Relevant bibliographies by topics / Fatty acid �-oxidation

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  2. Dissertations / Theses
  3. Books
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Academic literature on the topic 'Fatty acid �-oxidation'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 February 2022

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Journal articles on the topic "Fatty acid �-oxidation"

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Hardwick, James P., Douglas Osei-Hyiaman, Homer Wiland, Mohamed A. Abdelmegeed, and Byoung-Joon Song. "PPAR/RXR Regulation of Fatty Acid Metabolism and Fatty Acid -Hydroxylase (CYP4) Isozymes: Implications for Prevention of Lipotoxicity in Fatty Liver Disease." PPAR Research 2009 (2009): 1–20. http://dx.doi.org/10.1155/2009/952734.

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Fatty liver disease is a common lipid metabolism disorder influenced by the combination of individual genetic makeup, drug exposure, and life-style choices that are frequently associated with metabolic syndrome, which encompasses obesity, dyslipidemia, hypertension, hypertriglyceridemia, and insulin resistant diabetes. Common to obesity related dyslipidemia is the excessive storage of hepatic fatty acids (steatosis), due to a decrease in mitochondria -oxidation with an increase in both peroxisomal -oxidation, and microsomal -oxidation of fatty acids through peroxisome proliferator activated receptors (PPARs). How steatosis increases PPAR activated gene expression of fatty acid transport proteins, peroxisomal and mitochondrial fatty acid -oxidation and -oxidation of fatty acids genes regardless of whether dietary fatty acids are polyunsaturated (PUFA), monounsaturated (MUFA), or saturated (SFA) may be determined by the interplay of PPARs and HNF4 with the fatty acid transport proteins L-FABP and ACBP. In hepatic steatosis and steatohepatitis, the -oxidation cytochrome P450CYP4Agene expression is increased even with reduced hepatic levels of PPAR. Although numerous studies have suggested the role ethanol-inducibleCYP2E1in contributing to increased oxidative stress,Cyp2e1-null mice still develop steatohepatitis with a dramatic increase inCYP4Agene expression. This strongly implies thatCYP4Afatty acid -hydroxylase P450s may play an important role in the development of steatohepatitis. In this review and tutorial, we briefly describe how fatty acids are partitioned by fatty acid transport proteins to either anabolic or catabolic pathways regulated by PPARs, and we explore how medium-chain fatty acid (MCFA)CYP4Aand long-chain fatty acid (LCFA)CYP4F-hydroxylase genes are regulated in fatty liver. We finally propose a hypothesis that increasedCYP4Aexpression with a decrease inCYP4Fgenes may promote the progression of steatosis to steatohepatitis.
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Onibi, G. E., J. R. Scaife, V. R. Fowler, and I. Murray. "Influence of Dietary Fatty Acid and α-Tocopherol Supply on Tissue Fatty Acid Profiles, α-Tocopherol Content and Lipid Oxidation in Pigs." Proceedings of the British Society of Animal Science 1996 (March 1996): 147. http://dx.doi.org/10.1017/s0308229600031147.

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Unsaturated fatty acids especially n-3 polyunsaturated fatty acids (PUFA) are recognised as important components of a healthy human diets and increased intake has been shown to reduce the incidence of cardiovascular diseases (BNF, 1992). These fatty acids are susceptible to oxidation and lipid oxidation in meat may adversely affect meat quality and safety. However, tissue α-tocopherol (AT) may reduce oxidative changes. In this study, the effect of increased dietary supply of AT and unsaturated fatty acids on tissue AT content, fatty acid profiles and oxidative stability of pig muscle lipid was assessed.
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Sidossis, Labros S. "The Role of Glucose in the Regulation of Substrate Interaction During Exercise." Canadian Journal of Applied Physiology 23, no. 6 (December 1, 1998): 558–69. http://dx.doi.org/10.1139/h98-031.

