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

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Published: 4 June 2021

Last updated: 25 July 2025

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1

Gonzalez-Hurtado, Elsie, Jieun Lee, Joseph Choi, et al. "Loss of macrophage fatty acid oxidation does not potentiate systemic metabolic dysfunction." American Journal of Physiology-Endocrinology and Metabolism 312, no. 5 (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 C

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2

Chen, Chuck T., Marc-Olivier Trépanier, Kathryn E. Hopperton, Anthony F. Domenichiello, Mojgan Masoodi та 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, № 3 (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

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3

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 (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)

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4

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 (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

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5

Nickerson, James G., Hakam Alkhateeb, Carley R. Benton, 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 (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

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6

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/s1752756200593430.

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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 wa

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7

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 wa

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8

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

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9

Rinaldo, Piero, Dietrich Matern, and Michael J. Bennett. "Fatty Acid Oxidation Disorders." Annual Review of Physiology 64, no. 1 (2002): 477–502. http://dx.doi.org/10.1146/annurev.physiol.64.082201.154705.

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10

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

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11

Sidossis, Labros S. "The Role of Glucose in the Regulation of Substrate Interaction During Exercise." Canadian Journal of Applied Physiology 23, no. 6 (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. I

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12

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 (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 ef

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13

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 re

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14

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 (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 alon

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15

Ranea-Robles, Pablo, and Sander M. Houten. "The biochemistry and physiology of long-chain dicarboxylic acid metabolism." Biochemical Journal 480, no. 9 (2023): 607–27. http://dx.doi.org/10.1042/bcj20230041.

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Mitochondrial β-oxidation is the most prominent pathway for fatty acid oxidation but alternative oxidative metabolism exists. Fatty acid ω-oxidation is one of these pathways and forms dicarboxylic acids as products. These dicarboxylic acids are metabolized through peroxisomal β-oxidation representing an alternative pathway, which could potentially limit the toxic effects of fatty acid accumulation. Although dicarboxylic acid metabolism is highly active in liver and kidney, its role in physiology has not been explored in depth. In this review, we summarize the biochemical mechanism of the forma

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16

Chen, Xiaocui, Lin Shang, Senwen Deng, et al. "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 (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 malony

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17

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 (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 palmita

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18

Sirotová, Ľudmila, and Marcela Matulová. "DNA damage by oxidized fatty acids detected by DNA/SPE biosensor." Nova Biotechnologica et Chimica 8, no. 1 (2021): 45–53. http://dx.doi.org/10.36547/nbc.1307.

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Electrochemical DNA/screen-printed electrode biosensor (DNA/SPE biosensor) was tested for the detection of alterations in DNA formed as a consequence of the reaction between DNA and oxidative products of fatty acids. Interaction of DNA with a mixture of products generated during the oxidation of linoleic and oleic acids manifested DNA damage depending on a tested fatty acid and the presence of hydroperoxides and thiobarbituric acid reactive substances (TBARS) determined after the oxidation of fatty acids. A bigger extent of the DNA damage was registered in the case of the interaction with oxid

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19

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 (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 ox

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20

Lee, Shin-Hae, Su-Kyung Lee, Donggi Paik та Kyung-Jin Min. "Overexpression of Fatty-Acid-β-Oxidation-Related Genes Extends the Lifespan ofDrosophila melanogaster". Oxidative Medicine and Cellular Longevity 2012 (2012): 1–8. http://dx.doi.org/10.1155/2012/854502.

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A better understanding of the aging process is necessary to ensure that the healthcare needs of an aging population are met. With the trend toward increased human life expectancies, identification of candidate genes affecting the regulation of lifespan and its relationship to environmental factors is essential. Through misexpression screening of EP mutant lines, we previously isolated several genes extending lifespan when ubiquitously overexpressed, including the two genes encoding the fatty-acid-binding protein and dodecenoyl-CoA delta-isomerase involved in fatty-acidβ-oxidation, which is the

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21

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 (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

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22

Han, Xiao-Xia, Adrian Chabowski, Narendra N. Tandon, et al. "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 (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

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23

Prakash, Satyam. "Fatty Acid Alpha-oxidation and its Clinical Correlation." MedS Alliance Journal of Medicine and Medical Sciences 4, no. 7 (2024): 58–67. http://dx.doi.org/10.3126/mjmms.v4i7.71631.

