Готові списки джерел за темами / Lipid metabolism; Ketone body metabolism; Carnitine

Добірка наукової літератури з теми "Lipid metabolism; Ketone body metabolism; Carnitine"

Автор: Grafiati

Опубліковано: 10 грудня 2022

Оновлено: 28 січня 2023

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Статті в журналах з теми "Lipid metabolism; Ketone body metabolism; Carnitine"

Singer, Thomas D., Vhundi G. Mahadevappa, and James S. Ballantyne. "Aspects of the Energy Metabolism of Lake Sturgeon,Acipenser fulvescens, with Special Emphasis on Lipid and Ketone Body Metabolism." Canadian Journal of Fisheries and Aquatic Sciences 47, no. 5 (May 1, 1990): 873–81. http://dx.doi.org/10.1139/f90-100.

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Key enzymes in several metabolic pathways in five tissues were measured in a primitive osteichthyan, the lake sturgeon (Acipenser fulvescens). Levels of nonesterified fatty acids (NEFAs) were measured in the plasma as an indicator of fatty acid mobilization and differential utilization of individual NEFAs as substrates for lipid oxidation. The metabolism of lake sturgeon differs from that of most teleosts studied; it has detectable levels of beta-hydroxy-butyrate dehydrogenase in all tissues, possibly a primitive metabolic feature of vertebrates, subsequently lost in the teleosts. Based on HOAD and CPT activities lipid oxidation in extrahepatic tissues of sturgeon is intermediate between elasmobranch and teleost models. Sturgeon plasma NEFA concentrations are clearly higher than those detected in any elasmobranch, indicating that the acipenserid chondrosteans may be among the first jawed fish to mobilize and transport NEFAs. Oleic acid (18:1,n9) which amounts to 45% of total NEFA content of the plasma may be a preferred substrate of carnitine dependent oxidation. High levels of long chain fatty acid in the plasma may represent a high turnover of eicosanoid precursors. The low levels of LDH in the anoxia tolerant sturgeon may indicate that alternative anaerobic end products, perhaps ethanol, are used to survive under anoxic conditions.

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Singer, Thomas D., and James S. Ballantyne. "Metabolic Organization of a Primitive Fish, the Bowfin (Amia calva)." Canadian Journal of Fisheries and Aquatic Sciences 48, no. 4 (April 1, 1991): 611–18. http://dx.doi.org/10.1139/f91-078.

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Key enzymes in several metabolic pathways in five tissues were measured in primitive osteichthyan, the bowfin (Amia calva), the only living representative of the group of extant fishes most closely allied to the teleosts. Aspects of the metabolism of Amia differ from those of most teleosts studied. These differences include detectable levels of β-hydroxybutyrate dehydrogenase in all tissues, possibly a primitive metabolic feature of vertebrates, subsequently lost in most more advanced teleosts. Based on 3-hydroxyacyl CoA dehydrogenase and carnitine palmitoyltransferase activities, lipid metabolism in extrahepatic tissues of bowfin more closely resembles that of an elasmobranch rather than that of a teleost. The overall level of metabolism is lower than most teleosts as indicated by enzyme activities in red muscle and heart. Bowfin plasma nonesterified fatty acid concentrations are lower than most teleosts, but higher than those detected in any elasmobranch. These data suggest that the metabolic organization, especially lipid and ketone body metabolism, at least in part, reflects the evolutionary history of this group.

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ZORZANO, Antonio, César FANDOS, and Manuel PALACÍN. "Role of plasma membrane transporters in muscle metabolism." Biochemical Journal 349, no. 3 (July 25, 2000): 667–88. http://dx.doi.org/10.1042/bj3490667.

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Muscle plays a major role in metabolism. Thus it is a major glucose-utilizing tissue in the absorptive state, and changes in muscle insulin-stimulated glucose uptake alter whole-body glucose disposal. In some conditions, muscle preferentially uses lipid substrates, such as fatty acids or ketone bodies. Furthermore, muscle is the main reservoir of amino acids and protein. The activity of many different plasma membrane transporters, such as glucose carriers and transporters of carnitine, creatine and amino acids, play a crucial role in muscle metabolism by catalysing the influx or the efflux of substrates across the cell surface. In some cases, the membrane transport process is subjected to intense regulatory control and may become a potential pharmacological target, as is the case with the glucose transporter GLUT4. The goal of this review is the molecular characterization of muscle membrane transporter proteins, as well as the analysis of their possible regulatory role.