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Glucose and fatty acids are the main energy sources for oxidative metabolism in endurance exercise. Although a reciprocal relationship exists between glucose and fatty acid contribution to energy production for a given metabolic rate, the controlling mechanism remains debatable. Randle et al.'s (1963) glucose-fatty acid cycle hypothesis provides a potential mechanism for regulating substrate interaction during exercise. The cornerstone of this hypothesis is that the rate of lipolysis, and therefore fatty acid availability, controls how glucose and fatty acids contribute to energy production. Increasing fatty acid availability attenuates carbohydrate oxidation during exercise, mainly via sparing intramuscular glycogen. However, there is little evidence for a direct inhibitory effect of fatty acids on glucose oxidation. We found that glucose directly determines the rate of fat oxidation by controlling fatty acid transport into the mitochondria. We propose that the intracellular availability of glucose, rather than fatty acids, regulates substrate interaction during exercise. Key words: mitochondria, malonyl-coenzyme A, carnitine palmitoyltransferase, medium-chain fatty acids, free fatty acids
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Schönfeld, Peter, and Georg Reiser. "Why does Brain Metabolism not Favor Burning of Fatty Acids to Provide Energy? - Reflections on Disadvantages of the Use of Free Fatty Acids as Fuel for Brain." Journal of Cerebral Blood Flow & Metabolism 33, no. 10 (August 7, 2013): 1493–99. http://dx.doi.org/10.1038/jcbfm.2013.128.

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It is puzzling that hydrogen-rich fatty acids are used only poorly as fuel in the brain. The long-standing belief that a slow passage of fatty acids across the blood–brain barrier might be the reason. However, this has been corrected by experimental results. Otherwise, accumulated nonesterified fatty acids or their activated derivatives could exert detrimental activities on mitochondria, which might trigger the mitochondrial route of apoptosis. Here, we draw attention to three particular problems: (1) ATP generation linked to β-oxidation of fatty acids demands more oxygen than glucose, thereby enhancing the risk for neurons to become hypoxic; (2) β-oxidation of fatty acids generates superoxide, which, taken together with the poor anti-oxidative defense in neurons, causes severe oxidative stress;(3) the rate of ATP generation based on adipose tissue-derived fatty acids is slower than that using blood glucose as fuel. Thus, in periods of extended continuous and rapid neuronal firing, fatty acid oxidation cannot guarantee rapid ATP generation in neurons. We conjecture that the disadvantages connected with using fatty acids as fuel have created evolutionary pressure on lowering the expression of the β-oxidation enzyme equipment in brain mitochondria to avoid extensive fatty acid oxidation and to favor glucose oxidation in brain.
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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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Rinaldo, Piero, Dietrich Matern, and Michael J. Bennett. "Fatty Acid Oxidation Disorders." Annual Review of Physiology 64, no. 1 (March 2002): 477–502. http://dx.doi.org/10.1146/annurev.physiol.64.082201.154705.

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Döbeln, U. von. "Fatty acid oxidation defects." Acta Paediatrica 82, s390 (August 1993): 88–90. http://dx.doi.org/10.1111/j.1651-2227.1993.tb12888.x.

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Merritt II, J. Lawrence, Marie Norris, and Shibani Kanungo. "Fatty acid oxidation disorders." Annals of Translational Medicine 6, no. 24 (December 2018): 473. http://dx.doi.org/10.21037/atm.2018.10.57.

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Lepine, Allan J., Malcolm Watford, R. Dean BOYD, Deborah A. Ross, and Dana M. Whitehead. "Relationship between hepatic fatty acid oxidation and gluconeogenesis in the fasting neonatal pig." British Journal of Nutrition 70, no. 1 (July 1993): 81–91. http://dx.doi.org/10.1079/bjn19930106.

