Journal articles: '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 Î±-Tocopherol Supply on Tissue Fatty Acid Profiles, Î±-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 Î±-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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Gonzalez-Hurtado, Elsie, Jieun Lee, Joseph Choi, Ebru S. Selen Alpergin, Samuel L. Collins, Maureen R. Horton, and Michael J. Wolfgang. "Loss of macrophage fatty acid oxidation does not potentiate systemic metabolic dysfunction." American Journal of Physiology-Endocrinology and Metabolism 312, no. 5 (May 1, 2017): E381—E393. http://dx.doi.org/10.1152/ajpendo.00408.2016.

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Fatty acid oxidation in macrophages has been suggested to play a causative role in high-fat diet-induced metabolic dysfunction, particularly in the etiology of adipose-driven insulin resistance. To understand the contribution of macrophage fatty acid oxidation directly to metabolic dysfunction in high-fat diet-induced obesity, we generated mice with a myeloid-specific knockout of carnitine palmitoyltransferase II (CPT2 Mϕ-KO), an obligate step in mitochondrial long-chain fatty acid oxidation. While fatty acid oxidation was clearly induced upon IL-4 stimulation, fatty acid oxidation-deficient CPT2 Mϕ-KO bone marrow-derived macrophages displayed canonical markers of M2 polarization following IL-4 stimulation in vitro. In addition, loss of macrophage fatty acid oxidation in vivo did not alter the progression of high-fat diet-induced obesity, inflammation, macrophage polarization, oxidative stress, or glucose intolerance. These data suggest that although IL-4-stimulated alternatively activated macrophages upregulate fatty acid oxidation, fatty acid oxidation is dispensable for macrophage polarization and high-fat diet-induced metabolic dysfunction. Macrophage fatty acid oxidation likely plays a correlative, rather than causative, role in systemic metabolic dysfunction.

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Nickerson, James G., Hakam Alkhateeb, Carley R. Benton, James Lally, Jennifer Nickerson, Xiao-Xia Han, Meredith H. Wilson, et al. "Greater Transport Efficiencies of the Membrane Fatty Acid Transporters FAT/CD36 and FATP4 Compared with FABPpm and FATP1 and Differential Effects on Fatty Acid Esterification and Oxidation in Rat Skeletal Muscle." Journal of Biological Chemistry 284, no. 24 (April 20, 2009): 16522–30. http://dx.doi.org/10.1074/jbc.m109.004788.

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In selected mammalian tissues, long chain fatty acid transporters (FABPpm, FAT/CD36, FATP1, and FATP4) are co-expressed. There is controversy as to whether they all function as membrane-bound transporters and whether they channel fatty acids to oxidation and/or esterification. Among skeletal muscles, the protein expression of FABPpm, FAT/CD36, and FATP4, but not FATP1, correlated highly with the capacities for oxidative metabolism (r ≥ 0.94), fatty acid oxidation (r ≥ 0.88), and triacylglycerol esterification (r ≥ 0.87). We overexpressed independently FABPpm, FAT/CD36, FATP1, and FATP4, within a normal physiologic range, in rat skeletal muscle, to determine the effects on fatty acid transport and metabolism. Independent overexpression of each fatty acid transporter occurred without altering either the expression or plasmalemmal content of other fatty acid transporters. All transporters increased fatty acid transport, but FAT/CD36 and FATP4 were 2.3- and 1.7-fold more effective than FABPpm and FATP1, respectively. Fatty acid transporters failed to alter the rates of fatty acid esterification into triacylglycerols. In contrast, all transporters increased the rates of long chain fatty acid oxidation, but the effects of FABPpm and FAT/CD36 were 3-fold greater than for FATP1 and FATP4. Thus, fatty acid transporters exhibit different capacities for fatty acid transport and metabolism. In vivo, FAT/CD36 and FATP4 are the most effective fatty acid transporters, whereas FABPpm and FAT/CD36 are key for stimulating fatty acid oxidation.

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Brivet, Michèle, Abdelhamid Slama, Jean-Marie Saudubray, Alain Legrand, and Alain Lemonnier. "Rapid Diagnosis of Long Chain and Medium Chain Fatty Acid Oxidation Disorders Using Lymphocytes." Annals of Clinical Biochemistry: International Journal of Laboratory Medicine 32, no. 2 (March 1995): 154–59. http://dx.doi.org/10.1177/000456329503200204.

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A method based on the release of tritiated water from [9,10(n)-3H] palmitic and myristic acids previously described for fibroblasts, was adapted for lymphocytes for the rapid diagnosis of fatty acid oxidation disorders. Optimal concentrations for both substrates and linearity of the assay were established. Normal values were established in control subjects of different age groups (58 children and 117 adults) and 16 patients with known fatty acid oxidation disorders were tested. Tritiated water production from patients' lymphocytes was expressed as a ratio between residual oxidations of palmitate and myristate and the results show that this method allows good differentiation between long chain and medium chain fatty acid oxidation defects.

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Ballantyne, J. S., D. Flannigan, and T. B. White. "Effects of Temperature on the Oxidation of Fatty Acids, Acyl Carnitines, and Ketone Bodies by Mitochondria Isolated from the Liver of the Lake Charr, Salvelinus namaycush." Canadian Journal of Fisheries and Aquatic Sciences 46, no. 6 (June 1, 1989): 950–54. http://dx.doi.org/10.1139/f89-122.

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Mitochondria isolated from the liver of the Lake Charr Salvelinus namaycush oxidize a wide range of acyl chain lengths of fatty acids and acyl carnitines at 1, 10, and 20 °C. For most carbon chain lengths the relative importance of carnitine-dependent fatty acid oxidation increases with increasing temperature due to greater thermal enhancement of carnitine-dependent oxidation. At low temperatures the rate of carnitine-independent fatty acid oxidation rivals that of carnitine-dependent oxidation. Therefore, acute temperature shifts during excursions above the thermocline would have important effects on the oxidation of dietary and depot lipids. Temperature does not substantially affect the chain length preference for fatty acid oxidation either in the presence or absence of carnitine, suggesting acclimation-induced changes in substrate specificity of fatty acid oxidation may not be necessary. The importance of β-hydroxybutyrate as an oxidative substrate increases at low temperatures relative to other substrates while acetoacetate oxidation is greater than that of β-hydroxybutyrate at 10 and 20 °C. Altered ketone body metabolism may play a role in regulating cholesterol levels to alter membrane fluidity.