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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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Miki, C., A. D. Mayer, J. A. C. Buckels, K. Iriyama, H. Suzuki, and P. McMaster. "Serum hepatocyte growth factor as an index of extensive catabolism of patients awaiting liver transplantation." Gut 44, no. 6 (June 1, 1999): 862–66. http://dx.doi.org/10.1136/gut.44.6.862.

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BACKGROUNDWhole body catabolism as the result of intrahepatic metabolic derangement is common in liver transplant candidates. However, individual nutritional assessment parameters lack sensitivity and specificity in determining energy status of these patients. Recently, serum hepatocyte growth factor (HGF) has been shown to reflect the recovery of hepatic energy metabolism after liver transplantation.AIMSThe relation between preoperative levels of serum HGF and metabolic variables was investigated to clarify the clinical value of measuring HGF in evaluations of the catabolism.PATIENTS/METHODSBlood samples were obtained from 30 liver transplant recipients, and biopsy specimens were taken from each recipient’s rectus muscle and the explanted liver. Preoperative serum concentration of HGF was determined. Whole body energy metabolism was assessed by measuring glycogen contents of biopsy specimens and plasma or serum levels of glucose, insulin, total ketone bodies, total carnitine, and amino acids.RESULTSSerum HGF concentration was elevated in 22 of 30 patients and correlated with the Child-Pugh score. It showed a negative association with muscle glycogen content, and a positive correlation with serum levels of glucose, total carnitine, and total ketone bodies. Patients with elevated serum HGF concentrations had higher preoperative plasma levels of aromatic amino acids and branched chain amino acids, associated with lower branched chain to aromatic amino acid ratios.CONCLUSIONSThe elevated serum concentration of HGF in liver transplant candidates reflected inhibition of peripheral glucose storage, enhanced lipid oxidation, and increased peripheral release of branched chain amino acids, and thus extensive energy catabolism.

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Lytle, Kelli A., Nikki C. Bush, Jessica M. Triay, Todd A. Kellogg, Michael L. Kendrick, James M. Swain, Nicola W. Gathaiya, Kazanna C. Hames, and Michael D. Jensen. "Hepatic Fatty Acid Balance and Hepatic Fat Content in Humans With Severe Obesity." Journal of Clinical Endocrinology & Metabolism 104, no. 12 (August 13, 2019): 6171–81. http://dx.doi.org/10.1210/jc.2019-00875.

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Abstract Objective Nonalcoholic fatty liver disease can lead to hepatic inflammation/damage. Understanding the physiological mechanisms that contribute to excess hepatic lipid accumulation may help identify effective treatments. Design We recruited 25 nondiabetic patients with severe obesity scheduled for bariatric surgery. To evaluate liver export of triglyceride fatty acids, we measured very-low-density lipoprotein (VLDL)–triglyceride secretion rates the day prior to surgery using an infusion of autologous [1-14C]triolein-labeled VLDL particles. Ketone body response to fasting and intrahepatic long-chain acylcarnitine concentrations were used as indices of hepatic fatty acid oxidation. We measured intraoperative hepatic uptake rates of plasma free fatty acids using a continuous infusion of [U-13C]palmitate, combined with a bolus dose of [9,10-3H]palmitate and carefully timed liver biopsies. Total intrahepatic lipids were measured in liver biopsy samples to determine fatty liver status. The hepatic concentrations and enrichment from [U-13C]palmitate in diacylglycerols, sphingolipids, and acyl-carnitines were measured using liquid chromatography/tandem mass spectrometry. Results Among study participants with fatty liver disease, intrahepatic lipid was negatively correlated with VLDL-triglyceride secretion rates (r = −0.92, P = 0.01) but unrelated to hepatic free fatty acid uptake or indices of hepatic fatty acid oxidation. VLDL-triglyceride secretion rates were positively correlated with hepatic concentrations of saturated diacylglycerol (r = 0.46, P = 0.02) and sphingosine-1-phosphate (r = 0.44, P = 0.03). Conclusion We conclude that in nondiabetic humans with severe obesity, excess intrahepatic lipid is associated with limited export of triglyceride in VLDL particles rather than increased uptake of systemic free fatty acids.

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Li, Shangbiao, Xiaoxia Zhu, Lijuan Wang, and Zhihao Zheng. "The role of radiation dose-dependent enhancement of fatty acid oxidation in radiation surviving/resistant lung cancer cells." Journal of Clinical Oncology 38, no. 15_suppl (May 20, 2020): e21724-e21724. http://dx.doi.org/10.1200/jco.2020.38.15_suppl.e21724.

