous arachidonic acid (AA) from macrophage lipids and its subsequent metabolism to both cyclooxygenase and 5-lipoxygenase eicosanoids, including leukotrienes (LT), previous work suggests that exogenously supplied arachidonate is metabolized preferentially to cyclooxygenase products and mono-hydroxyeicosatetranenoic acids rather than LT. We have compared the metabolism of endogenous and exogenous AA in cultured rat alveolar macrophages and have further examined the effect of exogenous fatty acids on eicosanoid synthesis stimulated by the calcium ionophore A23187 and the particulate agonist zymosan. As reported by others, exogenous AA was metabolized to large amounts of cyclooxygenase products, 12-hydroxyeicosatetraenoic acid and 15-hydroxyeicosatetraenoic acid, but far lesser amounts of all 5-lipoxygenase products. However, whereas exogenous AA augmented the synthesis of cyclooxygenase metabolites in both A23187- and zymosan-stimulated cells, it dose-dependently inhibited the synthesis of LT. Inasmuch as unsaturated fatty acids, including AA, uncouple oxidative phosphorylation, and because 5-lipoxygenase activity depends on ATP, we examined the possibility that ATP depletion was responsible for the inhibition of LT synthesis by exogenous AA. Arachidonate depleted cellular ATP in a dose-dependent fashion similar to its inhibition of LT synthesis. In addition, the other unsaturated fatty acids, linolenic and eicosatrienoic, but not the saturated fatty acids, palmitic or stearic, both depleted ATP and inhibited A23187-induced LT synthesis. These data suggest that the relative lack of synthesis of LT from exogenous AA is related to the ability of this unsaturated fatty acid to function as an inhibitor, as well as a substrate, of 5-lipoxygenase. Our results further suggest that this inhibition of 5-lipoxygenase may be mediated by ATP depletion.
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Desfougères, Thomas, Thierry Ferreira, Thierry Bergès, and Matthieu Régnacq. "SFH2 regulates fatty acid synthase activity in the yeast Saccharomyces cerevisiae and is critical to prevent saturated fatty acid accumulation in response to haem and oleic acid depletion." Biochemical Journal 409, no. 1 (December 11, 2007): 299–309. http://dx.doi.org/10.1042/bj20071028.
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The yeast Saccharomyces cerevisiae is a facultative anaerobic organism. Under anaerobiosis, sustained growth relies on the presence of exogenously supplied unsaturated fatty acids and ergosterol that yeast is unable to synthesize in the absence of oxygen or upon haem depletion. In the absence of exogenous supplementation with unsaturated fatty acid, a net accumulation of SFA (saturated fatty acid) is observed that induces significant modification of phospholipid profile [Ferreira, Régnacq, Alimardani, Moreau-Vauzelle and Bergès (2004) Biochem. J. 378, 899–908]. In the present paper, we focus on the role of SFH2/CSR1, a hypoxic gene related to SEC14 and its involvement in lipid metabolism upon haem depletion in the absence of oleic acid supplementation. We observed that inactivation of SFH2 results in enhanced accumulation of SFA and phospholipid metabolism alterations. It results in premature growth arrest and leads to an exacerbated sensitivity to exogenous SFA. This phenotype is suppressed in the presence of exogenous oleic acid, or by a controlled expression of FAS1, one of the two genes encoding FAS. We present several lines of evidence to suggest that Sfh2p and oleic acid regulate SFA synthase in yeast at different levels: whereas oleic acid acts on FAS2 at the transcriptional level, we show that Sfh2p inhibits fatty acid synthase activity in response to haem depletion.
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Yao, Jiangwei, and Charles O. Rock. "Exogenous fatty acid metabolism in bacteria." Biochimie 141 (October 2017): 30–39. http://dx.doi.org/10.1016/j.biochi.2017.06.015.
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Mahajan, Sandeep, and G. K. Khuller. "Cerulenin inhibition of lipid synthesis and its reversal by exogenous fatty acids in Mycobacterium smegmatis ATCC 607." Canadian Journal of Biochemistry and Cell Biology 63, no. 2 (February 1, 1985): 85–90. http://dx.doi.org/10.1139/o85-012.
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Cerulenin inhibited the lipid synthesis of Mycobacterium smegmatis ATCC 607 over the range of 0.5–1.8 μg/mL with complete inhibition at 1.8 μg/mL, as monitored by [14C]glycerol incorporation into lipids. Exogenous fatty acids failed to restore the lipid synthesis at 1.8 μg/mL; however, the addition of palmitic acid to the growth medium partially restored the lipid synthesis when cerulenin concentration was decreased to 1.6 μg/mL. Fatty acid analysis of cerulenin plus palmitic acid supplemented cultures revealed that exogenously supplied fatty acid was incorporated into cellular phospholipids. Further investigations with 1.6 μg/mL of cerulenin and [14C]acetate and [32P]orthophosphoric acid showed that cerulenin inhibited the synthesis of saturated plus unsaturated fatty acids and phospholipids. Pulse–chase studies with [14C]acetate revealed decreased synthesis and degradation of each of the phospholipid components.
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Saito, Holly E., John R. Harp, and Elizabeth M. Fozo. "Incorporation of Exogenous Fatty Acids Protects Enterococcus faecalis from Membrane-Damaging Agents." Applied and Environmental Microbiology 80, no. 20 (August 15, 2014): 6527–38. http://dx.doi.org/10.1128/aem.02044-14.
