Relevant bibliographies by topics / Fatty acid metabolism

Academic literature on the topic 'Fatty acid metabolism'

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Published: 4 June 2021
Last updated: 6 July 2024

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Journal articles on the topic "Fatty acid metabolism"

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Harwood, J. L. "Fatty Acid Metabolism." Annual Review of Plant Physiology and Plant Molecular Biology 39, no. 1 (June 1988): 101–38. http://dx.doi.org/10.1146/annurev.pp.39.060188.000533.

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de las Fuentes, Lisa, Pilar Herrero, Linda R. Peterson, Daniel P. Kelly, Robert J. Gropler, and Víctor G. Dávila-Román. "Myocardial Fatty Acid Metabolism." Hypertension 41, no. 1 (January 2003): 83–87. http://dx.doi.org/10.1161/01.hyp.0000047668.48494.39.

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SPIECKERMANN, P., J. HUTTER, and C. ALVES. "Myocardial fatty acid metabolism." Journal of Molecular and Cellular Cardiology 18 (1986): 68. http://dx.doi.org/10.1016/s0022-2828(86)80233-4.

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Yamamoto, Tsunehisa, and Motoaki Sano. "Deranged Myocardial Fatty Acid Metabolism in Heart Failure." International Journal of Molecular Sciences 23, no. 2 (January 17, 2022): 996. http://dx.doi.org/10.3390/ijms23020996.

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The heart requires fatty acids to maintain its activity. Various mechanisms regulate myocardial fatty acid metabolism, such as energy production using fatty acids as fuel, for which it is known that coordinated control of fatty acid uptake, β-oxidation, and mitochondrial oxidative phosphorylation steps are important for efficient adenosine triphosphate (ATP) production without unwanted side effects. The fatty acids taken up by cardiomyocytes are not only used as substrates for energy production but also for the synthesis of triglycerides and the replacement reaction of fatty acid chains in cell membrane phospholipids. Alterations in fatty acid metabolism affect the structure and function of the heart. Recently, breakthrough studies have focused on the key transcription factors that regulate fatty acid metabolism in cardiomyocytes and the signaling systems that modify their functions. In this article, we reviewed the latest research on the role of fatty acid metabolism in the pathogenesis of heart failure and provide an outlook on future challenges.
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Lopaschuk, Gary D., John R. Ussher, Clifford D. L. Folmes, Jagdip S. Jaswal, and William C. Stanley. "Myocardial Fatty Acid Metabolism in Health and Disease." Physiological Reviews 90, no. 1 (January 2010): 207–58. http://dx.doi.org/10.1152/physrev.00015.2009.

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There is a constant high demand for energy to sustain the continuous contractile activity of the heart, which is met primarily by the β-oxidation of long-chain fatty acids. The control of fatty acid β-oxidation is complex and is aimed at ensuring that the supply and oxidation of the fatty acids is sufficient to meet the energy demands of the heart. The metabolism of fatty acids via β-oxidation is not regulated in isolation; rather, it occurs in response to alterations in contractile work, the presence of competing substrates (i.e., glucose, lactate, ketones, amino acids), changes in hormonal milieu, and limitations in oxygen supply. Alterations in fatty acid metabolism can contribute to cardiac pathology. For instance, the excessive uptake and β-oxidation of fatty acids in obesity and diabetes can compromise cardiac function. Furthermore, alterations in fatty acid β-oxidation both during and after ischemia and in the failing heart can also contribute to cardiac pathology. This paper reviews the regulation of myocardial fatty acid β-oxidation and how alterations in fatty acid β-oxidation can contribute to heart disease. The implications of inhibiting fatty acid β-oxidation as a potential novel therapeutic approach for the treatment of various forms of heart disease are also discussed.
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Koundouros, Nikos, and George Poulogiannis. "Reprogramming of fatty acid metabolism in cancer." British Journal of Cancer 122, no. 1 (December 10, 2019): 4–22. http://dx.doi.org/10.1038/s41416-019-0650-z.

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AbstractA common feature of cancer cells is their ability to rewire their metabolism to sustain the production of ATP and macromolecules needed for cell growth, division and survival. In particular, the importance of altered fatty acid metabolism in cancer has received renewed interest as, aside their principal role as structural components of the membrane matrix, they are important secondary messengers, and can also serve as fuel sources for energy production. In this review, we will examine the mechanisms through which cancer cells rewire their fatty acid metabolism with a focus on four main areas of research. (1) The role of de novo synthesis and exogenous uptake in the cellular pool of fatty acids. (2) The mechanisms through which molecular heterogeneity and oncogenic signal transduction pathways, such as PI3K–AKT–mTOR signalling, regulate fatty acid metabolism. (3) The role of fatty acids as essential mediators of cancer progression and metastasis, through remodelling of the tumour microenvironment. (4) Therapeutic strategies and considerations for successfully targeting fatty acid metabolism in cancer. Further research focusing on the complex interplay between oncogenic signalling and dysregulated fatty acid metabolism holds great promise to uncover novel metabolic vulnerabilities and improve the efficacy of targeted therapies.
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Strandberg, Ursula, Jussi Vesterinen, Timo Ilo, Jarkko Akkanen, Miina Melanen, and Paula Kankaala. "Fatty acid metabolism and modifications in Chironomus riparius." Philosophical Transactions of the Royal Society B: Biological Sciences 375, no. 1804 (June 15, 2020): 20190643. http://dx.doi.org/10.1098/rstb.2019.0643.

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A priori knowledge of fatty acid modifications in consumers is essential for studies using fatty acids as biomarkers. We investigated fatty acid metabolism and possible modification pathways in benthic invertebrate Chironomus riparius larvae (Diptera). We conducted diet manipulation experiments using natural food sources (two chlorophyte algae, a diatom and a non-toxic cyanobacterium). We also did a diet-switch experiment on two different resources, fish food flakes TetraMin ® and cyanobacterium Spirulina , to study fatty acid turnover in Chironomus . Results of the diet manipulation experiments indicate that Chironomus larvae have a strong tendency to biosynthesize 20:5n-3 and 20:4n-6 from precursor fatty acids, and that the dietary availability of polyunsaturated fatty acids (PUFA) does not control larval growth. Fatty acid modifications explain why low dietary availability of PUFA did not significantly limit growth. This has ecologically relevant implications on the role of benthic chironomids in conveying energy to upper trophic level consumers. A diet-switch experiment showed that the turnover rate of fatty acids in Chironomus is relatively fast––a few days. The compositional differences of algal diets were large enough to separate Chironomus larvae into distinct groups even if significant modification of PUFA was observed. In summary, fatty acids are excellent dietary biomarkers for Chironomus , if modifications of PUFA are considered, and will provide high-resolution data on resource use. This article is part of the theme issue ‘The next horizons for lipids as ‘trophic biomarkers': evidence and significance of consumer modification of dietary fatty acids'.
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Yoon, Hyunho, and Sanghoon Lee. "Fatty Acid Metabolism in Ovarian Cancer: Therapeutic Implications." International Journal of Molecular Sciences 23, no. 4 (February 16, 2022): 2170. http://dx.doi.org/10.3390/ijms23042170.