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Chen, Xiaocui, Lin Shang, Senwen Deng, Ping Li, Kai Chen, Ting Gao, Xiao Zhang, Zhilan Chen, and Jia Zeng. "Peroxisomal oxidation of erucic acid suppresses mitochondrial fatty acid oxidation by stimulating malonyl-CoA formation in the rat liver." Journal of Biological Chemistry 295, no. 30 (June 3, 2020): 10168–79. http://dx.doi.org/10.1074/jbc.ra120.013583.

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Feeding of rapeseed (canola) oil with a high erucic acid concentration is known to cause hepatic steatosis in animals. Mitochondrial fatty acid oxidation plays a central role in liver lipid homeostasis, so it is possible that hepatic metabolism of erucic acid might decrease mitochondrial fatty acid oxidation. However, the precise mechanistic relationship between erucic acid levels and mitochondrial fatty acid oxidation is unclear. Using male Sprague–Dawley rats, along with biochemical and molecular biology approaches, we report here that peroxisomal β-oxidation of erucic acid stimulates malonyl-CoA formation in the liver and thereby suppresses mitochondrial fatty acid oxidation. Excessive hepatic uptake and peroxisomal β-oxidation of erucic acid resulted in appreciable peroxisomal release of free acetate, which was then used in the synthesis of cytosolic acetyl-CoA. Peroxisomal metabolism of erucic acid also remarkably increased the cytosolic NADH/NAD+ ratio, suppressed sirtuin 1 (SIRT1) activity, and thereby activated acetyl-CoA carboxylase, which stimulated malonyl-CoA biosynthesis from acetyl-CoA. Chronic feeding of a diet including high-erucic-acid rapeseed oil diminished mitochondrial fatty acid oxidation and caused hepatic steatosis and insulin resistance in the rats. Of note, administration of a specific peroxisomal β-oxidation inhibitor attenuated these effects. Our findings establish a cross-talk between peroxisomal and mitochondrial fatty acid oxidation. They suggest that peroxisomal oxidation of long-chain fatty acids suppresses mitochondrial fatty acid oxidation by stimulating malonyl-CoA formation, which might play a role in fatty acid–induced hepatic steatosis and related metabolic disorders.

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Chen, Chuck T., Marc-Olivier Trépanier, Kathryn E. Hopperton, Anthony F. Domenichiello, Mojgan Masoodi, and Richard P. Bazinet. "Inhibiting Mitochondrial β-Oxidation Selectively Reduces Levels of Nonenzymatic Oxidative Polyunsaturated Fatty Acid Metabolites in the Brain." Journal of Cerebral Blood Flow & Metabolism 34, no. 3 (December 11, 2013): 376–79. http://dx.doi.org/10.1038/jcbfm.2013.221.

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Schönfeld and Reiser recently hypothesized that fatty acid β-oxidation is a source of oxidative stress in the brain. To test this hypothesis, we inhibited brain mitochondrial β-oxidation with methyl palmoxirate (MEP) and measured oxidative polyunsaturated fatty acid (PUFA) metabolites in the rat brain. Upon MEP treatment, levels of several nonenzymatic auto-oxidative PUFA metabolites were reduced with few effects on enzymatically derived metabolites. Our finding confirms the hypothesis that reduced fatty acid β-oxidation decreases oxidative stress in the brain and β-oxidation inhibitors may be a novel therapeutic approach for brain disorders associated with oxidative stress.

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Orkusz, Agnieszka, Wioletta Wolańska, and Urszula Krajinska. "The Assessment of Changes in the Fatty Acid Profile and Dietary Indicators Depending on the Storage Conditions of Goose Meat." Molecules 26, no. 17 (August 24, 2021): 5122. http://dx.doi.org/10.3390/molecules26175122.

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The deterioration of food quality due to lipid oxidation is a serious problem in the food sector. Oxidation reactions adversely affect the physicochemical properties of food, worsening its quality. Lipid oxidation products are formed during the production, processing, and storage of food products. In the human diet, the sources of lipid oxidation products are all fat-containing products, including goose meat with a high content of polyunsaturated fatty acids. This study aims at comparing the fatty acid profile of goose breast muscle lipids depending on the storage conditions: type of atmosphere, temperature, and storage time. Three-way variance analysis was used to evaluate changes in the fatty acids profile occurring in goose meat. The health aspect of fatty acid oxidation of goose meat is also discussed. In general, the fatty acid composition changed significantly during storage in the meat packed in the high-oxygen modified atmosphere at different temperatures (1 °C and 4 °C). Higher temperature led to a higher degree of lipid oxidation and nutrient loss. During the storage of samples in vacuum, no changes in the fatty acid content and dietary indices were found, regardless of the storage temperature, which indicates that the anaerobic atmosphere ensured the oxidative stability of goose meat during 11 days of refrigerated storage.

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Abo Alrob, Osama, and Gary D. Lopaschuk. "Role of CoA and acetyl-CoA in regulating cardiac fatty acid and glucose oxidation." Biochemical Society Transactions 42, no. 4 (August 1, 2014): 1043–51. http://dx.doi.org/10.1042/bst20140094.

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CoA (coenzyme A) and its derivatives have a critical role in regulating cardiac energy metabolism. This includes a key role as a substrate and product in the energy metabolic pathways, as well as serving as an allosteric regulator of cardiac energy metabolism. In addition, the CoA ester malonyl-CoA has an important role in regulating fatty acid oxidation, secondary to inhibiting CPT (carnitine palmitoyltransferase) 1, a key enzyme involved in mitochondrial fatty acid uptake. Alterations in malonyl-CoA synthesis by ACC (acetyl-CoA carboxylase) and degradation by MCD (malonyl-CoA decarboxylase) are important contributors to the high cardiac fatty acid oxidation rates seen in ischaemic heart disease, heart failure, obesity and diabetes. Additional control of fatty acid oxidation may also occur at the level of acetyl-CoA involvement in acetylation of mitochondrial fatty acid β-oxidative enzymes. We find that acetylation of the fatty acid β-oxidative enzymes, LCAD (long-chain acyl-CoA dehydrogenase) and β-HAD (β-hydroxyacyl-CoA dehydrogenase) is associated with an increase in activity and fatty acid oxidation in heart from obese mice with heart failure. This is associated with decreased SIRT3 (sirtuin 3) activity, an important mitochondrial deacetylase. In support of this, cardiac SIRT3 deletion increases acetylation of LCAD and β-HAD, and increases cardiac fatty acid oxidation. Acetylation of MCD is also associated with increased activity, decreases malonyl-CoA levels and an increase in fatty acid oxidation. Combined, these data suggest that malonyl-CoA and acetyl-CoA have an important role in mediating the alterations in fatty acid oxidation seen in heart failure.

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Lopaschuk, Gary D. "Fatty Acid Oxidation and Its Relation with Insulin Resistance and Associated Disorders." Annals of Nutrition and Metabolism 68, Suppl. 3 (2016): 15–20. http://dx.doi.org/10.1159/000448357.