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The human diet includes branched chain fatty acid phytanic acid (3,7,11,15-tetramethylhexadecanoic acid) and the degradation of 2-hydroxyphytanoyl-CoA, the initial step in the oxidation of phytanic acid was investigated. But, the long-standing controversy about the mechanism and subcellular location of phytanic acid alpha-oxidation has been debated and remain incompletely understood. Phytanic acid is known to undergo one cycle of alpha-oxidation initially due to its methyl group at the beta-position. The metabolic pathway known as Alpha oxidation of fatty acid is important for the production o

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24

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 (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 atmospher

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25

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 (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 m

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26

Martı́nez, G., G. Jiménez-Sánchez, P. Divry, et al. "Plasma free fatty acids in mitochondrial fatty acid oxidation defects." Clinica Chimica Acta 267, no. 2 (1997): 143–54. http://dx.doi.org/10.1016/s0009-8981(97)00130-7.

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27

Friedman, Mark I., Ruth B. Harris, Hong Ji, Israel Ramirez, and Michael G. Tordoff. "Fatty acid oxidation affects food intake by altering hepatic energy status." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 276, no. 4 (1999): R1046—R1053. http://dx.doi.org/10.1152/ajpregu.1999.276.4.r1046.

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Inhibition of fatty acid oxidation stimulates feeding behavior in rats. To determine whether a decrease in hepatic fatty acid oxidation triggers this behavioral response, we compared the effects of different doses of methyl palmoxirate (MP), an inhibitor of fatty acid oxidation, on food intake with those on in vivo and in vitro liver and muscle metabolism. Administration of 1 mg/kg MP selectively decreased hepatic fatty acid oxidation but did not stimulate food intake. In contrast, feeding behavior increased in rats given 5 or 10 mg/kg MP, which inhibited hepatic fatty acid oxidation to the sa

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28

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

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29

Srere, Paul A., and Balazs Sumegi. "Processivity and fatty acid oxidation." Biochemical Society Transactions 22, no. 2 (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 (1994): 116S. http://dx.doi.org/10.1042/bst022116s.

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31

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

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32

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

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33

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

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34

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

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35

Momken, Iman, Adrian Chabowski, Ellen Dirkx, et al. "A new leptin-mediated mechanism for stimulating fatty acid oxidation: a pivotal role for sarcolemmal FAT/CD36." Biochemical Journal 474, no. 1 (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-arabinofuran

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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 i

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37

Hulver, Matthew W., Jason R. Berggren, Ronald N. Cortright, et al. "Skeletal muscle lipid metabolism with obesity." American Journal of Physiology-Endocrinology and Metabolism 284, no. 4 (2003): E741—E747. http://dx.doi.org/10.1152/ajpendo.00514.2002.

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The objectives of this study were to 1) examine skeletal muscle fatty acid oxidation in individuals with varying degrees of adiposity and 2) determine the relationship between skeletal muscle fatty acid oxidation and the accumulation of long-chain fatty acyl-CoAs. Muscle was obtained from normal-weight [ n = 8; body mass index (BMI) 23.8 ± 0.58 kg/m2], overweight/obese ( n = 8; BMI 30.2 ± 0.81 kg/m2), and extremely obese ( n = 8; BMI 53.8 ± 3.5 kg/m2) females undergoing abdominal surgery. Skeletal muscle fatty acid oxidation was assessed in intact muscle strips. Long-chain fatty acyl-CoA conce

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Maher, A. C., J. McFarlan, J. Lally, L. A. Snook та A. Bonen. "TBC1D1 reduces palmitate oxidation by inhibiting β-HAD activity in skeletal muscle". American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 307, № 9 (2014): R1115—R1123. http://dx.doi.org/10.1152/ajpregu.00014.2014.

