scholarly journals Citrus Flavanones Affect Hepatic Fatty Acid Oxidation in Rats by Acting as Prooxidant Agents

2013 ◽  
Vol 2013 ◽  
pp. 1-12 ◽  
Author(s):  
Rodrigo Polimeni Constantin ◽  
Gilson Soares do Nascimento ◽  
Renato Polimeni Constantin ◽  
Clairce Luzia Salgueiro ◽  
Adelar Bracht ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Citric Acid ◽  
Oxygen Uptake ◽  
Fatty Acid Oxidation ◽  
Citric Acid Cycle ◽  
Acid Oxidation ◽  
Acid Cycle ◽  
Hepatic Fatty Acid ◽  
Wide Range ◽  
Hepatic Fatty Acid Oxidation

Citrus flavonoids have a wide range of biological activities and positive health effects on mammalian cells because of their antioxidant properties. However, they also act as prooxidants and thus may interfere with metabolic pathways. The purpose of this work was to evaluate the effects of three citrus flavanones, hesperidin, hesperetin, and naringenin, on several parameters linked to fatty acid oxidation in mitochondria, peroxisomes, and perfused livers of rats. When exogenous octanoate was used as substrate, hesperetin and naringenin reduced the mitochondrial NADH/NAD+ratio and stimulated the citric acid cycle without significant changes on oxygen uptake or ketogenesis. When fatty acid oxidation from endogenous sources was evaluated, hesperetin and naringenin strongly reduced the mitochondrial NADH/NAD+ratio. They also inhibited both oxygen uptake and ketogenesis and stimulated the citric acid cycle. Hesperidin, on the other hand, had little to no effect on these parameters. These results confirm the hypothesis that citrus flavanones are able to induce a more oxidised state in liver cells, altering parameters related to hepatic fatty acid oxidation. The prooxidant effect is most likely a consequence of the ability of these substances to oxidise NADH upon production of phenoxyl radicals in the presence of peroxidases and hydrogen peroxide.

scholarly journals Lipotoxic Palmitate Impairs the Rate of β-Oxidation and Citric Acid Cycle Flux in Rat Neonatal Cardiomyocytes

2016 ◽  
Vol 40 (5) ◽  
pp. 969-981 ◽  
Author(s):  
Taha Haffar ◽  
Ali Akoumi ◽  
Nicolas Bousette
Keyword(s):  
Fatty Acid ◽  
Citric Acid ◽  
Dehydrogenase Activity ◽  
Fatty Acid Oxidation ◽  
Isocitrate Dehydrogenase ◽  
Lipid Accumulation ◽  
Citric Acid Cycle ◽  
Acid Oxidation ◽  
Acid Cycle ◽  
Neonatal Cardiomyocytes

Background/Aims: Diabetic hearts exhibit intracellular lipid accumulation. This suggests that the degree of fatty acid oxidation (FAO) in these hearts is insufficient to handle the elevated lipid uptake. We previously showed that palmitate impaired the rate of FAO in primary rat neonatal cardiomyocytes. Here we were interested in characterizing the site of FAO impairment induced by palmitate since it may shed light on the metabolic dysfunction that leads to lipid accumulation in diabetic hearts. Methods: We measured fatty acid oxidation, acetyl-CoA oxidation, and carnitine palmitoyl transferase (Cpt1b) activity. We measured both forward and reverse aconitase activity, as well as NAD+ dependent isocitrate dehydrogenase activity. We also measured reactive oxygen species using the 2', 7'-Dichlorofluorescin Diacetate (DCFDA) assay. Finally we used thin layer chromatography to assess diacylglycerol (DAG) levels. Results: We found that palmitate significantly impaired mitochondrial β-oxidation as well as citric acid cycle flux, but not Cpt1b activity. Palmitate negatively affected net aconitase activity and isocitrate dehydrogenase activity. The impaired enzyme activities were not due to oxidative stress but may be due to DAG mediated PKC activation. Conclusion: This work demonstrates that palmitate, a highly abundant fatty acid in human diets, causes impaired β-oxidation and citric acid cycle flux in primary neonatal cardiomyocytes. This metabolic defect occurs prior to cell death suggesting that it is a cause, rather than a consequence of palmitate mediated lipotoxicity. This impaired mitochondrial metabolism can have important implications for metabolic diseases such as diabetes and obesity.