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Hepatocytes were isolated from sixteen fasting neonatal pigs and used in two experiments: (1) to determine the effect of various factors on the ability for hepatic oxidation of fatty acids and (2) to clarify the relationship between fatty acid oxidation and glucose synthesis. In Expt 1, newborn pigs were either fasted from birth for 24 h or allowed to suck ad lib. for 3 d followed by a 24 h fast. In the presence of pyruvate, oxidation of octanoate (2 mM) was about 30-fold greater than oleate (1 mM) regardless of age, but glucose synthesis was not enhanced beyond that observed for pyruvate alone. Inclusion of carnitine (1 mM), glucagon (100 nM) or dibutryl cAMP (50 μM) in the incubation media did not stimulate either fatty acid oxidation (octanoate or oleate) or glucose synthesis. Extending the period of fasting to 48 h (Expt 2) failed to enhance the fatty acid oxidative capacity or glucose synthesis rate. Likewise, the redox potential of the giuconeogenic substrate (lactate v. pyruvate) did not influence glucose synthesis regardless of the oxidative capacity exhibited for fatty acids. These data indicate that fatty acid oxidative capacity is not the first limiting factor to full expression of gluconeogenesis in hepatocytes isolated from fasted newborn pigs.
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Bonen, Arend, Xiao-Xia Han, Daphna D. J. Habets, Maria Febbraio, Jan F. C. Glatz, and Joost J. F. P. Luiken. "A null mutation in skeletal muscle FAT/CD36 reveals its essential role in insulin- and AICAR-stimulated fatty acid metabolism." American Journal of Physiology-Endocrinology and Metabolism 292, no. 6 (June 2007): E1740—E1749. http://dx.doi.org/10.1152/ajpendo.00579.2006.

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Fatty acid translocase (FAT)/CD36 is involved in regulating the uptake of long-chain fatty acids into muscle cells. However, the contribution of FAT/CD36 to fatty acid metabolism remains unknown. We examined the role of FAT/CD36 on fatty acid metabolism in perfused muscles (soleus and red and white gastrocnemius) of wild-type (WT) and FAT/CD36 null (KO) mice. In general, in muscles of KO mice, 1) insulin sensitivity and 5-aminoimidazole-4-carboxamide-1-β-d-ribofuranoside (AICAR) sensitivity were normal, 2) key enzymes involved in fatty acid oxidation were altered minimally or not at all, and 3) except for an increase in soleus muscle FATP1 and FATP4, these fatty acid transporters were not altered in red and white gastrocnemius muscles, whereas plasma membrane-bound fatty acid binding protein was not altered in any muscle. In KO muscles perfused under basal conditions (i.e., no insulin, no AICAR), rates of hindquarter fatty acid oxidation were reduced by 26%. Similarly, in oxidative but not glycolytic muscles, the basal rates of triacylglycerol esterification were reduced by 40%. When muscles were perfused with insulin, the net increase in fatty acid esterification was threefold greater in the oxidative muscles of WT mice compared with the oxidative muscles in KO mice. With AICAR-stimulation, the net increase in fatty acid oxidation by hindquarter muscles was 3.7-fold greater in WT compared with KO mice. In conclusion, the present studies demonstrate that FAT/CD36 has a critical role in regulating fatty acid esterification and oxidation, particularly during stimulation with insulin or AICAR.
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Dissertations / Theses on the topic "Fatty acid �-oxidation"

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Eaton, Simon. "Regulation of fatty acid #beta#-oxidation." Thesis, University of Newcastle Upon Tyne, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.311443.

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Spurway, Tracy Deborah. "Control of hepatic fatty acid oxidation." Thesis, University of Newcastle Upon Tyne, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.283671.

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Jackson, Sandra. "Enzymes of mitochondrial fatty acid oxidation." Thesis, University of Newcastle Upon Tyne, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.283069.

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Smith, Simon. "Polyunsaturated fatty acid oxidation in Alzheimer’s disease." Thesis, Aston University, 2011. http://publications.aston.ac.uk/16499/.

