Fatty acid oxidation in cultured skin fibroblasts from patients with inherited disorders of fatty acid metabolism: studies on the specificity of acyl-CoA dehydrogenases

1987 ◽  
Vol 15 (3) ◽  
pp. 489-490 ◽  
Author(s):  
RONALD A. CHALMERS ◽  
NICHOLAS ENGLISH
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Fatty Acid Metabolism ◽  
Acid Metabolism ◽  
Skin Fibroblasts ◽  
Acid Oxidation ◽  
Inherited Disorders ◽  
Cultured Skin ◽  
Acyl Coa Dehydrogenases

scholarly journals Fatty acid oxidation inhibitor etomoxir suppresses tumor progression and induces cell cycle arrest via PPARγ-mediated pathway in bladder cancer

2019 ◽  
Vol 133 (15) ◽  
pp. 1745-1758 ◽  
Author(s):  
Songtao Cheng ◽  
Gang Wang ◽  
Yejinpeng Wang ◽  
Liwei Cai ◽  
Kaiyu Qian ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Bladder Cancer ◽  
Fatty Acid ◽  
Tumor Progression ◽  
Cell Cycle Arrest ◽  
Fatty Acid Oxidation ◽  
Fatty Acid Metabolism ◽  
Acid Metabolism ◽  
Acid Oxidation ◽  
Cycle Arrest

Abstract Tumor cells rely on aerobic glycolysis as their main energy resource (Warburg effect). Recent research has highlighted the importance of lipid metabolism in tumor progression, and certain cancers even turn to fatty acids as the main fuel. Related studies have identified alterations of fatty acid metabolism in human bladder cancer (BCa). Our microarray analysis showed that fatty acid metabolism was activated in BCa compared with normal bladder. The free fatty acid (FFA) level was also increased in BCa compared with paracancerous tissues. Inhibition of fatty acid oxidation (FAO) with etomoxir caused lipid accumulation, decreased adenosine triphosphate (ATP) and nicotinamide adenine dinucleotide phosphate (NADPH) levels, suppressed BCa cell growth in vitro and in vivo, and reduced motility of BCa cells via affecting epithelial–mesenchymal transition (EMT)-related proteins. Furthermore, etomoxir induced BCa cell cycle arrest at G0/G1 phase through peroxisome proliferator-activated receptor (PPAR) γ-mediated pathway with alterations in fatty acid metabolism associated gene expression. The cell cycle arrest could be reversed by PPARγ antagonist GW9662. Taken together, our results suggest that inhibition of FAO with etomoxir may provide a novel avenue to investigate new therapeutic approaches to human BCa.

Effect of hyperglycemia-hyperinsulinemia on whole body and regional fatty acid metabolism

1999 ◽  
Vol 276 (3) ◽  
pp. E427-E434 ◽  
Author(s):  
Labros S. Sidossis ◽  
Bettina Mittendorfer ◽  
David Chinkes ◽  
Eric Walser ◽  
Robert R. Wolfe
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Fatty Acid Metabolism ◽  
Acid Metabolism ◽  
Fatty Acid Uptake ◽  
Whole Body ◽  
Acid Oxidation ◽  
Acid Uptake ◽  
Similar Extent ◽  
Body Level

The effects of combined hyperglycemia-hyperinsulinemia on whole body, splanchnic, and leg fatty acid metabolism were determined in five volunteers. Catheters were placed in a femoral artery and vein and a hepatic vein. U-13C-labeled fatty acids were infused, once in the basal state and, on a different occasion, during infusion of dextrose (clamp; arterial glucose 8.8 ± 0.5 mmol/l). Lipids and heparin were infused together with the dextrose to maintain plasma fatty acid concentrations at basal levels. Fatty acid availability in plasma and fatty acid uptake across the splanchnic region and the leg were similar during the basal and clamp experiments. Dextrose infusion decreased fatty acid oxidation by 51.8% (whole body), 47.4% (splanchnic), and 64.3% (leg). Similarly, the percent fatty acid uptake oxidized decreased at the whole body level (53 to 29%), across the splanchnic region (30 to 13%), and in the leg (48 to 22%) during the clamp. We conclude that, in healthy men, combined hyperglycemia-hyperinsulinemia inhibits fatty acid oxidation to a similar extent at the whole body level, across the leg, and across the splanchnic region, even when fatty acid availability is constant.

scholarly journals Allogeneic T Cells up-Regulate Fatty Acid Metabolism and Can Be Targeted Through Metabolic Inhibition of Fatty Acid Oxidation

2013 ◽  
Vol 19 (2) ◽  
pp. S318-S319
Author(s):  
Craig A. Byersdorfer ◽  
Victor Tkachev ◽  
Stefanie Goodell ◽  
Stacy Sandquist ◽  
Anthony W. Opipari ◽  
...  
Keyword(s):  
T Cells ◽  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Fatty Acid Metabolism ◽  
Acid Metabolism ◽  
Metabolic Inhibition ◽  
Acid Oxidation

scholarly journals Zonation of fatty acid metabolism in rat liver

1989 ◽  
Vol 264 (1) ◽  
pp. 107-113 ◽  
Author(s):  
M Guzmán ◽  
J Castro
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Fatty Acid Metabolism ◽  
Acid Metabolism ◽  
Carnitine Palmitoyltransferase ◽  
Acid Oxidation ◽  
Low Density ◽  
Short Term ◽  
Carnitine Palmitoyltransferase I ◽  
Term Response