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ABSTRACTEnterococcus faecalisis a commensal bacterium of the mammalian intestine that can persist in soil and aquatic systems and can be a nosocomial pathogen to humans. It employs multiple stress adaptation strategies in order to survive such a wide range of environments. Within this study, we sought to elucidate whether membrane fatty acid composition changes are an important component for stress adaptation. We noted thatE. faecalisOG1RF was capable of changing its membrane composition depending upon growth phase and temperature. The organism also readily incorporated fatty acids from bile, serum, and medium supplemented with individual fatty acids, often dramatically changing the membrane composition such that a single fatty acid was predominant. Growth in either low levels of bile or specific individual fatty acids was found to protect the organism from membrane challenges such as high bile exposure. In particular, we observed that when grown in low levels of bile, serum, or the host-derived fatty acids oleic acid and linoleic acid,E. faecaliswas better able to survive the antibiotic daptomycin. Interestingly, the degree of membrane saturation did not appear to be important for protection from the stressors examined here; instead, it appears that a specific fatty acid or combination of fatty acids is critical for stress resistance.
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Gibbons, G. F., and F. J. Burnham. "Effect of nutritional state on the utilization of fatty acids for hepatitic triacylglycerol synthesis and secretion as very-low-density lipoprotein." Biochemical Journal 275, no. 1 (April 1, 1991): 87–92. http://dx.doi.org/10.1042/bj2750087.
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The mass of very-low-density-lipoproteins (VLDL) triacylglycerol secreted from isolated hepatocytes was dependent on the nutritional state of the donor rats, and declined in the order sucrose-fed greater than chow-fed greater than polyunsaturated-fat-fed greater than starved. This was the case irrespective of the presence or absence of exogenous oleate. The contribution of newly synthesized fatty acids to the total mass of VLDL triacylglycerol also declined in the above order, and reflected the relative rates of fatty acid synthesis de novo in each of the groups. The contribution of exogenous oleate to VLDL triacylglycerol varied in a manner similar to that for newly synthesized fatty acid. However, the contribution either of exogenous oleate or of newly synthesized fatty acid never exceeded 17-20% of the total VLDL triacylglycerol fatty acid even in the sucrose-fed animals. The increased contribution of newly synthesized fatty acids in the sucrose-fed group was not sufficient to account for the increase in the total mass of VLDL triacylglycerol secreted. These results suggest that: (a) changes in the rate of triacylglycerol secretion are not a direct consequence of variations in the rate of fatty acid synthesis de novo; (b) in the short term, most of the triacylglycerol required for VLDL assembly and secretion is derived from an intracellular storage source: (c) the distribution of newly synthesized triacylglycerol between the cytosolic and secretory pools was similar irrespective of the source of fatty acids (i.e. synthesized de novo or exogenous).
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Black, Paul N., and Concetta C. DiRusso. "Transmembrane Movement of Exogenous Long-Chain Fatty Acids: Proteins, Enzymes, and Vectorial Esterification." Microbiology and Molecular Biology Reviews 67, no. 3 (September 2003): 454–72. http://dx.doi.org/10.1128/mmbr.67.3.454-472.2003.
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SUMMARY The processes that govern the regulated transport of long-chain fatty acids across the plasma membrane are quite distinct compared to counterparts involved in the transport of hydrophilic solutes such as sugars and amino acids. These differences stem from the unique physical and chemical properties of long-chain fatty acids. To date, several distinct classes of proteins have been shown to participate in the transport of exogenous long-chain fatty acids across the membrane. More recent work is consistent with the hypothesis that in addition to the role played by proteins in this process, there is a diffusional component which must also be considered. Central to the development of this hypothesis are the appropriate experimental systems, which can be manipulated using the tools of molecular genetics. Escherichia coli and Saccharomyces cerevisiae are ideally suited as model systems to study this process in that both (i) exhibit saturable long-chain fatty acid transport at low ligand concentrations, (ii) have specific membrane-bound and membrane-associated proteins that are components of the transport apparatus, and (iii) can be easily manipulated using the tools of molecular genetics. In both systems, central players in the process of fatty acid transport are fatty acid transport proteins (FadL or Fat1p) and fatty acyl coenzyme A (CoA) synthetase (FACS; fatty acid CoA ligase [AMP forming] [EC 6.2.1.3]). FACS appears to function in concert with FadL (bacteria) or Fat1p (yeast) in the conversion of the free fatty acid to CoA thioesters concomitant with transport, thereby rendering this process unidirectional. This process of trapping transported fatty acids represents one fundamental mechanism operational in the transport of exogenous fatty acids.
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Yamasaki, Tomohiro, Lumin Zhang, Tyrone Dowdy, Adrian Lita, Kazuhiko Kurozumi, and Mioara Larion. "TMET-15. THE COMBINATIONAL EFFECT OF INHIBITOR FOR A FATTY ACID DESATURASE AND A FATTY ACID TRANSPORTER ON GLIOMA GROWTH." Neuro-Oncology 25, Supplement_5 (November 1, 2023): v275—v276. http://dx.doi.org/10.1093/neuonc/noad179.1059.
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Abstract BACKGROUND It is not well understood how much exogenous fatty acids uptake and de novo fatty acid synthesis affect the cell proliferation in glioma. In this study, we examined the combinational effect of inhibitor for a fatty acid desaturase (SCD) and a fatty acid transporter (CD36) on glioma growth. METHODS Normal human astrocytes (NHA) were used as glial cells, and U251 transfected with IDH wild-type or IDH mutant gene and patient-derived glioma cells (BT142, TS603, GSC923S) were used as glioma cells. The function of SCD was suppressed by SCD inhibitor and SCD siRNA, and Sulfo-N-succinimidyl oleate (SSO) was used to inhibit the CD36 function. RESULTS We treated U251 cells with palmitic acid (C16:0), stearic acid (C18:0), palmitoleic acid (C16:1) or oleic acid (C18:1) after SCD inhibitors treatment or SCD knockdown, and cell proliferation was rescued only after the treatment with C16:1 and C18:1. NHA was not affected by SCD inhibitor, although CD36 inhibitor suppressed cell proliferation of both U251 and NHA. The combination of SCD inhibitor and CD36 inhibitor under the addition of exogenous fatty acid, oleic acid, suppressed the proliferation of U251 cells more effectively than SCD inhibitor or CD36 inhibitor alone. Discussion: The SCD inhibitory effect on gliomas was attenuated by the presence of exogenous monounsaturated fatty acids, whereas the CD36 inhibitor enhanced the cell-killing effect. On the other hand, it should be noted that CD36 inhibitors affect the proliferation of glial cells.