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Alzheimer’s disease is a neurodegenerative disorder which has been characterised with genetic (apolipoproteins), protein (ß-amyloid and tau) and lipid oxidation/metabolism alterations in its pathogenesis. In conjunction with the Dementia Research Group, Bristol University, investigation into genetic, protein and lipid oxidation in Alzheimer’s disease was conducted. A large sample cohort using the double-blind criteria, along with various clinical and chemical data sets were used to improve the statistical analysis and therefore the strength of this particular study. Bristol University completed genetic and protein analysis with lipid oxidation assays performed at Aston University. Lipid oxidation is a complex process that creates various biomarkers, from transient intermediates, to short carbon chain products and cyclic ring structures. Quantification of these products was performed on lipid extracts of donated clinical diseased and non-diseased frontal and temporal brain regions, from the Brain Bank within Frenchay Hospital. The initial unoxidised fatty acids, first transient oxidation intermediates the conjugated dienes and lipid hydroperoxides, the endpoint aldehyde biomarkers and finally the cyclic isoprostanes and neuroprostanes were determined to investigate lipid oxidation in Alzheimer’s. Antioxidant levels were also investigated to observe the effect of oxidation on the defence pathways. Assays utilised in this analysis included; fatty acid composition by GC-FID, conjugated diene levels by HPLC-UV and UV-spec, lipid hydroperoxide levels by FOX, aldehyde content by TBARs, antioxidant status by TEAC and finally isoprostane and neuroprostane quantification using a newly developed EI-MS method. This method involved the SIM of specific ions from F-ring isoprostane and neuroprostane fragmentation, which enabled EI-MS to be used for their quantification. Analyses demonstrated that there was no significant difference between control and Alzheimer samples across all the oxidation biomarkers for both brain regions. Antioxidants were the only marker that showed a clear variance; with Alzheimer samples having higher levels than the age matched controls. This unique finding is supported with the observed lower levels of lipid oxidation biomarkers in Alzheimer brain region samples. The increased antioxidant levels indicate protection against oxidation which may be a host response to counteract the oxidative pathways, but this requires further investigation. In terms of lipid oxidation, no definitive markers or target site for therapeutic intervention have been revealed. This study concludes that dietary supplementation of omega-3 fatty acids or antioxidants would most likely be ineffective against Alzheimer disease, although it may support improvement in other areas of general health.
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Rocha, Hugo Daniel Carvalho de Azevedo. "Mitochondrial dysfunction in fatty acid β-oxidation disorders." Doctoral thesis, Universidade de Aveiro, 2014. http://hdl.handle.net/10773/14297.