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Ovarian cancer is the most malignant gynecological tumor. Previous studies have reported that metabolic alterations resulting from deregulated lipid metabolism promote ovarian cancer aggressiveness. Lipid metabolism involves the oxidation of fatty acids, which leads to energy generation or new lipid metabolite synthesis. The upregulation of fatty acid synthesis and related signaling promote tumor cell proliferation and migration, and, consequently, lead to poor prognosis. Fatty acid-mediated lipid metabolism in the tumor microenvironment (TME) modulates tumor cell immunity by regulating immune cells, including T cells, B cells, macrophages, and natural killer cells, which play essential roles in ovarian cancer cell survival. Here, the types and sources of fatty acids and their interactions with the TME of ovarian cancer have been reviewed. Additionally, this review focuses on the role of fatty acid metabolism in tumor immunity and suggests that fatty acid and related lipid metabolic pathways are potential therapeutic targets for ovarian cancer.
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Xu, Huan, Yanbo Chen, Meng Gu, Chong Liu, Qi Chen, Ming Zhan, and Zhong Wang. "Fatty Acid Metabolism Reprogramming in Advanced Prostate Cancer." Metabolites 11, no. 11 (November 9, 2021): 765. http://dx.doi.org/10.3390/metabo11110765.

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Prostate cancer (PCa) is a carcinoma in which fatty acids are abundant. Fatty acid metabolism is rewired during PCa development. Although PCa can be treated with hormone therapy, after prolonged treatment, castration-resistant prostate cancer can develop and can lead to increased mortality. Changes to fatty acid metabolism occur systemically and locally in prostate cancer patients, and understanding these changes may lead to individualized treatments, especially in advanced, castration-resistant prostate cancers. The fatty acid metabolic changes are not merely reflective of oncogenic activity, but in many cases, these represent a critical factor in cancer initiation and development. In this review, we analyzed the literature regarding systemic changes to fatty acid metabolism in PCa patients and how these changes relate to obesity, diet, circulating metabolites, and peri-prostatic adipose tissue. We also analyzed cellular fatty acid metabolism in prostate cancer, including fatty acid uptake, de novo lipogenesis, fatty acid elongation, and oxidation. This review broadens our view of fatty acid switches in PCa and presents potential candidates for PCa treatment and diagnosis.
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Dikalov, Sergey, Alexander Panov, and Anna Dikalova. "Critical Role of Mitochondrial Fatty Acid Metabolism in Normal Cell Function and Pathological Conditions." International Journal of Molecular Sciences 25, no. 12 (June 12, 2024): 6498. http://dx.doi.org/10.3390/ijms25126498.

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Abstract: There is a “popular” belief that a fat-free diet is beneficial, supported by the scientific dogma indicating that high levels of fatty acids promote many pathological metabolic, cardiovascular, and neurodegenerative conditions. This dogma pressured scientists not to recognize the essential role of fatty acids in cellular metabolism and focus on the detrimental effects of fatty acids. In this work, we critically review several decades of studies and recent publications supporting the critical role of mitochondrial fatty acid metabolism in cellular homeostasis and many pathological conditions. Fatty acids are the primary fuel source and essential cell membrane building blocks from the origin of life. The essential cell membranes phospholipids were evolutionarily preserved from the earlier bacteria in human subjects. In the past century, the discovery of fatty acid metabolism was superseded by the epidemic growth of metabolic conditions and cardiovascular diseases. The association of fatty acids and pathological conditions is not due to their “harmful” effects but rather the result of impaired fatty acid metabolism and abnormal lifestyle. Mitochondrial dysfunction is linked to impaired metabolism and drives multiple pathological conditions. Despite metabolic flexibility, the loss of mitochondrial fatty acid oxidation cannot be fully compensated for by other sources of mitochondrial substrates, such as carbohydrates and amino acids, resulting in a pathogenic accumulation of long-chain fatty acids and a deficiency of medium-chain fatty acids. Despite popular belief, mitochondrial fatty acid oxidation is essential not only for energy-demanding organs such as the heart, skeletal muscle, and kidneys but also for metabolically “inactive” organs such as endothelial and epithelial cells. Recent studies indicate that the accumulation of long-chain fatty acids in specific organs and tissues support the impaired fatty acid oxidation in cell- and tissue-specific fashion. This work, therefore, provides a basis to challenge these established dogmas and articulate the need for a paradigm shift from the “pathogenic” role of fatty acids to the critical role of fatty acid oxidation. This is important to define the causative role of impaired mitochondrial fatty acid oxidation in specific pathological conditions and develop novel therapeutic approaches targeting mitochondrial fatty acid metabolism.
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Dissertations / Theses on the topic "Fatty acid metabolism"

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Taylor, George. "Fatty acid metabolism in cyanobacteria." Thesis, University of Exeter, 2012. http://hdl.handle.net/10871/9363.

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With crude oil demand rising and supplies being depleted, alternative energy, specifically biofuels, are of intense scientific interest. Current plant crop based biofuels suffer from several problems, most importantly the use of land needed for food. Cyanobacteria offer a solution to this problem as they do not compete with land for food and produce hydrocarbons that can be used as biofuels. Upon examination of metabolic pathways competing with hydrocarbon synthesis, it appeared that cyanobacteria lacked the major fatty acid degradative metabolic pathway β-oxidation, generally thought to be a universally occurring pathway. Lack of this pathway in cyanobacteria was confirmed by employing a range of analytical techniques. Bioinformatic analysis suggested that potential enzymes with β-oxidation activity were involved in other metabolic pathways. A sensitive assay was set up to detect acyl- CoAs, the substrates of β-oxidation, using liquid chromatography triple quadrupole mass spectrometry. None could be detected in cyanobacteria. No enzymatic activity from the rate-limiting acyl-CoA dehydrogenase/oxidase could be detected in cyanobacterial extracts. It was found that radiolabeled fatty acids fed to cyanobacteria were utilised for lipid membranes as opposed to being converted to CO2 by respiration or into other compounds by the TCA cycle. An element of the β-oxidation pathway, E. coli acyl-CoA synthetase was ectopically expressed in a strain of cyanobacteria and implications of the introduction of acyl-CoA synthesis were assessed. Finally, the regulation of the fatty acid biosynthetic pathway was investigated. It was determined that under conditions of excess fatty acid, the transcription of acetyl-CoA carboxylase and enoyl-ACP reductase was repressed and acyl-ACP synthetase involved in fatty acid recycling was induced. These results were discussed in relation to fatty acid oxidation and hydrocarbon biosynthesis in other organisms.
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Rose, Philip. "Indices of fatty acid metabolism." Thesis, Sheffield Hallam University, 1992. http://shura.shu.ac.uk/20296/.