The Role of Lipid in Adult Development and Flight-Muscle Metabolism in Hyalophora Cecropia

1964 ◽  
Vol 41 (3) ◽  
pp. 573-590
Author(s):  
LAWRENCE A. DOMROESE ◽  
LAWRENCE I. GILBERT
Keyword(s):  
Fatty Acid ◽  
Citric Acid ◽  
Fatty Acid Oxidation ◽  
Adult Development ◽  
Citric Acid Cycle ◽  
Flight Muscle ◽  
Muscle Metabolism ◽  
Metabolic Inhibitors ◽  
Acid Oxidation ◽  
Acid Cycle

1. Changes in total lipid and R.Q. show that female pupae of H. cecropia begin to catabolize lipid early in adult development. In males there is a conservation of lipid during adult development resulting in the male moth having about three times the lipid content of the female. In the adult moth both sexes utilize lipid as the major energy source. 2. Lipid is the available substrate as well as the preferred substrate in flight-muscle metabolism in male moths. 3. Flight-muscle homogenates show greater oxidative activity with fatty acids and citric acid cycle intermediates than with glucose or glycolytic intermediates, indicating that carbohydrate pathways are not prominent. 4. A fatty acid oxidizing system has been identified in flight muscle which requires ATP, magnesium and a citric acid cycle intermediate for optimum activity. 5. Experiments with radiotracers and metabolic inhibitors reveal that fatty acid oxidation in flight muscle proceeds via the citric acid cycle and the cytochrome chain. 6. Active fatty acid activating enzymes are present in flight muscle, and fatty acid oxidation in H. cecropia is discussed in relation to vertebrate and other invertebrate systems.

scholarly journals Neddylation inhibition ameliorates steatosis in NAFLD by boosting hepatic fatty acid oxidation via DEPTOR-mTOR axis

2021 ◽  
pp. 101275
Author(s):  
Marina Serrano-Maciá ◽  
Jorge Simón ◽  
Maria J. González-Rellan ◽  
Mikel Azkargorta ◽  
Naroa Goikoetxea-Usandizaga ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Acid Oxidation ◽  
Hepatic Fatty Acid ◽  
Hepatic Fatty Acid Oxidation

scholarly journals Agmatine Stimulates Hepatic Fatty Acid Oxidation

2006 ◽  
Vol 281 (13) ◽  
pp. 8486-8496 ◽  
Author(s):  
Itzhak Nissim ◽  
Yevgeny Daikhin ◽  
Ilana Nissim ◽  
Bohdan Luhovyy ◽  
Oksana Horyn ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Acid Oxidation ◽  
Hepatic Fatty Acid ◽  
Hepatic Fatty Acid Oxidation

RS4-type resistant starch prevents high-fat diet-induced obesity via increased hepatic fatty acid oxidation and decreased postprandial GIP in C57BL/6J mice

2010 ◽  
Vol 298 (3) ◽  
pp. E652-E662 ◽  
Author(s):  
Akira Shimotoyodome ◽  
Junko Suzuki ◽  
Daisuke Fukuoka ◽  
Ichiro Tokimitsu ◽  
Tadashi Hase
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Resistant Starch ◽  
High Fat Diet ◽  
Acid Oxidation ◽  
High Fat ◽  
Fat Utilization ◽  
Hepatic Fatty Acid ◽  
Diet Induced Obesity ◽  
Hepatic Fatty Acid Oxidation

Chemically modified starches (CMS) are RS4-type resistant starch, which shows a reduced availability, as well as high-amylose corn starch (HACS, RS2 type), compared with the corresponding unmodified starch. Previous studies have shown that RS4 increases fecal excretion of bile acids and reduces zinc and iron absorption in rats. The aim of this study was to investigate the effects of dietary RS4 supplementation on the development of diet-induced obesity in mice. Weight- and age-matched male C57BL/6J mice were fed for 24 wk on a high-fat diet containing unmodified starch, hydroxypropylated distarch phosphate (RS4), or HACS (RS2). Those fed the RS4 diet had significantly lower body weight and visceral fat weight than those fed either unmodified starch or the RS2 diet. Those fed the RS4 diet for 4 wk had a significantly higher hepatic fatty acid oxidation capacity and related gene expression and lower blood insulin than those fed either unmodified starch or the RS2 diet. Indirect calorimetry showed that the RS4 group exhibited higher energy expenditure and fat utilization compared with the RS2 group. When gavaged with fat (trioleate), RS4 stimulated a lower postprandial glucose-dependent insulinotropic polypeptide (GIP; incretin) response than RS2. Higher blood GIP levels induced by chronic GIP administration reduced fat utilization in high-fat diet-fed mice. In conclusion, dietary supplementation with RS4-type resistant starch attenuates high-fat diet-induced obesity more effectively than RS2 in C57BL/6J mice, which may be attributable to lower postprandial GIP and increased fat catabolism in the liver.

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