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Puteri Afiqah Abdul Wahab and Aziz Ahmad. "Effects of Exogenous Arachidonic Acid on Morphological Traits and Fatty Acid Profile of Rice (Oryza sativa L.) Grown on Saline Soil." Universiti Malaysia Terengganu Journal of Undergraduate Research 1, no. 3 (July 31, 2019): 68–78. http://dx.doi.org/10.46754/umtjur.v1i3.80.
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Salinity is one of the major constraints in the rice production worldwide. Rice plants have moderate tolerance towards salinity. Salinity changes cell membrane permeability and fatty acid compositions by releasing the free fatty acids. Nonetheless, the effect of exogenous fatty acid such as arachidonic acid (AA) on rice grown on saline soil is yet unknown. The objective of the current study is to determine the effect of AA on the morphological traits and free fatty acids of rice plant grown under saline conditions. Rice plants grown on saline soil (EC=12 ds/m) were treated with 50 mM AA on day 45 after transplant. Leaves and panicles were sampled after two weeks of treatment and analysed for fatty acid profile using GC-MS. The morphological traits were observed at the maturity stage. Results showed that AA treatment improved the grain fill-in of the saline stress rice and reduced the accumulation of free fatty acids in the cell. The AA treatment also increased the linoleic acid (18:2), linolenic acid (18:3) in panicles and, dihomo-y-linolenic acid (20:3) and nervonic acid (24:1) in leaves. The finding suggests that exogenous AA regulates salinity stress in rice by reducing the accumulation of free fatty acids.
Dissertations / Theses on the topic "Exogenous fatty acid"
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Murota, Kaeko. "INHIBTION OF DIETARY FATTY ACID ABSORPTION BY EXOGENOUS FATTY ACID DERIVATIVES IN THE SMALI INTESTINE." Kyoto University, 2001. http://hdl.handle.net/2433/150341.
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Litton, Leanne Kay. "Effects of flaxseed supplementation and exogenous hormones on finishing performance, carcass characteristics, and plasma and longissimus muscle fatty acid profiles in finishing cattle." Thesis, Kansas State University, 2011. http://hdl.handle.net/2097/8757.
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Master of ScienceDepartment of Animal Sciences and Industry
James S. Drouillard
Christopher D. Reinhardt
The effects of supplementing forms of flaxseed on plasma and longissimus muscle (LM) fatty acid (FA) composition, finishing performance, and carcass characteristics were evaluated in five studies. In study 1, steers were fed diets with soy oil (SO), ground flaxseed (Flaxseed), or urea formaldehyde condensation polymer treated flaxseed (UFCP). In study 2, steers were fed diets with SO, linseed oil (LO), or a combination of flaxseed and field peas that was extruded (LinPro). Feeding flaxseed products increased (P < 0.01) α-linolenic acid (ALA), omega-3 FA, and decreased (P < 0.01) n-6:n-3 in LM compared to cattle fed SO. Feeding LinPro increased (P < 0.01) ALA, omega-3 FA, and decreased (P < 0.01) n-6:n-3 in LM compared to steers fed SO or LO. In studies 3 and 4, steers were fed diets with and without Flaxseed and implanted or not. Implanting improved (P ≤ 0.05) DMI, ADG, feed efficiency, HCW, and LM area compared to cattle not implanted. In study 4, cattle fed Flaxseed had increased (P < 0.01) ALA and omega-3 FA, and decreased (P < 0.01) n-6:n-3 in LM compared to cattle fed SO. In study 5, heifers were fed diets with 0% or 5% linseed meal, and administered with or without exogenous hormones (NHTC). Administering exogenous hormones improved (P ≤ 0.02) DMI, ADG, G:F, and HCW compared to NHTC cattle. Omega-3 FA increased in LM when cattle were supplemented with flaxseed products. Cattle fed LinPro achieved the highest levels of ALA and omega-3 FA. Flaxseed products did not interact with implants as a natural growth promoter in finishing cattle.
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Herdmann, Andrea [Verfasser], Gerhard [Akademischer Betreuer] Jahreis, Steffen [Akademischer Betreuer] Maak, and Nigel [Akademischer Betreuer] Scollan. "Exogenous effects of alpha-linolenic and linoleic acid on the fatty acid distribution and the regulation of lipid metabolism in ruminant tissues / Andrea Herdmann. Gutachter: Gerhard Jahreis ; Steffen Maak ; Nigel Scollan." Jena : Thüringer Universitäts- und Landesbibliothek Jena, 2012. http://d-nb.info/1025255917/34.
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Quilleré, Aurore. "Décrypter les mécanismes d'adaptation au froid de Listeria monocytogenes en présence de lipides insaturés alimentaires." Electronic Thesis or Diss., université Paris-Saclay, 2024. http://www.theses.fr/2024UPASB037.