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During the fed state energy requirements are met by glycolysis of carbohydrates. When the stores of carbohydrates are diminished, for example during prolonged fasting, metabolism switches to that of fatty acids. Fatty acids are broken down by fi-oxidation within the mitochondrial matrix. Prolonged fasting results in the production of ketone bodies. These can also be used as an energy source by the brain. In defects of fatty acid metabolism where individual steps are inhibited or blocked, such as medium chain acyl-CoA dehydrogenase deficiency, an abnormal accumulation of the metabolites that lead up to the block, or their breakdown products, is often seen. Non-compensatory levels of metabolites following the site of the defect also occur. In the fed state, when flux through the defective fatty acid pathway is minimal, metabolic profiles can appear completely normal. It is therefore often necessary to induce metabolic stress before a full laboratory investigation can proceed. Interpretation of individual metabolite quantitations can often be difficult and a variation of 'normal values' according to metabolic state can lead to misinterpretation. Comparison between the concentrations of related metabolites along the fatty acid metabolic pathway may diminish the need for exact knowledge of the metabolic state and by correlation plotting could clearly identify abnormal relationships. This thesis describes an investigation into the efficacy of paired metabolite correlation plots in preliminary detection of defects in fatty acid metabolism. In certain inborn errors of fatty acid metabolism where the fi-oxidation cycle is affected, abnormal urine metabolite patterns have been used as diagnostic markers. Similar patterns have been reported in the urine of healthy newborns and termed generalised neonatal dicarboxylic aciduria177. This report documents an investigation of the connections between generalised neonatal dicarboxylic aciduria and a number of overlying factors (vis type of feed, gender, sibling history of sudden infant death syndrome and urine carnitine levels). Also discussed is the development of two laboratory assays. A radio-enzymatic method was developed and used to determine the levels of total, free and acyl carnitine in urine or blood. Suberyl, hexanoyl, and phenylpropionyl glycine in urine can be quantitated by use of stable isotope internal standards and gas chromatography / electron impact mode mass spectrometry. Synthesis and calibration of such internal standards is described. Finally, methods used to culture and store skin fibroblasts from biopsy samples are included as an appendix. These fibroblasts can then be used in various diagnostic tests such as carbon dioxide release and electron transfer flavoprotein enzyme analysis. The costs encountered during tissue culture could be avoided by medium term storage of the biopsy material prior to culture to await sufficient clinical evidence to merit such analyses. Preliminary results of extended cryogenic storage and viability of recovered specimens are also included.
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Cryle, Max Julian. "Fatty acid metabolism by cytochromes P450 /." [St. Lucia, Qld.], 2006. http://www.library.uq.edu.au/pdfserve.php?image=thesisabs/absthe19452.pdf.

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Lippmeier, James Casey. "Fatty acid metabolism of marine microalgae." Thesis, University of Hull, 2007. http://hydra.hull.ac.uk/resources/hull:7014.

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Pathways for the biosynthesis of docosahexaenoic acid (DHA) and other polyunsaturated fatty acids (PUFA) were elucidated in two heterotrophic, marine microalgae; Schizochytrium sp. and Crypthecodinium cohnii. PUFA-requiring auxotrophs of both of these algae were created and used as tools for studying PUFA biosynthetic pathways. Additionally, equilibrium radio-labeling techniques were applied to algal cultures fed 14C-fatty acids. Both organisms were found to possess two distinct pathways for PUFA biosynthesis. One pathway, mediated by classical elongases and desaturases, was incomplete in both organisms and was not capable of complementing PUFA auxotrophic phenotypes or of producing PUFA de novo, but could produce DHA from simpler PUFA precursors. The second PUFA pathway in each organism was desaturase and elongase independent. In C. cohnii, this pathway was distinguished by a capacity to produce DHA from acetate, in a manner similar to that of Schizochytrium which was shown to employ a polyketide synthase (PKS) complex for primary DHA biosynthesis. Additionally, genes of the Schizochytrium PUFA-PKS were successfully expressed in transgenic yeast, which produced DHA. Candidates for genes encoding C. cohnii PUFA-PKS components and other genes of C. cohnii PUFA biosynthesis were identified and discussed.
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Brolinson, Annelie. "Regulation of Elovl and fatty acid metabolism." Doctoral thesis, Stockholm : Wenner-Gren Institute for Experimental Biology, Stockholm university : Stockholm University Library [distributör], 2009. http://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-8469.

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Baker, Genevieve Elizabeth. "Molecular insights into bacterial fatty acid metabolism." Thesis, University of Bristol, 2016. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.715811.

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Price, Claire Louise. "Candida CYP52 : alkane and fatty acid metabolism." Thesis, Swansea University, 2012. https://cronfa.swan.ac.uk/Record/cronfa42696.

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Cytochromes P450 are a superfamily of haem-thiolate proteins found in all kingdoms of life. To date 11294 enzymes have been identified and have been shown to be involved in the metabolism of a wide variety of substrates, including hydrocarbons and xenobiotics. In yeast and fungi the hydroxylation of alkanes is associated with a family of cytochromes P450 enzymes known as CYP52s. These enzymes are involved in the terminal hydroxylation of long-chain alkanes resulting in the production of alcohols, which can be further converted to form fatty acids and diacids. In vivo such hydrocarbons can be subjected to beta-oxidation for use in growth. Alternatively, the products formed by CYP52 catalysed hydroxylation in vitro can be used in biotechnological applications. They can be used as platform chemicals in the production of a number of industrial products, including plastics, fragrances and antibiotics. The p-oxidation of fatty acids has been less well documented for Candida albicans than for other Candida species, therefore it was the aim of this study to investigate a) did cytochromes P450 exist in C. albicans that could possibly fulfil this function and b) to definitively assign function to a single cytochrome P450. Using a bioinformatic approach, five putative CYP52s were identified in C. albicans. Of these CYP52s, Alk1 was shown to have the greatest homology to the archetypal alkane-assimilating CYP52, CYP52A3 from C. maltosa. ALK1 heterologous gene expression in the brewer's yeast Saccharomyces cerevisiae allowed growth on hexadecane (C16:0) as the sole carbon source. This showed for the first time that Alk1 is involved in the hydroxylation of long-chain alkanes as normally S. cerevisiae is unable to utilise alkanes for growth. This study has also shown that Alk1 is able to interact with sterol substrates suggesting a possible role for CYP52s in sterol metabolism, which was previously unknown.
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Batugedara, Hashini Maneesha. "Fatty acid metabolism in Saccharomyces cerevisiae and effects of fatty acid metabolites on neutrophil function." Thesis, California State University, Long Beach, 2014. http://pqdtopen.proquest.com/#viewpdf?dispub=1526893.

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In the presence of arachidonic acid (AA), Saccharomyces cerevisiae produces prostaglandin E2 (PGE2). S. cerevisiae and its metabolites may be consumed in products manufactured using the yeast (e.g. beer). Neutrophils are immune cells present in the gastrointestinal (GI) tract during inflammation. As a lipid-signaling molecule, PGE2 can potentially modify neutrophil functions and exacerbate pre-existing inflammation. As neutrophil migration is a hallmark of inflammation, we investigated the impact of PGE2 on neutrophil chemotaxis. Chemotaxis assays were performed on neutrophils isolated from human whole blood using the chemotactic agents f-Met-Leu-Phe (fMLP) or interleukin-8 (IL-8). Neutrophil chemotaxis was concentration dependent as it was enhanced 3.5-fold at low concentrations of PGE2 (0.1 nM-10 nM) and reduced 3.0-fold at higher concentrations of PGE2 (100 nM).

The biochemical pathway utilized by S. cerevisiae to produce PGE2 is unknown. Identifying enzymes that metabolize AA may direct approaches to reduce the impact that yeast PGE2 may have on neutrophils. S. cerevisiae does not have genes homologous to those involved in mammalian AA metabolism. We employed RNAseq transcriptome sequencing to study the lipid biosynthetic pathway in S. cerevisiae and observed 1248 genes upregulated in yeast that were cultured in the presence of AA relative to yeast that were cultured without AA. Notably, genes that mediate beta-oxidation of fatty acids (Pot1, Pox1, Faa1 and Faa2) were upregulated up to 2.3-fold.

The results demonstrate that low concentrations of PGE2 enhance neutrophil chemotaxis that is mediated by fMLP or IL-8, suggesting that PGE 2 may aid in recruiting neutrophils from regions that are distant to a site of inflammation. Once a higher concentration of PGE2 is encountered by neutrophils, neutrophils may halt their migration and engage effector functions such as phagocytosis and superoxide production. Increased expression of genes involved with fatty acid metabolism points to enzymes that may utilize AA to produce PGE2 in S. cerevisiae. Experiments testing PGE2 levels in knock-out strains of yeast will identify genes involved in PGE2 production. Results of this study have implications to reduce potential off-target effects caused by yeast PGE 2 in consumables.