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Alterations in muscle fatty acid metabolism have been implicated in mediating the severity of insulin resistance. In the insulin resistant heart fatty acids are favored as an energy source over glucose, which is thus associated with increased fatty acid oxidation, and an overall decrease in glycolysis and glucose oxidation. In addition, excessive uptake and beta-oxidation of fatty acids in obesity and diabetes can compromise cardiac function. In animal studies, mice fed a high fat diet (HFD) show cardiac insulin resistance in which the accumulation of intra-myocardial diacylglycerol has been implicated, likely involving parallel signaling pathways. A HFD also results in accumulation of fatty acid oxidation byproducts in muscle, further contributing to insulin resistance. Carnitine acetyltransferase (CrAT) has an essential role in the cardiomyocyte because of its need for large amounts of carnitine. In the cardiomyocyte, carnitine switches energy substrate preference in the heart from fatty acid oxidation to glucose oxidation. This carnitine-induced switch in fatty acid oxidation to glucose oxidation is due to the presence of cytosolic CrAT and reverse CrAT activity. Accordingly, inhibition of fatty acid oxidation, or stimulation of CrAT, may be a novel approach to treatment of insulin resistance.

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Martı́nez, G., G. Jiménez-Sánchez, P. Divry, C. Vianey-Saban, E. Riudor, M. Rodés, P. Briones, and A. Ribes. "Plasma free fatty acids in mitochondrial fatty acid oxidation defects." Clinica Chimica Acta 267, no. 2 (November 1997): 143–54. http://dx.doi.org/10.1016/s0009-8981(97)00130-7.

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&NA;. "Ibuprofen inhibits fatty acid oxidation,." Reactions Weekly &NA;, no. 536 (February 1995): 3. http://dx.doi.org/10.2165/00128415-199505360-00006.

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Kompare, Michelle, and William B. Rizzo. "Mitochondrial Fatty-Acid Oxidation Disorders." Seminars in Pediatric Neurology 15, no. 3 (September 2008): 140–49. http://dx.doi.org/10.1016/j.spen.2008.05.008.

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Srere, Paul A., and Balazs Sumegi. "Processivity and fatty acid oxidation." Biochemical Society Transactions 22, no. 2 (May 1, 1994): 446–50. http://dx.doi.org/10.1042/bst0220446.

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YAQOOB, PARVEEN, ERIC A. NEWSHOLME, and PHILIP C. CALDER. "Fatty acid oxidation by lymphocytes." Biochemical Society Transactions 22, no. 2 (May 1, 1994): 116S. http://dx.doi.org/10.1042/bst022116s.

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Nyhan, William L. "Abnormalities of Fatty Acid Oxidation." New England Journal of Medicine 319, no. 20 (November 17, 1988): 1344–46. http://dx.doi.org/10.1056/nejm198811173192008.

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Schulz, Horst. "Inhibitors of fatty acid oxidation." Life Sciences 40, no. 15 (April 1987): 1443–49. http://dx.doi.org/10.1016/0024-3205(87)90375-4.

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Auvin, Stéphane. "Fatty acid oxidation and epilepsy." Epilepsy Research 100, no. 3 (July 2012): 224–28. http://dx.doi.org/10.1016/j.eplepsyres.2011.05.022.

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Romijn, J. A., E. F. Coyle, L. S. Sidossis, X. J. Zhang, and R. R. Wolfe. "Relationship between fatty acid delivery and fatty acid oxidation during strenuous exercise." Journal of Applied Physiology 79, no. 6 (December 1, 1995): 1939–45. http://dx.doi.org/10.1152/jappl.1995.79.6.1939.

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To evaluate the extent to which decreased plasma free fatty acid (FFA) concentration contributes to the relatively low rates of fat oxidation during high-intensity exercise, we studied FFA metabolism in six endurance-trained cyclists during 20–30 min of exercise [85% of maximal O2 uptake (VO2max)]. They were studied on two occasions: once during a control trial when plasma FFA concentration is normally low and again when plasma FFA concentration was maintained between 1 and 2 mM by intravenous infusion of lipid (Intralipid) and heparin. During the 20–30 min of exercise, fat and carbohydrate oxidation were measured by indirect calorimetry, and the rates of appearance (Ra) of plasma FFA and glucose were determined by the constant infusion of [6,6–2H2]glucose and [2H2]palmitate. Lipid-heparin infusion did not influence the Ra or rate of disappearance of glucose. During exercise in the control trial, Ra FFA failed to increase above resting levels (11.0 +/- 1.2 and 12.4 +/- 1.7 mumol.kg-1.min-1 for rest and exercise, respectively) and plasma FFA concentration dropped from a resting value of 0.53 +/- 0.08 to 0.29 +/- 0.02 mM. The restoration of plasma FFA concentration resulted in a 27% increase in total fat oxidation (26.7 +/- 2.6 vs. 34.0 +/- 4.4 mumol.kg-1.min-1, P < 0.05) with a concomitant reduction in carbohydrate oxidation, apparently due to a 15% (P < 0.05) reduction in muscle glycogen utilization. However, the elevation of plasma FFA concentration during exercise at 85% VO2max only partially restored fat oxidation compared with the levels observed during exercise at 65% VO2max. These findings indicate that fat oxidation is normally impaired during exercise at 85% VO2max because of the failure of FFA mobilization to increase above resting levels, but this explains only part of the decline in fat oxidation when exercise intensity is increased from 65 to 85% VO2max.

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Momken, Iman, Adrian Chabowski, Ellen Dirkx, Miranda Nabben, Swati S. Jain, Jay T. McFarlan, Jan F. C. Glatz, Joost J. F. P. Luiken, and Arend Bonen. "A new leptin-mediated mechanism for stimulating fatty acid oxidation: a pivotal role for sarcolemmal FAT/CD36." Biochemical Journal 474, no. 1 (December 22, 2016): 149–62. http://dx.doi.org/10.1042/bcj20160804.