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Doutoramento em Bioquímica
Mitochondria are central organelles for cell survival with particular relevance in energy production and signalling, being mitochondrial fatty acid β–oxidation (FAO) one of the metabolic pathways harboured in this organelle. FAO disorders (FAOD) are among the most well studied inborn errors of metabolism, mainly due to their impact in health. Nevertheless, some questions remain unsolved, as their prevalence in certain European regions and how pathophysiological determinants combine towards the phenotype. Analysis of data from newborn screening programs from Portugal and Spain allowed the estimation of the birth prevalence of FAOD revealing that this group of disorders presents in Iberia (and particularly in Portugal) one of the highest European birth prevalence, mainly due to the high birth prevalence of medium chain acyl-CoA dehydrogenase deficiency. These results highlight the impact of this group of genetic disorders in this European region. The characterization of mitochondrial proteome, from patients fibroblasts with FAOD, namely multiple acyl-CoA dehydrogenase deficiency (MADD) and long chain acyl-CoA dehydrogenase deficiency (LCHADD), provided a global perspective of the mitochondrial proteome plasticity in these disorders and highlights the main molecular pathways involved in their pathogenesis. Severe MADD forms show an overexpression of chaperones, antioxidant enzymes (MnSOD), and apoptotic proteins. An overexpression of glycolytic enzymes, which reflects cellular adaptation to energy deficiency due to FAO blockage, was also observed. When LCHADD fibroblasts were analysed a metabolic switching to glycolysis was also observed with overexpression of apoptotic proteins and modulation of the antioxidant defence system. Severe LCHADD present increased ROS alongside with up regulation of MnSOD while moderate forms have lower ROS and down-regulation of MnSOD. This probably reflects the role of MnSOD in buffering cellular ROS, maintain them at levels that allow cells to avoid damage and start a cellular response towards survival. When ROS levels are very high cells have to overexpress MnSOD for detoxifying proposes. When severe forms of MADD were compared to moderate forms no major differences were noticed, most probably because ROS levels in moderate MADD are high enough to trigger a response similar to that observed in severe forms. Our data highlights, for the first time, the differences in the modulation of antioxidant defence among FAOD spectrum. Overall, the data reveals the main pathways modulated in FAOD and the importance of ROS levels and antioxidant defence system modulation for disease severity. These results highlight the complex interaction between phenotypic determinants in FAOD that include genetic, epigenetic and environmental factors. The development of future better treatment approaches is dependent on the knowledge on how all these determinants interact towards phenotype.!
A mitocôndria desempenha um papel fundamental na regulação de vários processos celulares, com particular relevância na produção de energia, sendo a β-oxidação mitocondrial dos ácidos gordos uma das vias metabólicas que tem lugar neste organelo. Os défices da β-oxidação mitocondrial dos ácidos gordos estão entre os grupos de doenças metabólicas mais estudados, existindo contudo, algumas questões que continuam por esclarecer, como a sua prevalência ao nascimento em determinadas regiões da Europa e quais e de que forma os vários determinantes patofisiológicos interatuam para produzir um determinado fenótipo. A análise dos dados de programas de rastreio neonatal da península Ibérica possibilitou estimar a prevalência ao nascimento dos défices da β-oxidação mitocondrial, tendo-se observado um dos valores mais elevados (particularmente em Portugal) no âmbito das regiões europeias, fundamentalmente devido à grande prevalência ao nascimento dos défices da desidrogenase dos ácidos gordos de cadeia média. Estes resultados realçam o impacto deste grupo de doenças genéticas nesta região europeia. A caracterização do proteoma mitocondrial, a partir de fibroblastos em cultura, de doentes com défices da β-oxidação mitocondrial (especificamente défice múltiplo das desidogenases (MADD) e défice da desidrogenase dos ácidos 3- hidroxilados de cadeia longa (LCHADD)) permitiu obter uma perspetiva geral sobre a plasticidade do proteoma mitocondrial nestas doenças assim como avaliar quais as principais vias metabólicas envolvidas na sua patogénese. Em formas severas de MADD foi observada uma sobre-expressão de chaperones, enzimas antioxidantes e proteínas associadas à apoptose. Nestas células foi igualmente observada a sobre-expressão de enzimas glicolíticas, como adaptação ao bloqueio da β-oxidação. A análise de amostras de doentes com LCHADD também evidenciou uma sobre-expressão de enzimas glicolíticas, assim como de proteínas relacionadas com a apoptose, e a modulação do sistema de defesa antioxidante. O doente com uma forma severa de LCHADD apresentou níveis de stress oxidativo elevados, associados a uma sobre expressão da MnSOD, enquanto o doente com uma forma moderada apresentou níveis mais baixos de stress oxidativo e uma sub-expressão da MnSOD. Estes resultados são provavelmente o reflexo do papel da MnSOD na regulação dos níveis de ROS, mantendo-os em níveis que não provoquem danos, mas que permitam iniciar processos de sinalização com vista à manutenção celular. A comparação de forma moderadas com severas de MADD não revelou diferenças significativas, muito provavelmente porque os níveis de stress oxidativo são suficientemente altos para despoletar uma resposta semelhante às formas severas. Os presentes resultados realçam as diferenças na modulação do sistema de defesa antioxidante no espectro dos défices da β-oxidação mitocondrial. No seu conjunto os resultados obtidos revelam as principais vias moduladas nos défices da β-oxidação mitocondrial e a importância do stress oxidativo e sistema de defesa antioxidante para o fenótipo. Ao permitem compreender melhor a complexa interação entre os vários fatores que interagem com vista ao fenótipo e que podem ser de origem genética, epigenética ou ambiental, contribuem para o desenvolvimento de novas e mais eficazes abordagens terapêuticas.
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Wang, Wenzhong. "Mechanistic studies of flavoenzymes in fatty acid oxidation and oxidative protein folding." Access to citation, abstract and download form provided by ProQuest Information and Learning Company; downloadable PDF file, 233 p, 2007. http://proquest.umi.com/pqdweb?did=1362529911&sid=3&Fmt=2&clientId=8331&RQT=309&VName=PQD.