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Les pathologies infectieuses d'origine alimentaire, en particulier les listérioses avec leur fort taux de létalité, demeurent un véritable problème de santé publique. Ubiquitaire et psychrotrophe, Listeria monocytogenes est fréquemment présente dans les environnements alimentaires (matières premières, chaîne de production), et peut contaminer de nombreuses denrées, telles que les produits prêt à consommer. Pour cette catégorie de produits, la réfrigération est la principale méthode permettant de maitriser la croissance du pathogène et de garantir la sécurité sanitaire du produit. Une étude préliminaire de l'équipe a montré que plusieurs souches de L. monocytogenes sont capables d'incorporer des acides gras exogènes dans leur membrane, ce qui provoque un changement dans leur capacité de croissance à basse température. En effet, les acides gras saturés (AGS) limitent la croissance, alors que les acides gras insaturés (AGI) la favorisent. La tendance actuelle visant à privilégier les AGI dans les aliments au détriment des AGS pour répondre à des recommandations nutritionnelles pourrait donc augmenter le risque de listériose des produits réfrigérés riches en lipides.Dans ce contexte, le but de ce travail était de mieux comprendre le comportement de L. monocytogenes à basse température dans des environnements riches en acides gras. Dans un premier temps, nous avons caractérisé, génotypiquement et phénotypiquement, la souche Lm208 qui présentait le taux de croissance le plus important à basse température en présence d'acide oléique dans l'étude préliminaire. Le génome a été séquencé, annoté, et enrichi. Nous avons ensuite complété l'étude phénotypique en évaluant la réponse de L. monocytogenes à différents acides gras en fonction de leur structure (longueur de chaîne, insaturations). Les AGI induisant, après incorporation, une température de fusion des phospholipides membranaires comprise entre 18 et 23°C (AGI à 18 carbones) permettent la plus importante augmentation de croissance de Lm208 à basse température.Dans un deuxième temps, nous avons mené des études transcriptomiques non ciblée et ciblée pour mettre en évidence l'expression de gènes en relation avec le phénotype étudié. L'analyse RNA seq globale sur quatre conditions (croissance avec ou sans supplémentation en acide oléique à 5°C et 37°C) a permis de sélectionner les gènes impliqués dans ce phénomène de surcroissance. Une analyse par RT qPCR a ensuite été conduite sur les gènes ciblés en élargissant le panel des conditions de culture testées. Parmi les gènes d'intérêt, fabK impliqué dans la voie de biosynthèse des acides gras, cheY et flaA impliqués dans la mobilité et l'assemblage des flagelles sont respectivement sur exprimés ou sous exprimés en présence d'AGI ou AGS. L'expression différentielle de fabK pourrait avoir un lien avec la régulation de la voie de biosynthèse des AGI versus AGS. La présence de flagelles très longs et nombreux en présence d'AGI à basse température a été confirmée par microscopie électronique à transmission. Ce phénotype remarquable pourrait avoir des conséquences sur la capacité de L. monocytogenes à former des biofilms et à persister dans les environnements de production.En conclusion, ce travail a confirmé l'effet promoteur de croissance de nombreux AGI sur L. monocytogenes à basse température, et a mis en évidence un phénotype associé correspondant à la synthèse de flagelles longs et nombreux, ce qui peut avoir d'importantes conséquences en termes de sécurité sanitaire des aliments riches en lipides et des environnements de production associésFood-borne infectious diseases, especially listeriosis with its high case fatality rate, remain a real public health problem. Being ubiquitous and psychrotrophic, Listeria monocytogenes is frequently found in food environments (raw materials, production chain), and can contaminate numerous foodstuffs, such as ready to eat products (RTE). For RTE products, refrigeration is the main method for controlling pathogen growth and guaranteeing product food safety. A previous study performed in our laboratory showed that several strains of L. monocytogenes can incorporate exogenous fatty acids into their membranes, modifying their ability to grow at low temperature. Saturated fatty acids (SFA) limit growth, while unsaturated fatty acids (UFA) promote it. This ability could question new trends in reformulating food with unsaturated fatty acids to fit with nutritional claims that could increase the risk of listeriosis in lipid-rich refrigerated products.In this context, this work aimed at understanding the behavior of L. monocytogenes at low temperatures in fatty acid rich environments. First, we characterized, genotypically and phenotypically, Lm208, the strain that has shown the highest growth rate at low temperatures in the presence of oleic acid in the preliminary study. The genome was sequenced, annotated, and enriched. We then completed the phenotypic characterization by evaluating the behavior of L. monocytogenes in the presence of different FAs according to their structure (chain length, unsaturation). UFAs inducing, after incorporation, a membrane phospholipid melting temperature between 18 and 23°C (18 carbon UFA) enabled the greatest increase in Lm208 growth at low temperature.Secondly, we performed non targeted and targeted transcriptomic studies to study the gene expression related to the observed phenotype. Global RNA seq analysis over four conditions (growth with or without oleic acid supplementation at 5°C and 37°C) enabled us to select the genes involved in this overgrowth phenomenon. RT qPCR analysis was then carried out on the targeted genes, enlarging the range of culture conditions tested. Among the genes of interest, fabK, involved in the fatty acid biosynthesis pathway, and cheY and flaA, involved in flagellar mobility and assembly, were respectively over and under expressed in the presence of UFA or SFA. The differential expression of fabK could be linked to the regulation of the UFA versus SFA biosynthetic pathway. The presence of very long and numerous flagella in the presence of UFA at low temperatures was observed by transmission electron microscopy. This remarkable phenotype could be involved in the ability of L. monocytogenes to form biofilms and persist in production environments
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Oben, J. E. "The effects of exogenous fatty acids on rat mammary gland lipogenesis." Thesis, University of Reading, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.234451.
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Larsson, Mikael. "Endogenous and exogenous factors affecting lipoprotein lipase activity." Doctoral thesis, Umeå universitet, Fysiologisk kemi, 2014. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-91662.