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Leptin stimulates fatty acid oxidation in muscle and heart; but, the mechanism by which these tissues provide additional intracellular fatty acids for their oxidation remains unknown. We examined, in isolated muscle and cardiac myocytes, whether leptin, via AMP-activated protein kinase (AMPK) activation, stimulated fatty acid translocase (FAT/CD36)-mediated fatty acid uptake to enhance fatty acid oxidation. In both mouse skeletal muscle and rat cardiomyocytes, leptin increased fatty acid oxidation, an effect that was blocked when AMPK phosphorylation was inhibited by adenine 9-β-d-arabinofuranoside or Compound C. In wild-type mice, leptin induced the translocation of FAT/CD36 to the plasma membrane and increased fatty acid uptake into giant sarcolemmal vesicles and into cardiomyocytes. In muscles of FAT/CD36-KO mice, and in cardiomyocytes in which cell surface FAT/CD36 action was blocked by sulfo-N-succinimidyl oleate, the leptin-stimulated influx of fatty acids was inhibited; concomitantly, the normal leptin-stimulated increase in fatty acid oxidation was also prevented, despite the normal leptin-induced increase in AMPK phosphorylation. Conversely, in muscle of AMPK kinase-dead mice, leptin failed to induce the translocation of FAT/CD36, along with a failure to stimulate fatty acid uptake and oxidation. Similarly, when siRNA was used to reduce AMPK in HL-1 cardiomyocytes, leptin failed to induce the translocation of FAT/CD36. Our studies have revealed a novel mechanism of leptin-induced fatty acid oxidation in muscle tissue; namely, this process is dependent on the activation of AMPK to induce the translocation of FAT/CD36 to the plasma membrane, thereby stimulating fatty acid uptake. Without increasing this leptin-stimulated, FAT/CD36-dependent fatty acid uptake process, leptin-stimulated AMPK phosphorylation does not enhance fatty acid oxidation.

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Legako, Jerrad F. "114 Effect of altering fatty acid profile on fresh meat palatability." Journal of Animal Science 97, Supplement_3 (December 2019): 108–9. http://dx.doi.org/10.1093/jas/skz258.223.

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Abstract Fatty acids in fresh meat contribute to palatability in many ways. However, fatty acids primarily influence flavor and juiciness. Perceived juiciness is impacted through lubrication by fatty acids and stimulation of saliva during mastication. Therefore, the content of fatty acids primarily impacts juiciness. However, for flavor, fatty acid content and composition are each important. Volatile flavor compounds have been demonstrated to have greater expression as overall fatty acid content increases. This may be through the retention of fat-soluble volatile compounds leading up to consumption. In addition to content, fatty acid composition may also be altered. Factors, such as, species, muscle, and diet dictate fatty acid composition. In general, these factors mediate proportions of major fatty acids and thus alter levels of fatty acid saturation. As fatty acid saturation is decreased, there is greater propensity towards oxidation. Greater fatty acid oxidation generally leads to negative off-flavors. During storage and handling there is opportunity for less saturated fresh meats to undergo oxidation, ultimately impacting flavor. To summarize, both fatty acid content and composition play roles in fresh meat palatability. Understanding the role of fatty acids in palatability helps equip processors and meat scientist to maintain or improve meat palatability.

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Surina, D. M., W. Langhans, R. Pauli, and C. Wenk. "Meal composition affects postprandial fatty acid oxidation." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 264, no. 6 (June 1, 1993): R1065—R1070. http://dx.doi.org/10.1152/ajpregu.1993.264.6.r1065.

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The influence of macronutrient content of a meal on postprandial fatty acid oxidation was investigated in 13 Caucasian males after consumption of a high-fat (HF) breakfast (33% carbohydrate, 52% fat, 15% protein) and after an equicaloric high-carbohydrate (HC) breakfast (78% carbohydrate, 6% fat, 15% protein). The HF breakfast contained short- and medium-chain fatty acids, as well as long-chain fatty acids. Respiratory quotient (RQ) and plasma beta-hydroxybutyrate (BHB) were measured during the 3 h after the meal as indicators of whole body substrate oxidation and hepatic fatty acid oxidation, respectively. Plasma levels of free fatty acids (FFA), triglycerides, glucose, insulin, and lactate were also determined because of their relationship to nutrient utilization. RQ was significantly lower and plasma BHB was higher after the HF breakfast than after the HC breakfast, implying that more fat is burned in general and specifically in the liver after an HF meal. As expected, plasma FFA and triglycerides were higher after the HF meal, and insulin and lactate were higher after the HC meal. In sum, oxidation of ingested fat occurred in response to a single HF meal.

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Ceddia, RB, and R. Curi. "Leptin controls the fate of fatty acids in isolated rat white adipocytes." Journal of Endocrinology 175, no. 3 (December 1, 2002): 735–44. http://dx.doi.org/10.1677/joe.0.1750735.

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Leptin directly increases the rate of exogenous glucose and fatty acids oxidation in isolated adipocytes. However, the effects of leptin on fatty acid metabolism in white adipose tIssue have not been examined in detail. Here, we report that in adipocytes incubated for 6 h in the presence of leptin (10 ng/ml), the insulin-stimulated de novo fatty acid synthesis was inhibited by 36% (P<0.05), while the exogenous oxidation of acetic and oleic acids was increased by 50% and 76% respectively. Interestingly, leptin did not alter the oxidation of intracellular fatty acids. Leptin-incubated cells presented a 16-fold increase in the incorporation of oleic acid into triglyceride (TG) and a 123% increase in the intracellular TG hydrolysis (as measured by free fatty acids release). Fatty acid-TG cycling was not affected by leptin. By employing fatty acids radiolabeled with (3)H and (14)C, we could determine the concomitant influx of fatty acids (incorporation of fatty acids into TG) and efflux of fatty acids (intracellular fatty acids oxidation and free fatty acids release) in the incubated cells. Leptin increased by 30% the net efflux of fatty acids from adipocytes. We conclude that leptin directly inhibits de novo synthesis of fatty acids and increases the release and oxidation of fatty acids in isolated rat adipocytes. These direct energy-dissipating effects of leptin may play an important role in reducing accumulation of fatty acids into TG of rat adipose cells.

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Longnus, Sarah L., Richard B. Wambolt, Rick L. Barr, Gary D. Lopaschuk, and Michael F. Allard. "Regulation of myocardial fatty acid oxidation by substrate supply." American Journal of Physiology-Heart and Circulatory Physiology 281, no. 4 (October 1, 2001): H1561—H1567. http://dx.doi.org/10.1152/ajpheart.2001.281.4.h1561.

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We tested the hypothesis that myocardial substrate supply regulates fatty acid oxidation independent of changes in acetyl-CoA carboxylase (ACC) and 5′-AMP-activated protein kinase (AMPK) activities. Fatty acid oxidation was measured in isolated working rat hearts exposed to different concentrations of exogenous long-chain (0.4 or 1.2 mM palmitate) or medium-chain (0.6 or 2.4 mM octanoate) fatty acids. Fatty acid oxidation was increased with increasing exogenous substrate concentration in both palmitate and octanoate groups. Malonyl-CoA content only rose as acetyl-CoA supply from octanoate oxidation increased. The increases in octanoate oxidation and malonyl-CoA content were independent of changes in ACC and AMPK activity, except that ACC activity increased with very high acetyl-CoA supply levels. Our data suggest that myocardial substrate supply is the primary mechanism responsible for alterations in fatty acid oxidation rates under nonstressful conditions and when substrates are present at physiological concentrations. More extreme variations in substrate supply lead to changes in fatty acid oxidation by the additional involvement of intracellular regulatory pathways.