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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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Mansouri, Abdelhak. "Hepatic fatty acid oxidation and control of food intake /." Zürich : ETH, 2008. http://e-collection.ethbib.ethz.ch/show?type=diss&nr=17697.

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New, Karen Jayne. "Control of hepatic fatty acid oxidation in suckling rats." Thesis, University College London (University of London), 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.392103.

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Bacher, Mohamed A. "Induction of microsomal and peroxisomal fatty acid oxidation by chlorophenoxy acid herbicides." Thesis, University of Surrey, 1989. http://epubs.surrey.ac.uk/847223/.

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Induction of the cytochrome P-450 mixed-function oxidase and specifically the cytochrome P-450 IVA1 isoenzyme by seven phenoxy acid herbicides in rat liver and kidney, have been studied. results using liver microsomes demonstrated that the 12-hydroxylation of lauric acid was significantly induced by all compounds (3-8-fold), 4-chlorophenoxyacetic acid (CPA) (300 mg/kg) being the weakest and 2,4,5-trichlorophenoxypropionic acid (2,4,5-TP) (200 mg/kg) the most potent inducers respectively. This increase in lauric acid 12-hydroxylase-activity was accompanied by an increase in the hepatic content of cytochrome P-450 IVA1 as assessed by both a qualitative Western blot procedure and a quantitative ELISA method. Furthermore, there was a parallel increase in cytochrome P-450 IVA1 mRNA and a similar increase in peroxisomal B-oxidation subsequent to exposure to these compounds. In addition, benzphetamine-N-demethylase, a marker of cytochrome P-450 IIBl and IIB2 activities, was not affected by any of the herbicides, whereas cytochrome P-450 IA1 and IA2, as assayed by ethoxyresorufin-O-deethylase activity, was significantly increased (up to 2.2-fold) by some of the compounds. Kidney microsomal parameters were not affected by any of these compounds. My in vivo studies using antipyrine, pentobarbital and zoxazolamine indicated that the metabolism of these substrates was marginally affected by only some of the compounds. In order to highlight the possible involvement of a metabolite of the chlorophenoxy acids in the induction of cytochrome P-450, I investigated four related chlorophenols. There was no significant change in cytochrome P-450 isoenzyme levels in rat liver and kidney microsomes nor was there any increase in peroxisomal beta-oxidation. Taken collectively, the results presented in this thesis indicate that the chlorinated phenoxy acid herbicides studied preferentially induce the cytochrome P-450 IVA1 isoenzyme and peroxisomal beta-oxidation in a pattern similar to the typical inducers of this isoenzyme such as clofibrate. A scheme is presented whereby induction of catalytically competent cytochrome P-450 IVA1 is required for the phenomenon of peroxisome proliferation by these chlorophenoxy acid derivatives.
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Books on the topic "Fatty acid �-oxidation"

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Quant, Patti A., and Simon Eaton, eds. Current Views of Fatty Acid Oxidation and Ketogenesis. Boston, MA: Springer US, 2002. http://dx.doi.org/10.1007/b113063.

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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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M, Coates Paul, and Tanaka Kay, eds. New developments in fatty acid oxidation: Proceedings of the Second International Symposium on Clinical, Biochemical, and Molecular Aspects of Fatty Acid Oxidation, held in Philadelphia, Pennsylvania, November 1991. New York, N.Y: Wiley-Liss, 1992.

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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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Tomohito, Hamazaki, and Okuyama Harumi, eds. Fatty acids and lipids: New findings. Basel: Karger, 2001.

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Murphy, Elaine, Yann Nadjar, and Christine Vianey-Saban. Fatty Acid Oxidation, Electron Transfer and Riboflavin Metabolism Defects. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0008.