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Mardy, Jennifer Kai. "Fatty acid metabolism in isolated perfused mouse hearts." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp05/MQ64969.pdf.

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Masterson, Christine. "Carnitine and fatty acid metabolism in higher plants." Thesis, University of Newcastle Upon Tyne, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.254030.

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Books on the topic "Fatty acid metabolism"

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C, Glatz Jan F., and Vusse, G. J. van der., eds. Cellular fatty-acid binding proteins. Dordrecht: Kluwer Academic Publishers, 1990.

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Valentine, R. C. Omega-3 fatty acids and the DHA principle. Boca Raton, FL: CRC Press, 2010.

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L, Valentine David, ed. Omega-3 fatty acids and the DHA principle. Boca Raton: Taylor & Francis, 2010.

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International, Congress on Essential Fatty Acids and Eicosanoids (3rd 1992 Adelaide S. Aust ). Essential fatty acids and eicosanoids: Invited papers from the Third International Congress. Champaign, Ill: American Oil Chemists' Society, 1992.

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Simon, Eaton, and Fatty Acid Oxidation and Ketogenesis Conference (4th : 1998 : London, England), eds. Current views of fatty acid oxidation and ketogenesis: From organelles to point mutations. New York: Kluwer Academic/Plenum Publishers, 1999.

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Kay, Tanaka, and Coates Paul M, eds. Fatty acid oxidation: Clinical, biochemical, and molecular aspects : proceedings of the International Symposium on Clinical, Biochemical, and Molecular Aspects of Fatty Oxidation held in Philadelphia, November 6-9, 1988. New York: Liss, 1990.

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International Symposium on Clinical, Biochemical and Molecular Aspects of Fatty Acid Oxidation (1988 Philadelphia, Pa.). Fatty acid oxidation: Clinical biochemical, and molecular aspects : proceedings of the International Symposium on Clinical, Biochemical and Molecular Aspects of Fatty Acid Oxidation, held November 6-9, 1988 in Philadelphia. Edited by Tanaka Kay and Coates Paul M. New York: Liss, 1989.

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Simon, Eaton, and Fatty Acid Oxidation and Ketogenesis Conference (4th : 1998 : London, England), eds. Current views of fatty acid oxidation and ketogenesis: From organelles to point mutations. New York: Kluwer Academic/Plenum Publishers, 1999.

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Simon, Eaton, and Fatty Acid Oxidation and Ketogenesis Conference (4th : 1998 : London, England), eds. Current views of fatty acid oxidation and ketogenesis: From organelles to point mutations. New York: Kluwer Academic/Plenum Publishers, 1999.

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1933-, Simopoulos Artemis P., Meester Fabien De, and International Congress on the Columbus Concept (6th : 2008 : Geneva, Switzerland), eds. A balanced omega-6/omega-3 fatty acid ratio, cholesterol and coronary heart disease. Basel: Karger, 2009.

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Book chapters on the topic "Fatty acid metabolism"

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Park, Margaret A., and Charles Chalfant. "Fatty Acid Metabolism." In Molecular Life Sciences, 1–17. New York, NY: Springer New York, 2020. http://dx.doi.org/10.1007/978-1-4614-6436-5_613-1.

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Tiedemann, Anne, Catherine Sherrington, Daina L. Sturnieks, Stephen R. Lord, Mark W. Rogers, Marie-Laure Mille, Paavo V. Komi, et al. "Fatty Acid Metabolism." In Encyclopedia of Exercise Medicine in Health and Disease, 342. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-540-29807-6_4225.

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Park, Margaret A., and Charles Chalfant. "Fatty Acid Metabolism." In Molecular Life Sciences, 387–401. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4614-1531-2_613.

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Møller, Jens. "Free Fatty Acid Metabolism." In Cholesterol, 8. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-71600-3_5.

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Hamilton, James A., Kellen Brunaldi, Richard P. Bazinet, and Paul A. Watkins. "Brain Fatty Acid Uptake." In Neural Metabolism In Vivo, 793–817. Boston, MA: Springer US, 2011. http://dx.doi.org/10.1007/978-1-4614-1788-0_27.

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Storch, Judith. "The Role of Fatty Acid Binding Proteins in Enterocyte Fatty Acid Transport." In Intestinal Lipid Metabolism, 153–70. Boston, MA: Springer US, 2001. http://dx.doi.org/10.1007/978-1-4615-1195-3_9.

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Marinetti, Guido V. "Disorders of Fatty Acid Metabolism." In Disorders of Lipid Metabolism, 31–48. Boston, MA: Springer US, 1990. http://dx.doi.org/10.1007/978-1-4615-9564-9_3.

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Smith, Mark A., Johnathan A. Napier, Robert Browne, Peter R. Shewry, and A. Keith Stobart. "Cytochrome b5 and fatty acid desaturation." In Plant Lipid Metabolism, 24–26. Dordrecht: Springer Netherlands, 1995. http://dx.doi.org/10.1007/978-94-015-8394-7_6.

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Gurr, M. I., and J. L. Harwood. "Fatty acid structure and metabolism." In Lipid Biochemistry, 23–118. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4615-3862-2_3.

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Kiens, Bente. "Training and Fatty Acid Metabolism." In Advances in Experimental Medicine and Biology, 229–38. Boston, MA: Springer US, 1998. http://dx.doi.org/10.1007/978-1-4899-1928-1_21.

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Conference papers on the topic "Fatty acid metabolism"

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Sugiyama, Takeshi, Alison J. Hobro, Takayuki Umakoshi, Prabhat Verma, and Nicholas I. Smith. "Raman spectroscopy of macrophage uptake and cellular response during exposure to dietary lipids." In JSAP-OSA Joint Symposia. Washington, D.C.: Optica Publishing Group, 2019. http://dx.doi.org/10.1364/jsap.2019.18p_e208_8.

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The increase in patients suffering from ‘lifestyle diseases such as coronary heart disease, atherosclerosis, diabetes and gout has been associated with the amount and nature of fats in our diets. In many of these diseases, macrophages and their role in lipid metabolism greatly impacts the development and severity of the disease. Fatty acids, which are a sub-class of lipids, have many different types depending on the number of carbon atoms and the presence of carbon double bonds (i.e. saturated and unsaturated fatty acids). The chemical properties of each fatty acid depend on the number of carbon atoms and degree of saturation. Therefore, it is important to investigate how macrophages metabolize these different types of fatty acids. In this research, we focus on the distribution and the uptake of four fatty acids: palmitic acid, stearic acid, oleic acid, and linoleic acid, shown in Table 1.
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Blanksby, Stephen, Berwyck Poad, David Marshall, Philipp Menzel, and Reuben Young. "Unknown unknowns in lipidomics: A de novo method for fatty acid discovery." In 2022 AOCS Annual Meeting & Expo. American Oil Chemists' Society (AOCS), 2022. http://dx.doi.org/10.21748/nlsb8229.