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In skeletal muscle the Rab-GTPase-activating protein TBC1D1 has been implicated in the regulation of fatty acid oxidation by an unknown mechanism. We determined whether TBC1D1 altered fatty acid utilization via changes in protein-mediated fatty acid transport and/or selected enzymes regulating mitochondrial fatty acid oxidation. We also determined the effects of TBC1D1 on glucose transport and oxidation. Electrotransfection of mouse soleus muscles with TBC1D1 cDNA increased TBC1D1 protein after 2 wk ( P < 0.05), without altering its paralog AS160. TBC1D1 overexpression decreased basal palmi

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Wu, Jiang, Bo Shui Chen, Jian Hua Fang, and Jiu Wang. "Anti-Oxidation Stability and its Mechanism of Rapeseed Biodiesel." Advanced Materials Research 772 (September 2013): 287–91. http://dx.doi.org/10.4028/www.scientific.net/amr.772.287.

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The anti-oxidation stability of rapeseed biodiesel (RME) was evaluated on an oxidation simulator set up by the author. The results showed that oxidative stability of RME was worse than that of petrodiesel by exhibiting higher acid values and peroxide values, as well as greater viscosity increases after oxidation. Furthermore, a conjecture was taken about the configurational changes and the oxidation mechanisms of unsaturated fatty acid methyl ester molecules in the oxidation process, according to the principles of free radical reactions and the results of both infrared and ultraviolet spectros

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Wu, Jiang, Bo Shui Chen, Jian Hua Fang, and Jiu Wang. "Anti-Oxidation Stability and its Mechanism of Soybean Biodiesel." Applied Mechanics and Materials 339 (July 2013): 695–99. http://dx.doi.org/10.4028/www.scientific.net/amm.339.695.

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The anti-oxidation stability of soybean biodiesel (SME) was evaluated on an oxidation simulator set up by the author. The results showed that oxidative stability of SME was worse than that of petrodiesel by exhibiting higher acid values and peroxide values, as well as greater viscosity increases after oxidation. Furthermore, a conjecture was taken about the configurational changes and the oxidation mechanisms of unsaturated fatty acid methyl ester molecules in the oxidation process, according to the principles of free radical reactions and the results of both infrared and ultraviolet spectrosc

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Wu, Jiang, Bo Shui Chen, Jian Hua Fang, and Jiu Wang. "Anti-Oxidation Stability and its Mechanism of Waste Oil Biodiesel." Advanced Materials Research 739 (August 2013): 80–84. http://dx.doi.org/10.4028/www.scientific.net/amr.739.80.

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The anti-oxidation stability of waste oil biodiesel (WME) was evaluated on an oxidation simulator set up by the author. The results showed that oxidative stability of WME was worse than that of petrodiesel by exhibiting higher acid values and peroxide values, as well as greater viscosity increases after oxidation. Furthermore, a conjecture was taken about the configurational changes and the oxidation mechanisms of unsaturated fatty acid methyl ester molecules in the oxidation process, according to the principles of free radical reactions and the results of both infrared and ultraviolet spectro

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Pellieux, Corinne, Christophe Montessuit, Irène Papageorgiou, Thierry Pedrazzini, and René Lerch. "Differential effects of high-fat diet on myocardial lipid metabolism in failing and nonfailing hearts with angiotensin II-mediated cardiac remodeling in mice." American Journal of Physiology-Heart and Circulatory Physiology 302, no. 9 (2012): H1795—H1805. http://dx.doi.org/10.1152/ajpheart.01023.2011.

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Normal myocardium adapts to increase of nutritional fatty acid supply by upregulation of regulatory proteins of the fatty acid oxidation pathway. Because advanced heart failure is associated with reduction of regulatory proteins of fatty acid oxidation, we hypothesized that failing myocardium may not be able to adapt to increased fatty acid intake and therefore undergo lipid accumulation, potentially aggravating myocardial dysfunction. We determined the effect of high-fat diet in transgenic mice with overexpression of angiotensinogen in the myocardium (TG1306/R1). TG1306/R1 mice develop ANG II

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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 (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 hepar

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He, Fang, Jie-Qiong Jin, Qing-Qing Qin та ін. "Resistin Regulates Fatty Acid Β Oxidation by Suppressing Expression of Peroxisome Proliferator Activator Receptor Gamma-Coactivator 1α (PGC-1α)". Cellular Physiology and Biochemistry 46, № 5 (2018): 2165–72. http://dx.doi.org/10.1159/000489546.