Fatty acid metabolism was studied in periportal and perivenous hepatocytes isolated by the method of Chen & Katz [Biochem. J. (1988) 255, 99-104]. The rate of fatty acid synthesis and the activity of acetyl-CoA carboxylase were markedly enhanced in perivenous hepatocytes as compared with periportal cells. However, the response of these two parameters to short-term modulation by cellular effectors such as the hormones insulin and glucagon, the phorbol ester 4 beta-phorbol 12 beta-myristate 13 alpha-acetate and the xenobiotics ethanol and acetaldehyde was similar in the two zones of the liver. In addition, perivenous hepatocytes showed a higher capacity of esterification of exogenous fatty acids into both cellular and very-low-density-lipoprotein lipids. Nevertheless, no difference between the two cell sub-populations seemed to exist in relation to the secretion of very-low-density lipoproteins. On the other hand, the rate of fatty acid oxidation was increased in periportal cells. This could be accounted for by a higher activity of carnitine palmitoyltransferase I and a lower sensitivity of this enzyme to inhibition by malonyl-CoA in the periportal zone. No differences were observed between periportal and perivenous hepatocytes in relation to the short-term response of fatty acid oxidation and carnitine palmitoyltransferase I activity to the cellular modulators mentioned above. In conclusion, our results show that: (i) lipogenesis is achieved at higher rates in the perivenous zone of the liver, whereas the fatty-acid-oxidative process occurs with a certain preference in the periportal area of this organ; (ii) the short-term response of the different fatty-acid-metabolizing pathways to cellular effectors is quantitatively similar in the two zones of the liver.

Control of Fatty Acid Metabolism I. Induction of the Enzymes of Fatty Acid Oxidation in Escherichia coli

1969 ◽  
Vol 97 (2) ◽  
pp. 827-836 ◽  
Author(s):  
Gerald Weeks ◽  
Martin Shapiro ◽  
R. O. Burns ◽  
Salih J. Wakil
Keyword(s):  
Escherichia Coli ◽  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Fatty Acid Metabolism ◽  
Acid Metabolism ◽  
Acid Oxidation

scholarly journals Maternal Feeding of a Synthetic PPARα Agonist Alters Renal Development of Fatty Acid Metabolism in the Neonatal Piglet

2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 702-702
Author(s):  
Lin Xi ◽  
Brandon Pike ◽  
Jinan Zhao ◽  
Jack Odle
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Fatty Acid Metabolism ◽  
Acid Metabolism ◽  
Block Design ◽  
Energy Utilization ◽  
Detectable Effect ◽  
Acid Oxidation ◽  
Maternal Supplementation

Abstract Objectives Clofibrate as a therapeutic agent has been used for controlling hyperlipidemias of humans for more than 50 years. Its action, metabolism, half-life and excretion have been well documented in liver of adult humans and rodent species, but it has not been evaluated well in extrahepatic tissues in neonates as a stimulator of energy utilization. In this study, the role of maternal administration of clofibrate in development of renal fatty acid oxidation was evaluated using swine as a model. Methods A randomized complete block design was used with a total of 27 pregnant sows. The sows were fed standard gestation-lactation diets supplemented with either 0 (control), 0.25% or 0.5% clofibrate (w/w) from d 107 of gestation to d 7 of lactation. Fatty acid oxidation was measured in the presence or absence of carnitine (1 mM) or/and malonate (5 mM) in fresh kidney homogenates from piglets at d1, 7, 14 and 19 of age using 14C-oleic acid (1 mM) as substrate (9.9 mBq/mmol). Results Interactions (P < 0.001) were observed between maternal clofibrate levels and postnatal age on 14C accumulation in CO2 (14CO2), acid soluble products (14C-ASP) and esterified products (14C-ESP). The 14CO2 increased by 1.3 fold from d1 to d7, but showed no differences between d7, 14 and 19 in pigs from the control sows. Maternal supplementation of clofibrate increased 14CO2 in pigs across all ages, but the increase was higher in pigs from sows fed 0.5% versus 0.25% clofibrate at d14. The 14C-ASP was 7-fold higher in d1 pigs from control sows than all other ages. Maternal supplementation of clofibrate increased 14C-ASP by 2 fold in pigs at d1, but had no detectable effect at d 7, 14 and 19. The 14C-ESP increased from d1 to d7 and decreased from d7 to d19 in pigs from control sows. Maternal supplementation of clofibrate had no detectable impact on 14C-ESP at d1, 14 and 19, but decreased 14C-ESP measured in d7 pigs. In vitro carnitine supplementation increased 14CO2 and malonate supplementation decreased 14CO2, but neither carnitine nor malonate altered 14C-ASP or 14C-ESP. Conclusions The stimulatory effect of maternal clofibrate on renal fatty acid metabolism in offspring is associated with the postnatal age, being greater at d1 and d7 than d14 and d19. Funding Sources USDA National Institute of Food and Agriculture.

scholarly journals Correction of Fatty Acid Oxidation in Carnitine Palmitoyl Transferase 2–Deficient Cultured Skin Fibroblasts by Bezafibrate

2003 ◽  
Vol 54 (4) ◽  
pp. 446-451 ◽  
Author(s):  
Fatima Djouadi ◽  
Jean-Paul Bonnefont ◽  
Laure Thuillier ◽  
Véronique Droin ◽  
Noman Khadom ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Skin Fibroblasts ◽  
Acid Oxidation ◽  
Carnitine Palmitoyl Transferase ◽  
Cultured Skin
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