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Current technologies for fatty acid analysis are overly reliant on the availability of reference libraries, databases and standards. This reliance is hampering the discovery of novel fatty acids and obscuring a full view of lipid metabolism across the kingdoms of life. Recent high-profile discoveries of novel lipids with site(s) of unsaturation inconsistent with canonical lipid metabolism stress the need for new technologies that can provide robust identifications of fatty acids without reliance on prior assumptions. Herein we present advances in liquid chromatography-mass spectrometry for the de novo identification and quantification of fatty acids in lipid extracts. The workflow combines fixed-charge derivatization with ozone-induced dissociation (OzID) for sensitive detection of low-abundant fatty acids with unambiguous assignment of site(s) of unsaturation. Chromatographic alignment of precursor ions with OzID transitions is undertaken using a bespoke Skyline pipeline providing unbiased identification of fatty acids over a relative concentration range spanning more than 4-orders of magnitude. Application of this analytical workflow to lipid extracts from diverse sources including human plasma, cell lines and vernix caseosa has led to the discovery of new fatty acids that point to hitherto undescribed metabolism within the source cell or organism. The description of these “unknown unknowns” particularly in well-studied systems “such as human plasma” points to a substantially great diversity in the lipidome than previously appreciated.
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Schick, Paul K., Barbara P. Schick, and Pat Webster. "THE EFFECT OF OMEGA 3 FATTY ACIDS ON MEGAKARYOCYTE ARACHIDONIC ACID METABOLISM." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642953.

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Dietary omega 3 polyunsaturated fatty acids are thought to prevent atherosclerosis. It has been proposed that omega 3 fatty acids modify platelet arachidonic acid (20:4) metabolism and platelet function and thereby reduce the incidence of thrombosis. We have previously shown that megakaryocytes (MK), like platelets, contain large amounts of esterified 20:4. The study addresses the following questions: 1) Do omega 3 fatty acids have a primary action on 20:4 metabolism in MK rather than in platelets. 2) Do omega 3 marine oils, docosahexaenoic acid (22:6) and eicosapentaenoic acid (20:5), have a different effect on megakaryocyte 20:4 metabolism than does alpha linolenic acid (18:3), the major omega-3 fatty acid present in normal diets? 3) How do omega-3 fatty acids modify megakaryocyte 20:4 acid metabolism? MK and platelets were isolated from guinea pigs. Isolated cells were incubated with radiolabeled 20:4 acid and unlabeled 18:3, 20:5 or 22:6. Incubations were terminated by lipid extraction, lipid classes were separated by thin-layer chromatography and the incorporation of radiolabeled 20:4 into lipid species was measured by scintillation spectrometry.MK (106) can incorporate about 4 times more 20:4 than 109 platelets. We have previously shown that 20:4 is incorporated into all endogenous pools of 20:4 in MK while platelets appear to have a limited capacity to incorporate 20:4 into phosphatidyl-ethanolamine (PE). Marine oils, 22:6 and 20:5, had similar effects on the incorporation of radiolabeled 20:4 in MK. Both marine oils reduced the total uptake of 20:4 in megakaryocytes but the reduction occured primarily in PE and phosphatidylserine (PS) rather than in phosphatidylcholine (PC) and phosphatidylinositol (PI). Both 20:5 and 22:6 caused a 50% reduction in the incorporation of radiolabeled 20:4 into megakaryocyte PE and PS while only a 20% reduction into PC and PI. There was a striking difference in the effect of 18:3. Even though the incubation of megakaryocytes with 18:3 reduced the uptake of 20:4, the distribution of the incorporated 20:4 in phospholipids of megakaryocytes incubated with 18:3 was similar to that in controls. Thus, 18:3 did not have a selective effect on the incorporation of 20:4 into PE or PS. Whereas megakaryocyte 20:4 metabolism was significantly affected by omega-3 fatty acids, the incubation of guinea pig or human platelets with 22:6, 20:5 or 18:3 did not result in any alteration of the incorporation of 20:4 into platelet phospholipids.20:4 may be initially incorporated into megakaryocyte PC and subsequently transfered to PE and other phospholipids. Omega 3 marine oils, 20:5 and 22:6, appear to have a selective action on the incorporation or transfer of 20:4 into PE and PS. One mechanism for these observations would be an effect of marine oils on megakaryocyte acyltransferase and/or transacylases. Omega 3 linolenic acid appears to reduce the uptake of 20:4 but does not affect the transfer of 20:4 into PE and PS since there was no selective inhibition of uptake into PE or other megakaryocyte phospholipids. The observation that marine oils did not have any effect on 20:4 metabolism in platelets indicated that omega 3 polyunsaturated fatty acids primarily affect megakaryocytes. This phenomenon may result in the production of platelets with abnormal content and compartmentalization of arachidonic acid. The localization of 20:4 in different pools in these platelets could influence the availability of esterified 20:4 for the production of thromboxanes and other eicosanoids. Another implication of the study is that omega 3 fatty acids may have a greater effect on precursor cells than on differentiated cells and tissues and influence cellular maturation.
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Al-Qeraiwi, Maha, Manar Al-Rashid, Nasser Rizk, Abdelrahman El Gamal, and Amena Fadl. "Hepatic Gene Expression Profile of Lipid Metabolism of Obese Mice after treatment with Anti-obesity Drug." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0214.

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Obesity is a global disorder with multifactorial causes. The liver plays a vital role in fat metabolism. Disorder of hepatic fat metabolism is associated with obesity and causes fatty liver. High fat diet intake (HFD) to mice causes the development of dietinduced obesity (DIO). The study aimed to detect the effects of anti-obesity drugs (sulforaphane; SFN and leptin) on hepatic gene expression of fat metabolism in mice that were fed HFD during an early time of DIO. Twenty wild types (WT) CD1 male mice aged ten weeks were fed a high fat diet. The mice were treated with vehicle; Veh (control group), and SFN, then each group is treated with leptin or saline. Four groups of treatment were: control group (vehicle + saline), Group 2 (vehicle + leptin), group 3 (SFN + saline), and group 4 (SFN + leptin). Body weight and food intake were monitored during the treatment period. Following the treatments of leptin 24 hour, fasting blood samples and liver tissue was collected, and Total RNA was extracted then used to assess the gene expression of 84 genes involved in hepatic fat metabolism using RT-PCR profiler array technique. Leptin treatment upregulated fatty acid betaoxidation (Acsbg2, Acsm4) and fatty acyl-CoA biosynthesis (Acot6, Acsl6), and downregulated is fatty acid transport (Slc27a2). SFN upregulated acylCoA hydrolase (Acot3) and long chain fatty acid activation for lipids synthesis and beta oxidation (Acsl1). Leptin + SFN upregulated fatty acid beta oxidation (Acad11, Acam) and acyl-CoA hydrolase (Acot3, Acot7), and downregulated fatty acid elongation (Acot2). As a result, treatment of both SFN and leptin has more profound effects on ameliorating pathways involved in hepatic lipogenesis and TG accumulation and lipid profile of TG and TC than other types of intervention. We conclude that early intervention of obesity pa could ameliorate the metabolic changes of fat metabolism in liver as observed in WT mice on HFD in response to anti-obesity treatment.
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Alvarez, D. M., M. Bueno, L. Tu, B. Kimball, G. Eric, M. Rojas, and A. L. Mora. "Defective Fatty Acid Metabolism Promotes Fibrosis in the Lung." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a1245.

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Omelchenko, A. N., K. A. Okotrub, N. V. Surovtsev, T. N. Igonina, E. Yu Brusentsev, and S. Y. Amstislavsky. "APPLICATION OF RAMAN SPECTROSCOPY TO THE CHARACTERIZATION OF THE METABOLISM OF MOUSE PREIMPLANTATION EMBRYOS." In X Международная конференция молодых ученых: биоинформатиков, биотехнологов, биофизиков, вирусологов и молекулярных биологов — 2023. Novosibirsk State University, 2023. http://dx.doi.org/10.25205/978-5-4437-1526-1-200.