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Individuals with high levels of plasma triglycerides are at high risk to develop cardiovascular disease (CVD), currently one of the major causes of death worldwide. Recent epidemiological studies show that loss-of-function mutations in the APOC3 gene lower plasma triglyceride levels and reduce the incidence of coronary artery disease. The APOC3 gene encodes for apolipoprotein (APO) C3, known as an inhibitor of lipoprotein lipase (LPL) activity. Similarly, a common gain-of-function mutation in the LPL gene is associated with reduced risk for CVD. LPL is central for the metabolism of lipids in blood. The enzyme acts at the endothelial surface of the capillary bed where it hydrolyzes triglycerides in circulating triglyceride-rich lipoproteins (TRLs) and thereby allows uptake of fatty acids in adjacent tissues. LPL activity has to be rapidly modulated to adapt to the metabolic demands of different tissues. The current view is that LPL is constitutively expressed and that the rapid modulation of the enzymatic activity occurs by some different controller proteins. Angiopoietin-like protein 4 (ANGPTL4) is one of the main candidates for control of LPL activity. ANGPTL4 causes irreversible inactivation through dissociation of the active LPL dimer to inactive monomers. Other proteins that have effects on LPL activity are the APOCs which are surface components of the substrate TRLs. APOC2 is a well-known LPL co-factor, whereas APOC1 and APOC3 independently inhibit LPL activity. Given the important role of LPL for triglyceride homeostasis in blood, the aim of this thesis was to find small molecules that could increase LPL activity and serve as lead compounds in future drug discovery efforts. Another aim was to investigate the molecular mechanisms for how APOC1 and APOC3 inhibit LPL activity. Using a small molecule screening library we have identified small molecules that can protect LPL from inactivation by ANGPTL4 during incubations in vitro. Following a structure-activity relationship study we have synthesized lead compounds that more efficiently protect LPL from inactivation by ANGPTL4 in vitro and also have dramatic triglyceride-lowering properties in vivo. In a separate study we show that low concentrations of fatty acids possess the ability to prevent inactivation of LPL by ANGPTL4 under in vitro conditions. With regard to APOC1 and APOC3 we demonstrate that when bound to TRLs, these apolipoproteins prevent binding of LPL to the lipid/water interface. This results in decreased lipolysis and in an increased susceptibility of LPL to inactivation by ANGPTL4. We demonstrate that hydrophobic amino acid residues that are centrally located in the APOC3 molecule are critical for attachment of this protein to lipid emulsion particles and consequently for inhibition of LPL activity. In summary, this work has identified a lead compound that protects LPL from inactivation by ANGPTL4 in vitro and lowers triglycerides in vivo. In addition, we propose a molecular mechanism for inhibition of LPL activity by APOC1 and APOC3.
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Grandmaison, Paul Andrew. "The role of exogenous fatty acids and endogenous lipid in the synthesis and secretion of apolipoprotein B¦1¦0¦0-containing lipoproteins in the Hep G2 cell line." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp02/NQ49264.pdf.
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Mock, Thomas. "The role of exogenous free fatty acids in phosphatidylcholine and phosphatidylethanolamine biosynthesis in isolated hamster heart : incorporation and regulation." 1985. http://hdl.handle.net/1993/24401.
Full textBook chapters on the topic "Exogenous fatty acid"
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Mazière, Cécile, Jean-Claude Mazière, Liliana Mora, Martine Auclair, and Jacques Polonovski. "Hormonal Regulation of Exogenous Fatty-Acid Incorporation into Lipids in Cultured Hamster Fibroblasts." In Enzymes of Lipid Metabolism II, 467–71. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4684-5212-9_60.
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Grenier, Gilles, Alain Muanamputu Zimafuala, and Jean-Pierre Marier. "Effects of Exogenous Free Oleic Acid on Membrane Fatty Acid Composition and Physiology of Lemna Minor Fronds." In Physiology, Biochemistry and Molecular Biology of Plant Lipids, 163–65. Dordrecht: Springer Netherlands, 1997. http://dx.doi.org/10.1007/978-94-017-2662-7_52.
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Roughan, P. G., and G. A. Thompson. "Metabolism of Exogenous Fatty Acids by Leaves: Positional Specifications." In Biological Role of Plant Lipids, 119–22. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4684-1303-8_29.
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Nyarumenteng Adhipurnawan Winarno, Gatot. "Fatty Acid Metabolism as a Tumor Marker." In Fatty Acids - Recent Advances [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.106072.
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Cancer cells tend to make metabolism changes in the human body for their growth and survival. One of the most interesting changes is the alteration of fatty acid metabolism in order for the high rate of fatty acid synthesis required to increase the level of fatty acids needed for cancer cell proliferation. Thus, the reprogramming of fatty acid metabolism is needed for cancer cell survival. Fatty acid metabolic reprogramming is one of the hallmarks of the cancer condition since it can affect cellular functions. The reprogramming of fatty acid synthesis includes increased exogenous fatty acid uptake, de novo fatty acid synthesis, and oxidation of fatty acids. Identifying biochemical targets in fatty acid metabolism is useful for diagnosing and predicting the therapeutic efficiency in tumor treatment.
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Bagg, Jeremy, T. Wallace MacFarlane, Ian R. Poxton, and Andrew J. Smith. "Infections of the skin and soft tissues." In Essentials of microbiology for dental students, 136–46. Oxford University PressOxford, 2005. http://dx.doi.org/10.1093/oso/9780198564898.003.0013.
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Abstract The skin provides an excellent defence for the underlying tissues against invading, pathogenic micro-organisms (Chapter 8). The structural elements of normal skin that are important in this protection include its acid pH, the limited amount of moisture present and excreted chemicals such as sebum, fatty acids and urea. In addition, the skin is colonized by a large number of bacterial species, which comprise the resident normal flora. This resident flora includes coagulase negative staphylococci, micrococci and diphtheroids and plays an important defence role through prevention of colonization by exogenous pathogens.
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Ibrahim, Majid. "Role of Endogenous and Exogenous Hormones in Bioactive Compounds Production in Medicinal Plants Via In Vitro Culture Technique." In Plant Hormones - Recent Advances, New Perspectives and Applications [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.102814.