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The fatty acid oxidation disorders are a group of autosomally recessively inherited disorders of energy metabolism that may present with life-threatening hypoketotic hypoglycemia, encephalopathy and hepatic dysfunction, muscle symptoms, and/or cardiomyopathy. Milder phenotypes may present in adulthood, causing exercise intolerance, episodic rhabdomyolysis, and neuropathy. Specific investigations include acylcarnitine profiling, urine organic acid analysis, fibroblast or leucocyte studies of fatty acid oxidation flux/enzyme activity, and genetic testing. Management varies depending on the condition but includes avoidance of precipitants such as fasting, fever, and intense exercise, a high-carbohydrate, low-fat diet, and supplementation with carnitine or riboflavin. Inborn errors of riboflavin transport mainly present with Brown-Vialetto-Van Laere syndrome. Some patients respond dramatically to riboflavin supplementation; therefore it has to be tried in all suspected patients.
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Forrest, Rosemary, and Nicole Baugh. Genetic Mistakes: Understanding and Living with Fatty Acid Oxidation Disorders. Nova Science Publishers, Incorporated, 2017.

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Casteels, M. Differences in the Peroxisomal B-oxidation of Fatty Acids and Bile Acid Intermediates. Leuven University Press, 1990.

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Institution, British Standards, and European Committee for Standardization., eds. Fat and oil derivatives - Fatty Acid Methyl Esters (FAME): Determination of oxidation stability (accelerated oxidation test). BSI, 2003.

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Tanaka, Kay. Fatty Acid Oxidation: Clinical, Biochemical, and Molecular Aspects (Progress in Clinical and Biological Research). Wiley-Liss, 1990.

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Book chapters on the topic "Fatty acid �-oxidation"

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Wieser, Thomas. "Fatty acid oxidation disorders." In International Neurology, 658–61. Chichester, UK: John Wiley & Sons, Ltd, 2016. http://dx.doi.org/10.1002/9781118777329.ch165.

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Wieser, Thomas, and Thomas Deufel. "Fatty Acid Oxidation Disorders." In International Neurology, 631–34. Oxford, UK: Wiley-Blackwell, 2010. http://dx.doi.org/10.1002/9781444317008.ch160.

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Van Hove, Johan L. K. "Fatty Acid Oxidation Defects." In Nutrition Management of Inherited Metabolic Diseases, 241–54. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-14621-8_22.

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Stanley, C. A. "Disorders of Fatty Acid Oxidation." In Inborn Metabolic Diseases, 133–43. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-662-03147-6_11.

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Stanley, C. A. "Disorders of Fatty Acid Oxidation." In Inborn Metabolic Diseases, 140–50. Berlin, Heidelberg: Springer Berlin Heidelberg, 2000. http://dx.doi.org/10.1007/978-3-662-04285-4_11.

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Spiekerkoetter, Ute, and Marinus Duran. "Mitochondrial Fatty Acid Oxidation Disorders." In Physician's Guide to the Diagnosis, Treatment, and Follow-Up of Inherited Metabolic Diseases, 247–64. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-40337-8_17.

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Stanley, C. A. "Disorders of Fatty Acid Oxidation." In Inborn Metabolic Diseases, 395–410. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-662-02613-7_31.

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Fournier, N. C., and M. A. Richard. "Role of fatty acid-binding protein in cardiac fatty acid oxidation." In Cellular Fatty Acid-binding Proteins, 149–59. Boston, MA: Springer US, 1990. http://dx.doi.org/10.1007/978-1-4615-3936-0_19.

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Chesworth, J. M., T. Stuchbury, and J. R. Scaife. "Fatty Acid Oxidation and Lipid Breakdown." In An Introduction to Agricultural Biochemistry, 173–92. Dordrecht: Springer Netherlands, 1998. http://dx.doi.org/10.1007/978-94-009-1441-4_13.

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Veerkamp, J. H., and H. T. B. van Moerkerk. "Fatty acid-binding protein and its relation to fatty acid oxidation." In Cellular Fatty Acid-Binding Proteins II, 101–6. Boston, MA: Springer US, 1993. http://dx.doi.org/10.1007/978-1-4615-3096-1_13.