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The research demonstrates the description of the metabolism of mouse preimplantation embryos by Raman spectroscopy using deuterated labels. We observe changes in the transport of fatty acids (stearic acid), amino acids (phenylalanine and leucine) and glucose after embryos cryopreservation.
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Homma, Soichiro, and Mamoru Hashimoto. "Label free isomeric metabolism measurement with multiplex coherent anti-Stokes Raman scattering microspectroscopy." In Conference on Lasers and Electro-Optics/Pacific Rim. Washington, D.C.: Optica Publishing Group, 2022. http://dx.doi.org/10.1364/cleopr.2022.p_cm15_02.

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We observed beta-oxidation of trans-fatty acid for human hepatocarcinoma cell line HepG2 with multiplex coherent anti-Stokes Raman scattering microspectroscopy under time-series and found the isomerization of unsaturated fatty acid without staining.
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Arsić, Aleksandra, Milica Kojadinović, Snjezana Petrović, Danijela Ristić Medić, Milena Žuža Praštalo, and Vesna Vučić. "FFECTS OF POMEGRANATE JUICE ON LIPID METABOLISM IN WOMEN WITH DYSLIPIDEMIA AND METABOLIC SYNDROME." In 2nd International Symposium on Biotechnology. Faculty of Agronomy in Čačak, University of Kragujevac, 2024. http://dx.doi.org/10.46793/sbt29.79aa.

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The objective of this research was to evaluate the effects of the consumption of Pomegranate juice (PJ) on blood pressure and lipid metabolism in subjects with dyslipidemia and metabolic syndrome. Twelve females with established dyslipidemia and 12 females with metabolic syndrome consumed 300 mL of PJ daily for 2 and 6 weeks respectively. PJ consumption resulted in a significant decrease in diastolic blood pressure, and LDL-cholesterol, an increase in the estimated activity of stearoyl-CoA desaturase in the short study, and a significant decrease in the percentage of arachidonic acid and an increase in monounsaturated fatty acids in longer study. These results indicate a positive impact of the consumption of pomegranate juice, in both short and long periods, on lipid metabolism and suggest potential anti-inflammatory and cardio- protective effects
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Noto, Alessia, Maria Elena Pisanu, Claudia De Vitis, Debora Malpicci, Luigi Fattore, Nadia Lobello, Barbara Bonacci, Gennaro Ciliberto, and Rita Mancini. "Abstract 4230: Targeting lung cancer stem cells through fatty acid metabolism." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-4230.

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Evans, William, Jazmine Eccles, and William Baldwin. "Changes in Energy Metabolism Induced by PFOS and Dietary Oxylipins." In 2022 AOCS Annual Meeting & Expo. American Oil Chemists' Society (AOCS), 2022. http://dx.doi.org/10.21748/jnpe5541.

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CYP2B6 is a drug metabolizing cytochrome P450 (CYP) that has anti-obesity properties, but also increases non-alcoholic fatty liver disease (NAFLD) in hCYP2B6-transgenic mice compared to Cyp2b-null mice. hCYP2B6-transgenic mice are also more susceptible to perfluorooctane sulfonic acid (PFOS) toxicity, a lipid-like toxicant used in stains, varnishes and firefighting foams that increase NAFLD. Our recent research demonstrates that CYP2B6 metabolizes dietary polyunsaturated fatty acids into the oxylipins, 9-HODE and 9-HOTre, which are strong peroxisome proliferator activated receptor alpha (PPARa) agonists and weak PPARg agonists. The purpose of our studies is to better understand the mechanisms behind PFOS and oxylipin-mediated hepatic steatosis. To test whether PFOS, 9-HODE or 9-HOTrE alter mitochondrial metabolism, Seahorse Mitostress assays were performed using HepG2 cells treated with 0.2, 1 and 5mM PFOS, 9-HODE and 9-HOTrE for 24 hours (n=5). Both PFOS and 9-HOTrE increased spare respiratory capacity in a concentration-dependent manner with lesser effects by 9-HODE. qPCR was performed following exposure of HepG2 cells to 1 and 5 mM of each compound to investigate changes in gene expression that may explain alterations in mitochondrial respiration or hepatic steatosis. PFOS repressed expression of ANGPTL4, a biomarker of PPARgactivation. 9-HODE induced CD36 and FASN expression, genes involved in fatty acid uptake and synthesis. 9-HOTrE induced SREBF1 and Cpt1a expression, genes involved in sterol synthesis and fatty acid transport into the mitochondria and may partially explain the increase in SRC. Thus, based on current results, PFOS is associated with reduced transport of lipids from the liver and 9-HODE increases lipid uptake; both would increase steatosis through different mechanisms. 9-HOTre may increase metabolism and therefore reduce steatosis.
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Reports on the topic "Fatty acid metabolism"

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Monaco, Marie. The Role of Fatty Acid Metabolism in Estrogen Receptor-Negative Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, September 2011. http://dx.doi.org/10.21236/ada550883.

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Fridman, Eyal, and Eran Pichersky. Tomato Natural Insecticides: Elucidation of the Complex Pathway of Methylketone Biosynthesis. United States Department of Agriculture, December 2009. http://dx.doi.org/10.32747/2009.7696543.bard.

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Plant species synthesize a multitude of specialized compounds 10 help ward off pests. and these in turn may well serve as an alternative to synthetic pesticides to reduce environmental damage and health risks to humans. The general goal of this research was to perform a genetic and biochemical dissection of the natural-insecticides methylketone pathway that is specific to the glandular trichomes of the wild species of tomato, Solanumhabrochaites f. glabratum (accession PI126449). Previous study conducted by us have demonstrated that these compounds are synthesized de novo as a derivate pathway of the fatty acid biosynthesis, and that a key enzyme. designated MethylketoneSynthase 1 (MKS 1). catalyzes conversion of the intermediate B-ketoacyl- ACPs to the corresponding Cn-1 methylketones. The approach taken in this proposed project was to use an interspecific F2 population. derived from the cross between the cultivated lV182 and the wild species PIl26449. for three objectives: (i) Analyze the association between allelic status of candidate genes from the fatty acid biosynthesis pathway with the methylketone content in the leaves (ii) Perform bulk segregant analysis of genetic markers along the tomato genome for identifying genomic regions that harbor QTLs for 2TD content (iii) Apply differential gene expression analysis using the isolated glands of bulk segregant for identifying new genes that are involved in the pathway. The genetic mapping in the interspecific F2 population included app. 60 genetic markers, including the candidate genes from the FAS pathway and SSR markers spread evenly across the genome. This initial; screening identified 5 loci associated with MK content including the candidate genes MKS1, ACC and MaCoA:ACP trans. Interesting observation in this genetic analysis was the connection between shape and content of the glands, i.e. the globularity of the four cells, typical to the wild species. was associated with increased MK in the segregating population. In the next step of the research transcriptomic analysis of trichomes from high- and 10w-MK plants was conducted. This analysis identified a new gene, Methy1ketone synthase 2 (MKS2), whose protein product share sequence similarity to the thioesterase super family of hot-dog enzymes. Genetic analysis in the segregating population confirmed its association with MK content, as well as its overexpression in E. coli that led to formation of MK in the media. There are several conclusions drawn from this research project: (i) the genetic control of MK accumulation in the trichomes is composed of biochemical components in the FAS pathway and its vicinity (MKS 1 and MKS2). as well as genetic factors that mediate the morphology of these specialized cells. (ii) the biochemical pathway is now realized different from what was hypothesized before with MKS2 working upstream to I\1KS 1 and serves as the interface between primary (fatty acids) and secondary (MK) metabolism. We are currently testing the possible physical interactions between these two proteins in vitro after the genetic analysis showed clear epistatic interactions. (iii) the regulation of the pathway that lead to specialized metabolism in the wild species is largely mediated by transcription and one of the achievements of this project is that we were able to isolate and verify the specificity of the MKS1 promoter to the trichomes which allows manipulation of the pathways in these cells (currently in progress). The scientific implications of this research project is the advancement in our knowledge of hitherto unknown biochemical pathway in plants and new leads for studying a new family in plants (hot dog thioesterase). The agricultural and biotechnological implication are : (i) generation of new genetic markers that could assist in importing this pathway to cultivated tomato hence enhancing its natural resistance to insecticides, (ii) the discovery of MKS2 adds a new gene for genetic engineering of plants for making new fatty acid derived compounds. This could be assisted with the use of the isolated and verified MKS1 promoter. The results of this research were summarized to a manuscript that was published in Plant Physiology (cover paper). to a chapter in a proceeding book. and one patent was submitted in the US.
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Porat, Ron, Gregory T. McCollum, Amnon Lers, and Charles L. Guy. Identification and characterization of genes involved in the acquisition of chilling tolerance in citrus fruit. United States Department of Agriculture, December 2007. http://dx.doi.org/10.32747/2007.7587727.bard.