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Background/Aims: Abnormal fatty acid β oxidation has been associated with obesity and type 2 diabetes. Resistin is an adipokine that has been considered as a potential factor in obesity-mediated insulin resistance and type 2 diabetes. However, the effect of resistin on fatty acid β oxidation needs to be elucidated. Methods: We detected the effects of resistin on the expression of fatty acid oxidation (FAO) transcriptional regulatory genes, the fatty acid transport gene, and mitochondrial β-oxidation genes using real-time PCR. The rate of FAO was measured using 14C-palmitate. Immunofluorescence

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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 (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

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Zhou, Lufang, Hazel Huang, Tracy A. McElfresh, Domenick A. Prosdocimo, and William C. Stanley. "Impact of anaerobic glycolysis and oxidative substrate selection on contractile function and mechanical efficiency during moderate severity ischemia." American Journal of Physiology-Heart and Circulatory Physiology 295, no. 3 (2008): H939—H945. http://dx.doi.org/10.1152/ajpheart.00561.2008.

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The role of anaerobic glycolysis and oxidative substrate selection on contractile function and mechanical efficiency during moderate severity myocardial ischemia is unclear. We hypothesize that 1) preventing anaerobic glycolysis worsens contractile function and mechanical efficiency and 2) increasing glycolysis and glucose oxidation while inhibiting free fatty acid oxidation improves contractile function during ischemia. Experiments were performed in anesthetized pigs, with regional ischemia induced by a 60% decrease in left anterior descending coronary artery blood flow for 40 min. Three grou

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Lu, Qinyue, Weicheng Zong, Mingyixing Zhang, Zhi Chen та Zhangping Yang. "The Overlooked Transformation Mechanisms of VLCFAs: Peroxisomal β-Oxidation". Agriculture 12, № 7 (2022): 947. http://dx.doi.org/10.3390/agriculture12070947.

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Beta-oxidation(β-oxidation) is an important metabolic process involving multiple steps by which fatty acid molecules are broken down to produce energy. The very long-chain fatty acids (VLCFAs), a type of fatty acid (FA), are usually highly toxic when free in vivo, and their oxidative metabolism depends on the peroxisomal β-oxidation. For a long time, although β-oxidation takes place in both mitochondria and peroxisomes, most studies have been keen to explore the mechanism of β-oxidation in mitochondria while ignoring the importance of peroxisomal β-oxidation. However, current studies indicate

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Stanley, William C., Eric E. Morgan, Hazel Huang, et al. "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 (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 ac

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Luglio, Harry Freitag. "Genetic Variation of Fatty Acid Oxidation and Obesity, A Literature Review." International Journal of Biomedical Science 12, no. 1 (2016): 1–8. http://dx.doi.org/10.59566/ijbs.2016.12001.

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Modulation of fat metabolism is an important component of the etiology of obesity as well as individual response to weight loss program. The influence of lipolysis process had receives many attentions in recent decades. Compared to that, fatty acid oxidation which occurred after lipolysis seems to be less exposed. There are limited publications on how fatty acid oxidation influences predisposition to obesity, especially the importance of genetic variations of fatty acid oxidation proteins on development of obesity. The aim of this review is to provide recent knowledge on how polymorphism of ge

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Shekhawat, Prem, Michael J. Bennett, Yoel Sadovsky, D. Michael Nelson, Dinesh Rakheja, and Arnold W. Strauss. "Human placenta metabolizes fatty acids: implications for fetal fatty acid oxidation disorders and maternal liver diseases." American Journal of Physiology-Endocrinology and Metabolism 284, no. 6 (2003): E1098—E1105. http://dx.doi.org/10.1152/ajpendo.00481.2002.

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The role of fat metabolism during human pregnancy and in placental growth and function is poorly understood. Mitochondrial fatty acid oxidation disorders in an affected fetus are associated with maternal diseases of pregnancy, including preeclampsia, acute fatty liver of pregnancy, and the hemolysis, elevated liver enzymes, and low platelets syndrome called HELLP. We have investigated the developmental expression and activity of six fatty acid β-oxidation enzymes at various gestational-age human placentas. Placental specimens exhibited abundant expression of all six enzymes, as assessed by imm

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