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Han, Xiao-Xia, Adrian Chabowski, Narendra N. Tandon, Jorge Calles-Escandon, Jan F. C. Glatz, Joost J. F. P. Luiken, and Arend Bonen. "Metabolic challenges reveal impaired fatty acid metabolism and translocation of FAT/CD36 but not FABPpm in obese Zucker rat muscle." American Journal of Physiology-Endocrinology and Metabolism 293, no. 2 (August 2007): E566—E575. http://dx.doi.org/10.1152/ajpendo.00106.2007.

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We examined, in muscle of lean and obese Zucker rats, basal, insulin-induced, and contraction-induced fatty acid transporter translocation and fatty acid uptake, esterification, and oxidation. In lean rats, insulin and contraction induced the translocation of the fatty acid transporter FAT/CD36 (43 and 41%, respectively) and plasma membrane-associated fatty acid binding protein (FABPpm; 19 and 60%) and increased fatty acid uptake (63 and 40%, respectively). Insulin and contraction increased lean muscle palmitate esterification and oxidation 72 and 61%, respectively. In obese rat muscle, basal levels of sarcolemmal FAT/CD36 (+33%) and FABPpm (+14%) and fatty acid uptake (+30%) and esterification (+32%) were increased, whereas fatty acid oxidation was reduced (−28%). Insulin stimulation of obese rat muscle increased plasmalemmal FABPpm (+15%) but not plasmalemmal FAT/CD36, blunted fatty acid uptake and esterification, and failed to reduce fatty acid oxidation. In contracting obese rat muscle, the increases in fatty acid uptake and esterification and FABPpm translocation were normal, but FAT/CD36 translocation was impaired and fatty acid oxidation was blunted. There was no relationship between plasmalemmal fatty acid transporters and palmitate partitioning. In conclusion, fatty acid metabolism is impaired at several levels in muscles of obese Zucker rats; specifically, they are 1) insulin resistant with respect to FAT/CD36 translocation and fatty acid uptake, esterification, and oxidation and 2) contraction resistant with respect to fatty acid oxidation and FAT/CD36 translocation, but, conversely, 3) obese muscles are neither insulin nor contraction resistant at the level of FABPpm. Finally, 4) there is no evidence that plasmalemmal fatty acid transporters contribute to the channeling of fatty acids to specific metabolic destinations within the muscle.

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Parsons, H. G., and V. C. Dias. "Intramitochondrial fatty acid metabolism: riboflavin deficiency and energy production." Biochemistry and Cell Biology 69, no. 7 (July 1, 1991): 490–97. http://dx.doi.org/10.1139/o91-073.

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Inborn errors of fatty acid β-oxidation have contributed significantly to our understanding of intracellular fatty acid metabolism. The first intramitochondrial step in β-oxidation of fatty acyl-CoA of different chain lengths is catalyzed by the three chain length specific acyl-CoA dehydrogenases. Inherited deficiency of these enzymes has been reported. Some are riboflavin responsive. The first step of fatty acid oxidation is reviewed with specific emphasis on β-oxidation in newborn infants, rendered riboflavin deficient by phototherapy. Given that medium chain fatty acids are not stored as triacylglycerols and undergo rapid β-oxidation, they have been proposed as superior substrates compared with long chain triglycerides in times of metabolic stress. This review also examines medium chain triglycerides as an alternate energy source. When medium chain triglycerides were fed as 50% of total energy, glucose sparing was present with little loss of energy as dicarboxylic acids.Key words: β-oxidation, acyl-CoA dehydrogenase, riboflavin, medium chain triglycerides, dicarboxylic acids.

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BERGE, Rolf K., Lise MADSEN, Hege VAAGENES, Karl Johan TRONSTAD, Martin GÖTTLICHER, and Arild C. RUSTAN. "In contrast with docosahexaenoic acid, eicosapentaenoic acid and hypolipidaemic derivatives decrease hepatic synthesis and secretion of triacylglycerol by decreased diacylglycerol acyltransferase activity and stimulation of fatty acid oxidation." Biochemical Journal 343, no. 1 (September 24, 1999): 191–97. http://dx.doi.org/10.1042/bj3430191.

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Hypolipidaemic fatty acid derivatives and polyunsaturated fatty acids decrease concentrations of plasma triacylglycerol by mechanisms that are not fully understood. Because poor susceptibility to β- and/or ω-oxidation is apparently a determinant of the peroxisome proliferating and hypolipidaemic capacity of fatty acids and derivatives, the relative importance of activation of the peroxisome-proliferator-activated receptor α (PPARα), fatty acid oxidation and triacylglycerol synthesis were examined. We have compared the effects of differentially β-oxidizable fatty acids on these parameters in primary cultures of rat hepatocytes. Tetradecylthioacetic acid (TTA), 2-methyleicosapentaenoic acid and 3-thia-octadecatetraenoic acid, which are non-β-oxidizable fatty acid derivatives, were potent activators of a glucocorticoid receptor (GR)-PPARα chimaera. This activation was paradoxically reflected in an substantially increased oxidation of [1-14C]palmitic acid and/or oleic acid. The incorporation of [1-14C]palmitic acid and/or oleic acid into cell-associated and secreted triacylglycerol was decreased by 15-20% and 30% respectively with these non-β-oxidizable fatty acid derivatives. The CoA ester of TTA inhibited the esterification of 1,2-diacylglycerol in rat liver microsomes. Both eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) activated GR-PPARα. EPA increased the oxidation of [1-14C]palmitic acid but DHA had no effect. The CoA ester of EPA inhibited the esterification of 1,2-diacylglycerol, whereas DHA-CoA had no effect. The ratio between synthesized triacylglycerol and diacylglycerol was lower in hepatocytes cultured with EPA in the medium compared with DHA or oleic acid, indicating a decreased conversion of diacylglycerol to triacylglycerol. Indeed, the incorporation of [1-14C]oleic acid into secreted triacylglycerol was decreased by 20% in the presence of EPA. In conclusion, a decreased availability of fatty acids for triacylglycerol synthesis by increased mitochondrial β-oxidation and decreased triacylglycerol formation caused by inhibition of diacylglycerol acyltransferase might explain the hypolipidaemic effect of TTA and EPA.