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Citrus, like many other tropical and subtropical fruit are sensitive to chilling temperatures. However, application of a pre-storage temperature conditioning (CD) treatment at 16°C for 7 d or of a hot water brushing (HWB) treatment at 60°C for 20 sec remarkably enhances chilling tolerance and reduces the development of chilling injuries (CI) upon storage at 5°C. In the current research, we proposed to identify and characterize grapefruit genes that are induced by CD, and may contribute to the acquisition of fruit chilling tolerance, by two different molecular approaches: cDNA array analysis and PCR cDNA subtraction. In addition, following the recent development and commercialization of the new Affymetrix Citrus Genome Array, we further performed genome-wide transcript profiling analysis following exposure to CD and chilling treatments. To conduct the cDNA array analysis, we constructed cDNA libraries from the peel tissue of CD- and HWB-treated grapefruit, and performed an EST sequencing project including sequencing of 3,456 cDNAs from each library. Based on the obtained sequence information, we chose 70 stress-responsive and chilling-related genes and spotted them on nylon membranes. Following hybridization the constructed cDNA arrays with RNA probes from control and CD-treated fruit and detailed confirmations by RT-PCR analysis, we found that six genes: lipid-transfer protein, metallothionein-like protein, catalase, GTP-binding protein, Lea5, and stress-responsive zinc finger protein, showed higher transcript levels in flavedo of conditioned than in non-conditioned fruit stored at 5 ᵒC. The transcript levels of another four genes: galactinol synthase, ACC oxidase, temperature-induced lipocalin, and chilling-inducible oxygenase, increased only in control untreated fruit but not in chilling-tolerant CD-treated fruit. By PCR cDNA subtraction analysis we identified 17 new chilling-responsive and HWB- and CD-induced genes. Overall, characterization of the expression patterns of these genes as well as of 11 more stress-related genes by RNA gel blot hybridizations revealed that the HWB treatment activated mainly the expression of stress-related genes(HSP19-I, HSP19-II, dehydrin, universal stress protein, EIN2, 1,3;4-β-D-glucanase, and SOD), whereas the CD treatment activated mainly the expression of lipid modification enzymes, including fatty acid disaturase2 (FAD2) and lipid transfer protein (LTP). Genome wide transcriptional profiling analysis using the newly developed Affymetrix Citrus GeneChip® microarray (including 30,171 citrus probe sets) revealed the identification of three different chilling-related regulons: 1,345 probe sets were significantly affected by chilling in both control and CD-treated fruits (chilling-response regulon), 509 probe sets were unique to the CD-treated fruits (chilling tolerance regulon), and 417 probe sets were unique to the chilling-sensitive control fruits (chilling stress regulon). Overall, exposure to chilling led to expression governed arrest of general cellular metabolic activity, including concretive down-regulation of cell wall, pathogen defense, photosynthesis, respiration, and protein, nucleic acid and secondary metabolism. On the other hand, chilling enhanced various adaptation processes, such as changes in the expression levels of transcripts related to membranes, lipid, sterol and carbohydrate metabolism, stress stimuli, hormone biosynthesis, and modifications in DNA binding and transcription factors.
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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.

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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.
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Butler, Walter R., Uzi Moallem, Amichai Arieli, Robert O. Gilbert, and David Sklan. Peripartum dietary supplementation to enhance fertility in high yielding dairy cows. United States Department of Agriculture, April 2007. http://dx.doi.org/10.32747/2007.7587723.bard.

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Objectives of the project: To evaluate the effects of a glucogenic supplement during the peripartum transition period on insulin, hepatic triglyceride accumulation, interval to first ovulation, and progesterone profile in dairy cows. To compare benefits of supplemental fats differing in fatty acid composition and fed prepartum on hepatic triglyceride accumulation, interval to first ovulation, progesterone profile, and uterine prostaglandin production in lactating dairy cows. To assess the differential and carry-over effects of glucogenic and fat supplements fed to peripartum dairy cows on steroidogenesis and fatty acids in ovarian follicles. To determine the carry-over effects of peripartum glucogenic or fat supplements on fertility in high producing dairy cows (modified in year 3 to Israel only). Added during year 3 of project: To assess the activity of genes related to hepatic lipid oxidation and gluconeogenesis following dietary supplementation (USA only). Background: High milk yields in dairy cattle are generally associated with poor reproductive performance. Low fertility results from negative energy balance (NEBAL) of early lactation that delays resumption of ovarian cycles and exerts other carryover effects. During NEBAL, ovulation of ovarian follicles is compromised by low availability of insulin and insulin-like growth factor-I (IGF-I), but fatty acid mobilization from body stores is augmented. Liver function during NEBAL is linked to the resumption of ovulation and fertility: 1) Accumulation of fatty acids by the liver and ketone production are associated with delayed first ovulation; 2) The liver is the main source of IGF-I. NEBAL will continue as a consequence of high milk yield, but dietary supplements are currently available to circumvent the effects on liver function. For this project, supplementation was begun prepartum prior to NEBAL in an effort to reduce detrimental effects on liver and ovarian function. Fats either high or low in unsaturated fatty acids were compared for their ability to reduce liver triglyceride accumulation. Secondarily, feeding specific fats during a period of high lipid turnover caused by NEBAL provides a novel approach for manipulating phospholipid pools in tissues including ovary and uterus. Increased insulin from propylene glycol (glucogenic) was anticipated to reduce lipolysis and increase IGF-I. The same supplements were utilized in both the USA and Israel, to compare effects across different diets and environments. Conclusions: High milk production and very good postpartum health was achieved by dietary supplementation. Peripartum PGLY supplementation had no significant effects on reproductive variables. Prepartum fat supplementation either did not improve metabolic profile and ovarian and uterine responses in early lactation (USA) or decreased intake when added to dry cow diets (Israel). Steroid production in ovarian follicles was greater in lactating dairy cows receiving supplemental fat (unsaturated), although in a field trail fertility to insemination was not improved.
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McInerney, M. J. Energetics of end product excretion in anaerobic bacteria and the metabolism of fatty acids by Syntrophomonas wolfei. Office of Scientific and Technical Information (OSTI), January 1986. http://dx.doi.org/10.2172/7245908.

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McInerney, M. Energetics of end product excretion in anaerboic bacteria and the metabolism of fatty acids by Syntrophomonas wolfei. Office of Scientific and Technical Information (OSTI), October 1989. http://dx.doi.org/10.2172/7013135.