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e21724 Background: Radiotherapy plays a critical role in the integrated management of lung cancer. However, radioresistance limits the long-term control. Exploring the dynamic changes of metabolic reprogramming in radiation surviving/resistant (S/R) lung cancer cells is helpful to clarify the metabolic mechanism of radiation resistance and to develop new targets for intervention and early detection. Methods: Cell lines were irradiated with different doses (2Gy × 20F, 2Gy × 30F, 2Gy × 40F) in conventional dose fractionation. The cellular radiosensitivity was verified by colony formation assay and neutral comet assay. Cell proliferation ability was determined by EdU assay. Metabonomic analysis was used to identify the differentially expressed metabolites between high-dose radiation-resistant cells and their parent cells. Lipid droplet content was detected by Oil Red O (ORO) staining. Cell oxygen consumption rate (OCR) was measured by Seahorse XF24e analyzer. Western blot was used to detect the expression of metabolic enzymes. The growth of xenograft tumors from these cell lines in BALB/c nude mice were measured after the treatment of radiation (2Gy×5F), Etomoxir, or radiation combined with Etomoxir. Results: Compared with parent cells, the radioresitance of S/R lung cancer cells after different doses of radiationwas significantly increased with the increase of radiation exposure. ORO staining showed that fatty deposition of radiation S/R cells was obviously higher than their parent cells, and more fatty deposition in cells received higher dose of radiation. The ketone body metabolism-related substances, including acetoacetic acid, a metabolite of FAO, were significantly enriched in high-dose radiation-resistant cells. The expression of carnitine palmitoyltransferase1 (CPT1) and the OCR in radiation S/R cells were also radiation-dose dependently increased. Etomoxir, an inhibitor of fatty acid oxidation, significantly enhanced the radiosensitivity and decreased the OCR and DNA repair ability of various S/R cells exposed to radiation. We further confirmed that Etomoxir could significantly inhibit proliferation of radiation S/R cells in vivo, which also presented with radiation-dose dependent model. Conclusions: The enhancement of radiation dose-dependent FAO promotes radiation surviving/resistance of lung cancer cells. CPT1A, a key metabolic enzyme mediating FAO, may be a potential target for treatment of radiation resistant lung cancer. Funding: 81972853, 81572279, 2016J004, LC2019ZD009, 2018CR033.

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Miyamoto, Junki, Ryuji Ohue-Kitano, Hiromi Mukouyama, Akari Nishida, Keita Watanabe, Miki Igarashi, Junichiro Irie, et al. "Ketone body receptor GPR43 regulates lipid metabolism under ketogenic conditions." Proceedings of the National Academy of Sciences 116, no. 47 (November 4, 2019): 23813–21. http://dx.doi.org/10.1073/pnas.1912573116.

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Ketone bodies, including β-hydroxybutyrate and acetoacetate, are important alternative energy sources during energy shortage. β-Hydroxybutyrate also acts as a signaling molecule via specific G protein-coupled receptors (GPCRs); however, the specific associated GPCRs and physiological functions of acetoacetate remain unknown. Here we identified acetoacetate as an endogenous agonist for short-chain fatty acid (SCFA) receptor GPR43 by ligand screening in a heterologous expression system. Under ketogenic conditions, such as starvation and low-carbohydrate diets, plasma acetoacetate levels increased markedly, whereas plasma and cecal SCFA levels decreased dramatically, along with an altered gut microbiota composition. In addition, Gpr43-deficient mice showed reduced weight loss and suppressed plasma lipoprotein lipase activity during fasting and eucaloric ketogenic diet feeding. Moreover, Gpr43-deficient mice exhibited minimal weight decrease after intermittent fasting. These observations provide insight into the role of ketone bodies in energy metabolism under shifts in nutrition and may contribute to the development of preventive medicine via diet and foods.

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Nosadini, R., C. Angelini, C. Trevisan, S. Vigili de Kreutzenberg, P. Fioretto, R. Trevisan, A. Avogaro, et al. "Glucose and ketone body turnover in carnitine-palmitoyl-transferase deficiency." Metabolism 36, no. 9 (September 1987): 821–26. http://dx.doi.org/10.1016/0026-0495(87)90088-6.

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Inokuchi, Toshiki, Kenji Imamura, Kayoko Nomura, Keiko Nomoto, and Sho Isogai. "Changes in carnitine metabolism with ketone body production in obese glucose-intolerant patients." Diabetes Research and Clinical Practice 30, no. 1 (October 1995): 1–7. http://dx.doi.org/10.1016/0168-8227(95)01140-4.

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Дисертації з теми "Lipid metabolism; Ketone body metabolism; Carnitine"

Stuart, Jeffrey Alan. "Evolutionary and adaptive aspects of lipid and ketone body metabolism in gastropod molluscs." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp02/NQ31903.pdf.

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