Full textAbstract:
The natural compounds produced in plants are classified into two major groups (Primary and secondary metabolic compounds). These compounds are the precursor materials for thecompounds of the second group, which are represented by secondary metabolites, most of which produce from three main compounds: shikimic acid, acetate, and fatty acids. Primary metabolites are the basic units in the metabolism of secondary compounds. Tissue cultures of plants are used to produce large quantities of secondary metabolic products, although cultures of callus and cell suspensions often do not produce higher levels of the whole plant. Therefore, some technologies were used to increase the production of secondary metabolites by plant tissue culture techniques through the selection of high-production cells. The growth of plant cells in tissue cultures occurs when the requirements for division and growth are available for them from nutrients, growth regulators, and any other additives that all affect the metabolic activities within the cells. To achieve optimal productivity of secondary metabolites, it is preferable to produce cells in a medium that is optimal for increasing biomass. Plant growth regulators such as auxins and cytokinins affect cell division, various metabolic processes, and plant growth in tissue cultures.
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Clark, Gregory O., and William J. Kovacs. "Glucose, Lipid, and Protein Metabolism." In Textbook of Endocrine Physiology. Oxford University Press, 2011. http://dx.doi.org/10.1093/oso/9780199744121.003.0018.
Full textAbstract:
The maintenance of life requires a constant supply of substrate for the generation of energy and preservation of the structure of cells and tissues. The process in principle is simple, yet the individual metabolic pathways and the regulation of substrate fluxes through these pathways can be complex. Energy is derived when fuel substrates are oxidized to carbon dioxide and water in the presence of oxygen, generating adenosine triphosphate (ATP). A portion of the ingested foodstuff is also utilized, either directly or after transformation into other substrates, to repair and replace cell membranes, structural proteins, and organelles. The remainder is stored as potential energy in the form of glycogen or fat. Under normal circumstances, each individual remains in a near-steady state where weight and appearance are stable over prolonged periods. In the short term, fuel metabolism changes dramatically several times a day during alternating periods of feeding and fasting. An anabolic phase begins with food ingestion and lasts for several hours. Energy storage occurs during this period when caloric intake exceeds caloric demands. The catabolic phase usually begins 4 to 6 hours after a meal and lasts until the person eats once again. During this phase, utilization shifts from exogenous to endogenous fuels, a change heralded by the mobilization of substrate stored in liver, muscle, and adipose tissue. Both anabolic and catabolic phases are characterized by specific biochemical processes regulated by distinct hormonal profiles. In the anabolic phase that follows ingestion of a mixed meal, substrate flux is directed from the intestine through the liver to storage and utilization sites. Glucose, triglyceride, and amino acid concentrations increase in plasma, whereas those of fatty acids, ketones (acetoacetic and β -hydroxy-butyric acids), and glycerol decrease. Both glycogen and protein synthesis begin in liver and muscle, while fatty acid synthesis and triglyceride esterification are stimulated in hepatocytes and adipose tissue. In the catabolic phase, the biochemical activities are reversed and the flux of fuel is directed from storage depots to liver and other utilization sites.
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Heidari, Reza, and M. Mehdi Ommati. "Taurine and the Liver: A Focus on Mitochondria related Liver Disease." In Taurine and the Mitochondrion: Applications in the Pharmacotherapy of Human Diseases, 108–36. BENTHAM SCIENCE PUBLISHERS, 2023. http://dx.doi.org/10.2174/9789815124484123010007.
Full textAbstract:
Although the liver is the leading site for taurine (TAU) synthesis, the level of this amino acid in hepatic tissue is relatively low. It is well-known that TAU is efficiently redistributed from hepatocytes to the circulation. However, the human body’s capacity for TAU synthesis is negligible, and we receive a very high percentage of our body TAU from exogenous sources. Plasma TAU is taken up by several tissues, such as the skeletal muscle and the heart. The roles of TAU in liver function are the subject of many investigations. It has been found that TAU could have beneficial effects against xenobiotics-induced liver injury, alcoholism-associated hepatic damage, non-alcoholic fatty liver disease (NAFLD), non-alcoholic steatohepatitis (NASH), or even viral hepatitis infections. The inhibition of cytochrome P450, alleviation of oxidative stress, inhibition of inflammatory reactions, and the mitigation of tissue fibrosis are fundamental mechanisms proposed for the hepatoprotective properties of TAU. On the other hand, many studies indicate that hepatocytes’ mitochondria are essential targets for the cytoprotective properties of TAU. The current chapter reviews the beneficial role of TAU on the most common liver disorders, focusing on the effects of this amino acid on mitochondrial function and energy metabolism.<br>
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Auchus, Richard J., and Keith L. Parker. "The Adrenal Glands." In Textbook of Endocrine Physiology. Oxford University Press, 2011. http://dx.doi.org/10.1093/oso/9780199744121.003.0016.