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Splitter, Gary A., Menachem Banai, and Jerome S. Harms. Brucella second messenger coordinates stages of infection. United States Department of Agriculture, January 2011. http://dx.doi.org/10.32747/2011.7699864.bard.

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Aim 1: To determine levels of this second messenger in: a) B. melitensiscyclic-dimericguanosinemonophosphate-regulating mutants (BMEI1448, BMEI1453, and BMEI1520), and b) B. melitensis16M (wild type) and mutant infections of macrophages and immune competent mice. (US lab primary) Aim 2: To determine proteomic differences between Brucelladeletion mutants BMEI1453 (high cyclic-dimericguanosinemonophosphate, chronic persistent state) and BMEI1520 (low cyclicdimericguanosinemonophosphate, acute virulent state) compared to wild type B. melitensisto identify the role of this second messenger in establishing the two polar states of brucellosis. (US lab primary with synergistic assistance from the Israel lab Aim 3: Determine the level of Brucellacyclic-dimericguanosinemonophosphate and transcriptional expression from naturally infected placenta. (Israel lab primary with synergistic assistance from the US lab). B. Background Brucellaspecies are Gram-negative, facultative intracellular bacterial pathogens that cause brucellosis, the most prevalent zoonosis worldwide. Brucellosis is characterized by increased abortion, weak offspring, and decreased milk production in animals. Humans are infected with Brucellaby consuming contaminated milk products or via inhalation of aerosolized bacteria from occupational hazards. Chronic human infections can result in complications such as liver damage, orchitis, endocarditis, and arthritis. Brucellaspp. have the ability to infect both professional and non-professional phagocytes. Because of this, Brucellaencounter varied environments both throughout the body and within a cell and must adapt accordingly. To date, few virulence factors have been identified in B. melitensisand even less is known about how these virulence factors are regulated. Subsequently, little is known about how Brucellaadapt to its rapidly changing environments, and how it alternates between acute and chronic virulence. Our studies suggest that decreased concentrations of cyclic dimericguanosinemonophosphate (c-di-GMP) lead to an acute virulent state and increased concentrations of c-di-GMP lead to persistent, chronic state of B. melitensisin a mouse model of infection. We hypothesize that B. melitensisuses c-di-GMP to transition from the chronic state of an infected host to the acute, virulent stage of infection in the placenta where the bacteria prepare to infect a new host. Studies on environmental pathogens such as Vibrio choleraeand Pseudomonas aeruginosasupport a mechanism where changes in c-di-GMP levels cause the bacterium to alternate between virulent and chronic states. Little work exists on understanding the role of c-di-GMP in dangerous intracellular pathogens, like Brucellathat is a frequent pathogen in Israeli domestic animals and U.S. elk and bison. Brucellamust carefully regulate virulence factors during infection of a host to ensure proper expression at appropriate times in response to host cues. Recently, the novel secondary signaling molecule c-di-GMP has been identified as a major component of bacterial regulation and we have identified c-di-GMP as an important signaling factor in B. melitensishost adaptation. C. Major conclusions, solutions, achievements 1. The B. melitensis1453 deletion mutant has increased c-di-GMP, while the 1520 deletion mutant has decreased c-di-GMP. 2. Both mutants grow similarly in in vitro cultures; however, the 1453 mutant has a microcolony phenotype both in vitro and in vivo 3. The 1453 mutant has increased crystal violet staining suggesting biofilm formation. 4. Scanning electron microscopy revealed an abnormal coccus appearance with in increased cell area. 5. Proteomic analysis revealed the 1453 mutant possessed increased production of proteins involved in cell wall processes, cell division, and the Type IV secretion system, and a decrease in proteins involved in amino acid transport/metabolism, carbohydrate metabolism, fatty acid production, and iron acquisition suggesting less preparedness for intracellular survival. 6. RNAseq analysis of bone marrow derived macrophages infected with the mutants revealed the host immune response is greatly reduced with the 1453 mutant infection. These findings support that microlocalization of proteins involved in c-di-GMP homeostasis serve a second messenger to B. melitensisregulating functions of the bacteria during infection of the host.
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9

Firon, Nurit, Prem Chourey, Etan Pressman, Allen Hartwell, and Kenneth J. Boote. Molecular Identification and Characterization of Heat-Stress-Responsive Microgametogenesis Genes in Tomato and Sorghum - A Feasibility Study. United States Department of Agriculture, October 2007. http://dx.doi.org/10.32747/2007.7591741.bard.

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Exposure to higher than optimal temperatures - heat-stress (HS) - is becoming increasingly common to all crop plants worldwide. Heat stress coinciding with microgametogenesis, especially during the post-meiotic phase that is marked by starch biosynthesis, is often associated with starch-deficient pollen and male sterility and ultimately, greatly reduced crop yields. The molecular basis for the high sensitivity of developing pollen grains, on one hand, and factors involved in pollen heat-tolerance, on the other, is poorly understood. The long-term goal of this project is to provide a better understanding of the genes that control pollen quality under heat-stress conditions. The specific objectives of this project were: (1) Determination of the threshold heat stress temperature(s) that affects tomato and sorghum pollen quality whether: a) Chronic mild heat stress conditions (CMHS), or b) Acute heat stress (AHS). (2) Isolation of heat-responsive, microgametogenesis-specific sequences. During our one-year feasibility project, we have accomplished the proposed objectives as follows: Objectrive 1: We have determined the threshold HS conditions in tomato and sorghum. This was essential for achieving the 2nd objective, since our accumulated experience (both Israeli and US labs) indicate that when temperature is raised too high above "threshold HS levels" it may cause massive death of the developing pollen grains. Above-threshold conditions have additional major disadvantages including the "noise" caused by induced expression of genes involved in cell death and masking of the differences between heatsensitive and heat-tolerant pollen grains. Two different types of HS conditions were determined: a) Season-long CMHS conditions: 32/26°C day/night temperatures confirmed in tomato and 36/26°C day maximum/night minimum temperatures in sorghum. b) Short-term AHS: In tomato, 2 hour exposure to 42-45°C (at 7 to 3 days before anthesis) followed by transfer to 28/22±2oC day/night temperatures until flower opening and pollen maturation, caused 50% reduced germinating pollen in the heat-sensitive 3017 cv.. In sorghum, 36/26°C day/night temperatures 10 to 5 days prior to panicle emergence, occurring at 35 days after sowing (DAS) in cv. DeKalb28E, produced starch-deficient and sterile pollen. Objective 2: We have established protocols for the high throughput transcriptomic approach, cDNA-AFLP, for identifying and isolating genes exhibiting differential expression in developing microspores exposed to either ambient or HS conditions and created a databank of HS-responsivemicrogametogenesis-expressed genes. A subset of differentially displayed Transcript-Derived Fragments (TDFs) that were cloned and sequenced (35 & 23 TDFs in tomato and sorghum, respectively) show close sequence similarities with metabolic genes, genes involved in regulation of carbohydrate metabolism, genes implicated in thermotolerance (heat shock proteins), genes involved in long chain fatty acids elongation, genes involved in proteolysis, in oxidation-reduction, vesicle-mediated transport, cell division and transcription factors. T-DNA-tagged Arabidopsis mutants for part of these genes were obtained to be used for their functional analysis. These studies are planned for a continuation project. Following functional analyses of these genes under HS – a valuable resource of genes, engaged in the HS-response of developing pollen grains, that could be modulated for the improvement of pollen quality under HS in both dicots and monocots and/or used to look for natural variability of such genes for selecting heat-tolerant germplasm - is expected.
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