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Conference papers on the topic "Fatty acid �-oxidation"

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Lecuona, Emilia, Ermelinda Ceco, Samuel Weinberg, Masahiko Shigemura, Lynn Welch, Diego Celli, Lena Volpe, Navdeep Chandel, and Jabob Sznajder. "Increased fatty acid oxidation impairs myoblast differentiation in hypercapnia." In ERS International Congress 2017 abstracts. European Respiratory Society, 2017. http://dx.doi.org/10.1183/1393003.congress-2017.pa384.

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Liu, Xi, Yun Lu, Zibo Chen, Xiuxia Liu, Weiguo Hu, Lin Zheng, Yulong Chen, et al. "Abstract 2547: USP18 promotes lipolysis, fatty acid oxidation and lung cancer growth." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-2547.

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Hansen, Karyn J., and Bennett Van Houten. "Abstract POSTER-BIOL-1314: Investigating fatty acid beta-oxidation in ovarian cancer cells." In Abstracts: 10th Biennial Ovarian Cancer Research Symposium; September 8-9, 2014; Seattle, WA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1557-3265.ovcasymp14-poster-biol-1314.

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Jung, Kwang Hwa, Jun Hyoung Park, Tirupataiah Sirupangi, Sajna Vithayathil, Lee-Jun Wong, and Benny A. Kaipparettu. "Abstract 1507: Fatty acid oxidation mediated autophagy regulation in triple negative breast cancer." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-1507.

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Patella, Francesca, Zachary T. Schug, Erez Persi, Lisa J. Neilson, Zahra Erami, Daniele Avanzato, Federica Maione, et al. "Abstract B17: In-depth proteomics unveils fatty acid oxidation role in controlling vascular permeability." In Abstracts: AACR Special Conference: Tumor Angiogenesis and Vascular Normalization: Bench to Bedside to Biomarkers; March 5-8, 2015; Orlando, FL. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-8514.tumang15-b17.

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Gu, L., J. L. Casey, D. Davis, and A. B. Carter. "MCU Modulates Transcriptional Network for PGC-1a-Mediated Fatty Acid Oxidation During Pulmonary Fibrosis." 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.a7223.

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Lee, M. H., J. Harral, D. Hernandez-Saavedra, L. Sanders, A. Gandjeva, B. B. Graham, and R. M. Tuder. "Pathogenetic Role of Fatty Acid Oxidation in Human Lungs Affected by Pulmonary Arterial Hypertension." 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.a5871.

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Rada, Miran, Jennifer Cha, Jessica Sage, Bo Zhou, Wei Yang, Sandra Orsulic, and Dong-Joo Cheon. "Abstract A16: COL11A1 confers cisplatin resistance through fatty acid oxidation in ovarian cancer cells." In Abstracts: AACR Special Conference: Addressing Critical Questions in Ovarian Cancer Research and Treatment; October 1-4, 2017; Pittsburgh, PA. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1557-3265.ovca17-a16.

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Bitler, Benjamin Guy, Brandon Sawyer, Lubna Qamar, Jennifer K. Richer, Kian Behbakht, and Isabel R. Schlaepfer. "Abstract 5029: Targeting fatty acid oxidation to promote anoikis and inhibit ovarian cancer progression." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-5029.

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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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Abstract:
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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Reports on the topic "Fatty acid �-oxidation"

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Fillmore, Natasha, Osama Abo Alrob, and Gary D. Lopaschuk. Fatty Acid beta-Oxidation. AOCS, July 2011. http://dx.doi.org/10.21748/lipidlibrary.39187.

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Yamane, Koji, Kiyoshi Kawasaki, Kazutaka Sone, Takeru Hara, and Tirto Prakoso. A Fundamental Study for the Prevention of Biodiesel Fuel Oxidation Deterioration (1st Report)~Unsaturated Fatty Acid Methyl Esters and Thermal Oxidation Characteristics. Warrendale, PA: SAE International, September 2005. http://dx.doi.org/10.4271/2005-08-0556.

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Wilson, George R. Diesel Lubricity Additive Effect on Jet Fuel Thermal Oxidative Stability with Supplementary Information on Fatty Acid Methyl Ester and Jet Engine Nozzle Performance. Coordinating Research Council, Inc., August 2011. http://dx.doi.org/10.21813/crcav-03-04.

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