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Calles-Escandon, J., and P. Driscoll. "Free fatty acid metabolism in aerobically fit individuals." Journal of Applied Physiology 77, no. 5 (November 1, 1994): 2374–79. http://dx.doi.org/10.1152/jappl.1994.77.5.2374.

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The impact of aerobic fitness level on the production and disposal of serum free fatty acids was investigated in 26 normal young volunteers. The fitness level was ascertained by history and confirmed by determination of maximal aerobic capacity. Energy expenditure and substrate oxidation at rest were measured with indirect calorimetry. Free fatty acid turnover was measured with an infusion of [14C]palmitic acid. All tests were done > or = 48 h after the last bout of exercise. The sedentary (SED) volunteers had higher rates of systemic delivery of fatty acids than aerobically fit (FIT) individuals (532 +/- 53.4 vs. 353 +/- 62.3 mumol/min; P = 0.05). This difference was accentuated when the values were normalized to fat-free mass (9.2 +/- 0.8 and 5.9 +/- 0.98 mumol.kg-1.min-1 for SED and FIT, respectively). Fatty acid oxidation was similar between FIT and SED volunteers in absolute numbers (209 +/- 25 vs. 202 +/- 21 mumol/min, respectively; NS) as well as when normalized to fat-free mass (3.8 +/- 0.9 vs. 3.6 +/- 1.4 mumol.kg-1.min-1, respectively; NS). In contrast, the nonoxidative disposal of serum fatty acids was higher in SED (330 +/- 46.1 mumol/min) than in FIT individuals (144 +/- 52 mumol/min; P = 0.026). Thus, the ratio of nonoxidative to oxidative disposal rates of fatty acids was higher in SED than in FIT individuals (1.65 +/- 0.29 vs. 0.75 +/- 0.17; P = 0.021). The data support the hypothesis that high aerobic fitness level is associated with a low rate of systemic delivery of fatty acids at rest. Nevertheless, subjects with high aerobic fitness levels have fat oxidation at the same rate as unfit individuals.

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Stanley, William C., Eric E. Morgan, Hazel Huang, Tracy A. McElfresh, Joseph P. Sterk, Isidore C. Okere, Margaret P. Chandler, Jiefei Cheng, Jason R. B. Dyck, and Gary D. Lopaschuk. "Malonyl-CoA decarboxylase inhibition suppresses fatty acid oxidation and reduces lactate production during demand-induced ischemia." American Journal of Physiology-Heart and Circulatory Physiology 289, no. 6 (December 2005): H2304—H2309. http://dx.doi.org/10.1152/ajpheart.00599.2005.

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The rate of cardiac fatty acid oxidation is regulated by the activity of carnitine palmitoyltransferase-I (CPT-I), which is inhibited by malonyl-CoA. We tested the hypothesis that the activity of the enzyme responsible for malonyl-CoA degradation, malonyl-CoA decarboxlyase (MCD), regulates myocardial malonyl-CoA content and the rate of fatty acid oxidation during demand-induced ischemia in vivo. The myocardial content of malonyl-CoA was increased in anesthetized pigs using a specific inhibitor of MCD (CBM-301106), which we hypothesized would result in inhibition of CPT-I, reduction in fatty acid oxidation, a reciprocal activation of glucose oxidation, and diminished lactate production during demand-induced ischemia. Under normal-flow conditions, treatment with the MCD inhibitor significantly reduced oxidation of exogenous fatty acids by 82%, shifted the relationship between arterial fatty acids and fatty acid oxidation downward, and increased glucose oxidation by 50%. Ischemia was induced by a 20% flow reduction and β-adrenergic stimulation, which resulted in myocardial lactate production. During ischemia MCD inhibition elevated malonyl-CoA content fourfold, reduced free fatty acid oxidation rate by 87%, and resulted in a 50% decrease in lactate production. Moreover, fatty acid oxidation during ischemia was inversely related to the tissue malonyl-CoA content ( r = −0.63). There were no differences between groups in myocardial ATP content, the activity of pyruvate dehydrogenase, or myocardial contractile function during ischemia. Thus modulation of MCD activity is an effective means of regulating myocardial fatty acid oxidation under normal and ischemic conditions and reducing lactate production during demand-induced ischemia.

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Onay-Besikci, Arzu, and Nandakumar Sambandam. "Malonyl CoA control of fatty acid oxidation in the newborn heart in response to increased fatty acid supply." Canadian Journal of Physiology and Pharmacology 84, no. 11 (November 2006): 1215–22. http://dx.doi.org/10.1139/y06-062.

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The concentration of fatty acids in the blood or perfusate is a major determinant of the extent of myocardial fatty acid oxidation. Increasing fatty acid supply in adult rat increases myocardial fatty acid oxidation. Plasma levels of fatty acids increase post-surgery in infants undergoing cardiac bypass operation to correct congenital heart defects. How a newborn heart responds to increased fatty acid supply remains to be determined. In this study, we examined whether the tissue levels of malonyl CoA decrease to relieve the inhibition on carnitine palmitoyltransferase (CPT) I when the myocardium is exposed to higher concentrations of long-chain fatty acids in newborn rabbit heart. We then tested the contribution of the enzymes that regulate tissue levels of malonyl CoA, acetyl CoA carboxylase (ACC), and malonyl CoA decarboxylase (MCD). Our results showed that increasing fatty acid supply from 0.4 mmol/L (physiological) to 1.2 mmol/L (pathological) resulted in an increase in cardiac fatty acid oxidation rates and this was accompanied by a decrease in tissue malonyl CoA levels. The decrease in malonyl CoA was not related to any alterations in total and phosphorylated acetyl CoA carboxylase protein or the activities of acetyl CoA carboxylase and malonyl CoA decarboxylase. Our results suggest that the regulatory role of malonyl CoA remained when the hearts were exposed to high levels of fatty acids.

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Hopkins, T. A., J. R. B. Dyck, and G. D. Lopaschuk. "AMP-activated protein kinase regulation of fatty acid oxidation in the ischaemic heart." Biochemical Society Transactions 31, no. 1 (February 1, 2003): 207–12. http://dx.doi.org/10.1042/bst0310207.