Full textAbstract:
The basic function of the adrenal glands is to protect the organism against acute and chronic stress, a concept popularized as the fight-or-flight response for the medulla and as the alarm reaction for the cortex. The steroid hormones of the cortex and the catecholamines of the medulla probably developed as protection against immediate stress or injury and more prolonged deprivation of food and water. In acute stress, catecholamines mobilize glucose and fatty acids for energy and prepare the heart, lungs, and muscles for action, while glucocorticoids protect against overreactions from the body’s responses to stress. In the more chronic stress of food and fluid deprivation, adrenocortical steroid hormones stimulate gluconeogenesis to maintain the supply of glucose and increase sodium reabsorption to maintain body fluid volume. Based on the widespread effects of its secreted products in multiple tissues, adrenal dysfunction is associated with protean manifestations. Diseases associated with adrenocortical hypofunction are relatively rare, while those associated with adrenocortical hyperfunction are slightly more common. However, both of these conditions are life threatening if untreated, and a high index of suspicion must therefore be maintained. Subtle increases in cortisol secretion or tissue sensitivity to glucocorticoids may be involved in many of the devastating effects of chronic stress, including visceral obesity, hypertension, diabetes mellitus, dyslipidemia, infertility, and depression. Moreover, exogenous glucocorticoids are widely used to treat numerous diseases and, when used in supraphysiological doses, can induce all of the manifestations of glucocorticoid excess. Perhaps because the adrenal medulla accounts for only 10 % of total sympathetic nervous activation, we can live quite well without it, and syndromes due to hypofunction are not clinically significant. However, conditions of excess catecholamine output due to tumors called pheochromocytomas are a rare but potentially life-threatening cause of secondary hypertension.
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Caputo, Emilia, Carlos Alberto Meinardi, and Luigi Mandrich. "CHEESE MAKING: NEW PERSPECTIVE IN LIPOLYSIS AND INFLUENCE OF EXOGENOUS ENZYMES IN FATTY ACIDS AND VOLATILE COMPOUND PROFILE OF SEMI HARD CHEESES." In Avanços em Ciência e Tecnologia de Alimentos - Volume 3, 606–23. Editora Científica Digital, 2021. http://dx.doi.org/10.37885/210303470.
Full textConference papers on the topic "Exogenous fatty acid"
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Purdon, A. D., and J. B. Smith. "RELEASE AND TRANSACYLATION OF ARACHIDONATE FROM A COMMON POOL OF 1-ACYL-2-ARACHIDONOYL GLYCEROPHOSPHOCHOLINE IN HUMAN PLATELETS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643391.
Full textAbstract:
We have previously shown that the main source of arachidonate in thrombin-stimulated human platelets is 1-acyl-2-arachidonoyl (AA) glycerophosphocholine (GPC) and release of 3H-AA from this phospholipid also was correlated with increased 3H-AA in ether phospholipid. This ATP independent transfer of 3H-AA from 1,2 diacyl GPC to ether phospholipid (transacylation) also occurs in resting cells. Human platelets in 1/10 volume of plasma (ACD anticoagulant, pH 6.5) were radiolabelled with 3H-AA for 60 min at 37°C and then exogenous 3H-AA was removed by gel filtration into Tyrode's buffer, pH 7.4, 0.2% albumin. These radiolabelled cells were incubated in the absence of exogenous 3H-AA for four hours followed by Bligh and Dyer extraction and thin layer chromatography purification of phospholipids. 3H-AA in 1,2 diacyl GPC was found to decrease by over 20% and increase substantially in 1-0-alkyl-2-acyl GPC and 1-0-alk-1'-enyl-2-acyl glycerophospho ethanolamine (GPE), In this same time interval the mass of AA released by thrombin (5 U/ml, 10 min, 37°C, no stirring)in the presence of BIT 775C and measured by GLC, stayed the same (30 nmoles/109 cells), however, the specific activity decreased. Using reverse phase HPLC to resolve diradylglycerobenzoate derivatives of phospholipids: acylation, deacylation, and transacylation were observed for individual AA-containing molecular species of phospholipid, including those with an unsaturated fatty acid at sn-1. In particular the radiolabellinq of the 1-unsaturate-2-arachidonoyl GPC correlated with the specific activity of the 3H-AA released by stimulation with thrombin. Furthermore, 1-arachidonoyl-2-3H-arachidonoyl GPC was completely deacylated while 50 % of its mass remained. This contrasted with 16:0, and 18:0-2-arachidonoyl GPC in which the specific activity remained the same before and after deacylation. We conclude that deacylation of AA-containing molecular species of 1,2 diacyl GPC in stimulated cells includes molecular species which are also a source of arachidonic acid for transacylation reactions.
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Radošević, Draginja, Kristina Stevanović, Vladimir Perović, and Sanja Glišić. "Coumarins as promising PPARα agonists. Novel in silico insights." In 2nd International Conference on Chemo and Bioinformatics. Institute for Information Technologies, University of Kragujevac, 2023. http://dx.doi.org/10.46793/iccbi23.597r.
Full textAbstract:
The occurrence of metabolic syndrome, which includes several chronic severe diseases such as cardiovascular disease, dyslipidemia, hypertension, stroke, and type 2 diabetes mellitus, is becoming a serious public health concern on a global scale. Peroxisome proliferator-activated receptor alpha (PPARα) is a ligand-activated transcription factor that are members of the nuclear hormone receptor superfamily. PPARα plays a crucial function in regulating the expression of genes involved in fatty acid beta-oxidation and glucose homeostasis, making it a potential drug target for treating metabolic syndrome. In experimental models, several coumarins, such as graphene, ostiole, and interruption B, have been found to activate PPARα. In this study, we focus our attention on exogenous natural ligands known as coumarins. Using in silico screening, we searched for the most promising coumarin candidates from the Chemical Synthesis Database. Using a combination of ligand-based virtual screening and molecular docking, we identified (E)-3-[(2-oxo-chromen-3-yl)-methyleneamino]-acrylaldehyde as the most favorable candidate PPARα agonist and proposed it for subsequent experimental testing.
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Kockmann, V., E. Véricel, M. Croset, and M. Lagarde. "IN VITRO AND IN VIVO EFFECT OF VITAMIN E ON NORMAL HUMAN PLATELETS. AGGREGATION AND ARACHIDONIC ACID (AA) METABOLISM." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644624.