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The heart relies predominantly on a balance between fatty acids and glucose to generate its energy supply. There is an important interaction between the metabolic pathways of these two substrates in the heart. When circulating levels of fatty acids are high, fatty acid oxidation can dominate over glucose oxidation as a source of energy through feedback inhibition of the glucose oxidation pathway. Following an ischaemic episode, fatty acid oxidation rates increase further, resulting in an uncoupling between glycolysis and glucose oxidation. This uncoupling results in an increased proton production, which worsens ischaemic damage. Since high rates of fatty acid oxidation can contribute to ischaemic damage by inhibiting glucose oxidation, it is important to maintain proper control of fatty acid oxidation both during and following ischaemia. An important molecule that controls myocardial fatty acid oxidation is malonyl-CoA, which inhibits uptake of fatty acids into the mitochondria. The levels of malonyl-CoA in the heart are controlled both by its synthesis and degradation. Three enzymes, namely AMP-activated protein kinase (AMPK), acetyl-CoA carboxylase (ACC) and malonyl-CoA decarboxylase (MCD), appear to be extremely important in this process. AMPK causes phosphorylation and inhibition of ACC, which reduces the production of malonyl-CoA. In addition, it is suggested that AMPK also phosphorylates and activates MCD, promoting degradation of malonyl-CoA levels. As a result malonyl-CoA levels can be dramatically altered by activation of AMPK. In ischaemia, AMPK is rapidly activated and inhibits ACC, subsequently decreasing malonyl-CoA levels and increasing fatty acid oxidation rates. The consequence of this is a decrease in glucose oxidation rates. In addition to altering malonyl-CoA levels, AMPK can also increase glycolytic rates, resulting in an increased uncoupling of glycolysis from glucose oxidation and an enhanced production of protons and lactate. This decreases cardiac efficiency and contributes to the severity of ischaemic damage. Decreasing the ischaemic-induced activation of AMPK or preventing the downstream decrease in malonyl-CoA levels may be a therapeutic approach to treating ischaemic heart disease.

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Wanders, Ronald J. A., Jasper Komen, and Stephan Kemp. "Fatty acid omega-oxidation as a rescue pathway for fatty acid oxidation disorders in humans." FEBS Journal 278, no. 2 (December 13, 2010): 182–94. http://dx.doi.org/10.1111/j.1742-4658.2010.07947.x.

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Scharrer, E., and W. Langhans. "Control of food intake by fatty acid oxidation." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 250, no. 6 (June 1, 1986): R1003—R1006. http://dx.doi.org/10.1152/ajpregu.1986.250.6.r1003.

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The role of fatty acid oxidation in the control of food intake was studied using mercaptoacetate (MA), an inhibitor of fatty acid oxidation. Food intake, plasma free fatty acids (FFA) and ketone bodies, and blood glucose were measured. Rats were fed either a low-fat (LF, 3.33% fat) or a medium-fat (MF, 18% fat) diet. At the onset of the dark phase of the lighting cycle, MA did not affect food intake in LF rats but increased it 74% in MF rats in comparison to control. Four hours after the injection the effect of MA on food intake disappeared. In the middle of the bright phase of the lighting cycle, MA increased food intake in MF rats approximately 120% up to 6 h postinjection. After MA, plasma FFA concentration was elevated, and plasma 3-hydroxybutyrate concentration was lowered, indicating that fatty acid oxidation had been successfully reduced. MA did not affect blood glucose. These results indicate fatty acid oxidation is involved in the control of food intake, at least when the dietary fat level is relatively high.

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Beverly, J. L., and R. J. Martin. "Influence of fatty acid oxidation in lateral hypothalamus on food intake and body composition." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 261, no. 2 (August 1, 1991): R339—R343. http://dx.doi.org/10.1152/ajpregu.1991.261.2.r339.

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This study tested the concept that the level of fatty acid oxidation in the ventrolateral hypothalamus (VLH) reflects peripheral energy stores and elicits compensatory responses to changes in energy balance status. Fatty acid oxidation rates in the VLH were chronically altered over a 14-day period by infusing into the VLH either 0.1 mM 4-pentenoic acid (4-PA; 5 ng/h) or 1.0 mM L-carnitine (L-Carn; 98 ng/h). Fatty acid oxidation rates in the VLH were altered to a similar extent as by overfeeding (reduced 37% by 4-PA) and dietary restriction (increased 28% by L-Carn). Diffusion of infusates was limited, since there were normal rates of fatty acid oxidation in the ventromedial hypothalamus and cortex. There were no significant effects of altering fatty acid oxidation in the VLH on food intake, body weight, body composition, or serum levels of glucose, insulin, and free fatty acids. The results of this experiment indicate that the level of fatty acid oxidation in the VLH is unlikely to independently elicit changes in food intake or peripheral metabolism.

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Górecka, M., M. Synak, L. Budohoski, J. Langfort, S. Moskalewski, and E. Żernicka. "Palmitic acid uptake by the rat soleus muscle in vitro." Biochemistry and Cell Biology 79, no. 4 (August 1, 2001): 419–24. http://dx.doi.org/10.1139/o01-028.

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The rate of fatty acid uptake, oxidation, and deposition in skeletal muscles in relation to total and unbound to albumin fatty acids concentration in the medium were investigated in the incubated rat soleus muscle. An immunohistochemical technique was applied to demonstrate whether the albumin-bound fatty acid complex from the medium penetrates well within all areas of the muscle strips. It was found that the percentage of incorporation of palmitic acid into intramuscular lipids was fairly constant, independently of the fatty acid concentration in the medium, and amounted to 6372% for triacylglycerols, 712% for diacylglycerols-monoacylglycerols, and 1926% for phospholipids. Both palmitic acid incorporation into the muscle triacylglycerol stores and its oxidation to CO2closely correlated with an increase in both total and unbound to albumin fatty acid concentrations in the incubation medium. Under conditions of increased total but constant unbound to albumin palmitic acid concentrations, the incorporation of palmitic acid into triacylglycerols and its oxidation to CO2were also increased, but to a lower extent. This supports the hypothesis that the cellular fatty acid metabolism depends not only on the availability of fatty acids unbound to albumin, but also on the availability of fatty acids complexed to albumin.Key words: skeletal muscle, fatty acids, triacylglycerols, phospholipids.

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Robergs, R. A., and C. Frankel. "Relationship between fatty acid delivery and fatty acid oxidation during exercise." Journal of Applied Physiology 81, no. 3 (September 1, 1996): 1450–52. http://dx.doi.org/10.1152/jappl.1996.81.3.1450.

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Veerkamp, J. H., and H. T. B. van Moerkerk. "Fatty acid-binding protein and its relation to fatty acid oxidation." Molecular and Cellular Biochemistry 123, no. 1-2 (June 1993): 101–6. http://dx.doi.org/10.1007/bf01076480.

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Song, Jae-Eun, Tiago C. Alves, Bernardo Stutz, Matija Šestan-Peša, Nicole Kilian, Sungho Jin, Sabrina Diano, Richard G. Kibbey, and Tamas L. Horvath. "Mitochondrial Fission Governed by Drp1 Regulates Exogenous Fatty Acid Usage and Storage in Hela Cells." Metabolites 11, no. 5 (May 18, 2021): 322. http://dx.doi.org/10.3390/metabo11050322.