Full textAbstract:
Oxygenated metabolism of AA through cyclooxygenase and lipoxygenase pathways involves peroxide species and vitamin E has been extensively studied as an agent that could reduce this lipid peroxidation. In the present study, effects of vitamin E has been investigated upon AA metabolism in normal human platelets with both in vivo and in vitro approaches. Using low doses of vitamin E either in vivo or in vitro, we have succeeded to almost double plasma and platelet a-tocopherol (determinated by HPLC). Despite such an enrichment platelet aggregation induced by agents involved in the AA cascade (collagen, arachidonate and U46619) was not affected. Similarly, the oxygenation of exogenous AA determined by HHT, HETE and TxB2 production was not modified. When the oxygenated products were measured after thrombin stimulation, some variations could be noted, although rarely significant. The tendency was a decrease after in vitro enrichment and an increase when enrichment occured in vivo. Basal oxygenated metabolism of AA in vivo was assessed by measuring 6-Keto-PGFla, 2,3-dinor-6-Keto-PGFla, TxB2 and 2,3-dinor-TxB2 in urine. All of them tended to increase after vitamin E intake, although not significantly. The oxygenation of eicosapentaenoic acid, which is markedly potentiated by AA through its hydroperoxide, 12 HPETE, was not altered after vitamin E treatment, confirming that vitamin E does not alter the specific peroxidation of polyunsaturated fatty acids in normal platelets. We conclude that vitamin E supplement does not affect the AA dependent aggregation neither the oxygenated metabolism of AA in normal human platelets. This does not exclude that it might be however useful in platelets that exhibit a relative deficiency in this vitamin (e.g. diabetes and aging) where it could slow down both AA peroxidation and aggregation.
Reports on the topic "Exogenous fatty acid"
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Meidan, Rina, and Robert Milvae. Regulation of Bovine Corpus Luteum Function. United States Department of Agriculture, March 1995. http://dx.doi.org/10.32747/1995.7604935.bard.
Full textAbstract:
The main goal of this research plan was to elucidate regulatory mechanisms controlling the development, function of the bovine corpus luteum (CL). The CL contains two different sterodigenic cell types and therefore it was necessary to obtain pure cell population. A system was developed in which granulosa and theca interna cells, isolated from a preovulatory follicle, acquired characteristics typical of large (LL) and small (SL) luteal cells, respectively, as judged by several biochemical and morphological criteria. Experiments were conducted to determine the effects of granulosa cells removal on subsequent CL function, the results obtained support the concept that granulosa cells make a substaintial contribution to the output of progesterone by the cyclic CL but may have a limited role in determining the functional lifespan of the CL. This experimental model was also used to better understand the contribution of follicular granulosa cells to subsequent luteal SCC mRNA expression. The mitochondrial cytochrome side-chain cleavage enzyme (SCC), which converts cholesterol to pregnenolone, is the first and rate-limiting enzyme of the steroidogenic pathway. Experiments were conducted to characterize the gene expression of P450scc in bovine CL. Levels of P450scc mRNA were higher during mid-luteal phase than in either the early or late luteal phases. PGF 2a injection decreased luteal P450scc mRNA in a time-dependent manner; levels were significantly reduced by 2h after treatment. CLs obtained from heifers on day 8 of the estrous cycle which had granulosa cells removed had a 45% reduction in the levels of mRNA for SCC enzymes as well as a 78% reduction in the numbers of LL cells. To characterize SCC expression in each steroidogenic cell type we utilized pure cell populations. Upon luteinization, LL expressed 2-3 fold higher amounts of both SCC enzymes mRNAs than SL. Moreover, eight days after stimulant removal, LL retained their P4 production capacity, expressed P450scc mRNA and contained this protein. In our attempts to establish the in vitro luteinization model, we had to select the prevulatory and pre-gonadotropin surge follicles. The ratio of estradiol:P4 which is often used was unreliable since P4 levels are high in atretic follicles and also in preovulatory post-gonadotropin follicles. We have therefore examined whether oxytocin (OT) levels in follicular fluids could enhance our ability to correctly and easily define follicular status. Based on E2 and OT concentrations in follicular fluids we could more accurately identify follicles that are preovulatory and post gonadotropin surge. Next we studied OT biosynthesis in granulosa cells, cells which were incubated with forskolin contained stores of the precursor indicating that forskolin (which mimics gonadotropin action) is an effective stimulator of OT biosynthesis and release. While studying in vitro luteinization, we noticed that IGF-I induced effects were not identical to those induced by insulin despite the fact that megadoses of insulin were used. This was the first indication that the cells may secrete IGF binding protein(s) which regonize IGFs and not insulin. In a detailed study involving several techniques, we characterized the species of IGF binding proteins secreted by luteal cells. The effects of exogenous polyunsaturated fatty acids and arachidonic acid on the production of P4 and prostanoids by dispersed bovine luteal cells was examined. The addition of eicosapentaenoic acid and arachidonic acid resulted in a dose-dependent reduction in basal and LH-stimulated biosynthesis of P4 and PGI2 and an increase in production of PGF 2a and 5-HETE production. Indomethacin, an inhibitor of arachidonic acid metabolism via the production of 5-HETE was unaffected. Results of these experiments suggest that the inhibitory effect of arachidonic acid on the biosynthesis of luteal P4 is due to either a direct action of arachidonic acid, or its conversion to 5-HETE via the lipoxgenase pathway of metabolism. The detailed and important information gained by the two labs elucidated the mode of action of factors crucially important to the function of the bovine CL. The data indicate that follicular granulosa cells make a major contribution to numbers of large luteal cells, OT and basal P4 production, as well as the content of cytochrome P450 scc. Granulosa-derived large luteal cells have distinct features: when luteinized, the cell no longer possesses LH receptors, its cAMP response is diminished yet P4 synthesis is sustained. This may imply that maintenance of P4 (even in the absence of a Luteotropic signal) during critical periods such as pregnancy recognition, is dependent on the proper luteinization and function of the large luteal cell.