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In the presence of high abundance of exogenous fatty acids, cells either store fatty acids in lipid droplets or oxidize them in mitochondria. In this study, we aimed to explore a novel and direct role of mitochondrial fission in lipid homeostasis in HeLa cells. We observed the association between mitochondrial morphology and lipid droplet accumulation in response to high exogenous fatty acids. We inhibited mitochondrial fission by silencing dynamin-related protein 1(DRP1) and observed the shift in fatty acid storage-usage balance. Inhibition of mitochondrial fission resulted in an increase in fatty acid content of lipid droplets and a decrease in mitochondrial fatty acid oxidation. Next, we overexpressed carnitine palmitoyltransferase-1 (CPT1), a key mitochondrial protein in fatty acid oxidation, to further examine the relationship between mitochondrial fatty acid usage and mitochondrial morphology. Mitochondrial fission plays a role in distributing exogenous fatty acids. CPT1A controlled the respiratory rate of mitochondrial fatty acid oxidation but did not cause a shift in the distribution of fatty acids between mitochondria and lipid droplets. Our data reveals a novel function for mitochondrial fission in balancing exogenous fatty acids between usage and storage, assigning a role for mitochondrial dynamics in control of intracellular fuel utilization and partitioning.

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Sidossis, L. S., and R. R. Wolfe. "Glucose and insulin-induced inhibition of fatty acid oxidation: the glucose-fatty acid cycle reversed." American Journal of Physiology-Endocrinology and Metabolism 270, no. 4 (April 1, 1996): E733—E738. http://dx.doi.org/10.1152/ajpendo.1996.270.4.e733.

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In this study we have investigated a hypothesis that proposes the reverse of the so-called "glucose-fatty acid cycle, " i.e., that accelerated carbohydrate metabolism directly inhibits fatty acid oxidation. We studied normal volunteers in the basal state and during a hyperinsulinemic, hyperglycemic clamp (plasma insulin = 1,789 +/- 119 pmol/l, plasma glucose = 7.7 +/- 0.2 mmol/l). We quantified fat oxidation using indirect calorimetry and stable isotopes ([1-13C]oleate). Plasma oleate enrichment and free fatty acid (FFA) concentration were kept constant by means of infusion of lipids and heparin. Glucose oxidation increased from basal 6.2 +/- 0.8 to 22.3 +/- 1.4 mumol.kg-1.min-1 during the clamp (P < 0.01). Total (indirect calorimetry) and plasma fatty acid oxidation (isotopic determination) decreased from 2.6 +/- 0.2 to 0.4 +/- 0.3 (P < 0.01) and 2.2 +/- 0.2 to 1.4 +/- 0.1 mumol.kg-1.min-1 (P <0.05), respectively. We conclude that under the conditions of the present experiment, glucose and/or insulin directly inhibits fatty acid oxidation. Our findings suggest that, contrary to the prediction of the glucose-fatty acid cycle, the intracellular availability of glucose (rather than FFA) determines the nature of substrate oxidation in human subjects.

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Schönfeld, Peter, and Georg Reiser. "Inhibition of β-oxidation is not a valid therapeutic tool for reducing oxidative stress in conditions of neurodegeneration." Journal of Cerebral Blood Flow & Metabolism 37, no. 3 (July 20, 2016): 848–54. http://dx.doi.org/10.1177/0271678x16642448.

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According to recent reports, systemic treatment of rats with methylpalmoxirate (carnitine palmitoyltransferase-1 inhibitor) decreased peroxidation of polyunsaturated fatty acids in brain tissue. This was taken as evidence of mitochondrial β-oxidation in brain, thereby contradicting long-standing paradigms of cerebral metabolism, which claim that β-oxidation of activated fatty acids has minor importance for brain energy homeostasis. We addressed this controversy. Our experiments are the first direct experimental analysis of this question. We fueled isolated brain mitochondria or rat brain astrocytes with octanoic acid, but octanoic acid does not enhance formation of reactive oxygen species, neither in isolated brain mitochondria nor in astrocytes, even at limited hydrogen delivery to mitochondria. Thus, octanoic acid or l-octanoylcarnitine does not stimulate H2O2 release from brain mitochondria fueled with malate, in contrast to liver mitochondria (2.25-fold rise). This does obviously not support the possible occurrence of β-oxidation of the fatty acid octanoate in the brain. We conclude that a proposed inhibition of β-oxidation does not seem to be a helpful strategy for therapies aiming at lowering oxidative stress in cerebral tissue. This question is important, since oxidative stress is the cause of neurodegeneration in numerous neurodegenerative or inflammatory disease situations.

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Vega, Gloria Lena, Fredrick L. Dunn, and Scott M. Grundy. "Impaired Hepatic Ketogenesis in Moderately Obese Men With Hypertriglyceridemia." Journal of Investigative Medicine 57, no. 4 (April 1, 2009): 590–94. http://dx.doi.org/10.2310/jim.0b013e31819e2f61.

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BackgroundSeveral studies suggest that increased nonesterified fatty acid flux and increased de novo lipogenesis may contribute to hypertriglyceridemia, but few studies have examined fatty acid oxidation as a factor.RationaleEndogenous hypertriglyceridemia (increased very low density lipoprotein triglyceride) could result from (a) re-esterification of excess nonesterified fatty acids entering the liver, (b) activation of hepatic lipogenesis, and/or (c) defective oxidation of hepatic fatty acids leading to greater triglyceride synthesis. Therefore, this study used plasma levels of 3-hydroxybutyrate as a marker for fatty acid oxidation. The study was carried out in hypertriglyceridemic and normotriglyceridemic subjects under 3 conditions: (a) in the fasting state, (b) after a fatty meal that should enhance fatty acid oxidation, and (c) after an oxandrolone challenge, which we recently showed increases fatty acid oxidation.ResultsIn the fasting state, 3-hydroxybutyrate concentrations in hypertriglyceridemic patients were only 53% of levels in normotriglyceridemic subjects. After a fatty meal, moderate increases in 3-hydroxybutyrate were observed, but values for patients with hypertriglceridemia remained 62% of the levels in the normotriglyceridemic group. A similar pattern of response was observed with oxandrolone challenge. There were no significant changes in fasting or postprandial levels of nonesterfified fatty acids, glycerol, or triglycerides before and during the oxandrolone challenge.ConclusionPatients with endogenous hypertriglyceridemia seem to have a defect in fatty acid oxidation as indicated by reduced levels of 3-hydroxybutyrate. This defect was observed during fasting, postprandially, and during oxandrolone challenge. We propose that this defect contributes to the development of hypertriglyceridemia.

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

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