scholarly journals Species differences in the physiological activity of dietary lignan (sesamin and episesamin) in affecting hepatic fatty acid metabolism

2004 ◽  
Vol 91 (3) ◽  
pp. 377-386 ◽  
Author(s):  
Masayo Kushiro ◽  
Yoko Takahashi ◽  
Takashi Ide
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Fatty Acid Metabolism ◽  
Animal Species ◽  
Acid Metabolism ◽  
Physiological Activity ◽  
Acid Oxidation ◽  
Mrna Levels ◽  
Hepatic Fatty Acid ◽  
Degradation Rates

The effect of sesame (Sesamum orientale) lignan preparation containing equivalent amounts of sesamin and episesamin on hepatic fatty acid metabolism was compared in rats, mice and hamsters. Animals were fed on either a diet free of lignan or a diet containing 2glignan/kg for 15d. The lignan preparation greatly increased hepatic activity and the mRNA levels of enzymes involved in fatty acid oxidation, while it strongly down-regulated those of enzymes involved in lipogenesis in rats. In contrast, lignan did not modify these variables in mice and hamsters. Changes observed, if any, were more attenuated in these mice and hamsters than in rats. Sesamin and episesamin concentrations in serum and liver of animals fed on lignan-containing diets were significantly greater (P<0·05) in rats than in mice and hamsters. Moreover, sesamin:episesamin values in tissues were far from that expected from the value in the lignan preparation given to the animals and were dependent on the animal species. Liver microsomes from each animal species degraded sesamin and episesamin in the presence of NADPH. The combined value of sesamin and episesamin degradation rates was lower in rats than in mice and hamsters. In addition, there was considerable diversity in the specificity of the enzyme reaction toward sesamin and episesamin among animal species. The differences in the amounts of lignan remaining in the tissues may account for the species dependence of the physiological activity of sesame lignan in affecting hepatic fatty acid oxidation and synthesis.

scholarly journals Comparative analysis of sesame lignans (sesamin and sesamolin) in affecting hepatic fatty acid metabolism in rats

2007 ◽  
Vol 97 (1) ◽  
pp. 85-95 ◽  
Author(s):  
Jin Seon Lim ◽  
Yoshikazu Adachi ◽  
Yoko Takahashi ◽  
Takashi Ide
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Fatty Acid Metabolism ◽  
Acid Metabolism ◽  
Liver Lipid ◽  
Mrna Abundance ◽  
Acid Oxidation ◽  
Hepatic Fatty Acid ◽  
Sesame Lignans ◽  
Hepatic Fatty Acid Oxidation

Effects of sesamin and sesamolin (sesame lignans) on hepatic fatty acid metabolism were compared in rats. Rats were fed either a lignan-free diet, a diet containing 0·6 or 2 g/kg lignan (sesamin or sesamolin), or a diet containing both sesamin (1·4 g/kg) and sesamolin (0·6 g/kg), for 10 d. Sesamin and sesamolin dose-dependently increased the activity and mRNA abundance of various enzymes involved in hepatic fatty acid oxidation. The increase was much greater with sesamolin than with sesamin. These lignans increased parameters of hepatic fatty acid oxidation in an additive manner when added simultaneously to an experimental diet. In contrast, they decreased the activity and mRNA abundance of hepatic lipogenic enzymes despite dose-dependent effects not being necessarily obvious. Sesamin and sesamolin were equally effective in lowering parameters of lipogenesis. Sesamolin accumulated in serum at 33- and 46-fold the level of sesamin at dietary concentrations of 0·6 and 2 g/kg, respectively. The amount of sesamolin accumulated in liver was 10- and 7-fold that of sesamin at the respective dietary levels. Sesamolin rather than sesamin can account for the potent physiological effect of sesame seeds in increasing hepatic fatty acid oxidation observed previously. Differences in bio-availability may contribute to the divergent effects of sesamin and sesamolin on hepatic fatty acid oxidation. Sesamin compared to sesamolin was more effective in reducing serum and liver lipid levels despite sesamolin more strongly increasing hepatic fatty acid oxidation.

scholarly journals Maternal Supplementation of Clofibrate Stimulates Hepatic Fatty Acid Oxidation in Newborn Suckling Piglets

2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 703-703
Author(s):  
Jinan Zhao ◽  
Brandon Pike ◽  
Jack Odle ◽  
Lin Xi
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Fatty Acid Metabolism ◽  
Acid Metabolism ◽  
Acid Oxidation ◽  
Standard Diet ◽  
Hepatic Fatty Acid ◽  
Food And Agriculture ◽  
Hepatic Fatty Acid Oxidation

Abstract Objectives To evaluate effects of maternal feeding of clofibrate, a PPARα agonist, on development of hepatic fatty acid metabolism in offspring using pig as a model. Methods Pregnant sows (N = 27) were randomly assigned into three treatment groups. Each group was fed a standard diet (3265 kcal ME/kg) supplemented with either 0, 0.25% or 5% clofibrate (w/w) from d 107 of gestation to d 7 of lactation. Liver tissue was collected from piglets at birth, d1, 7, 14 and 19. Fatty acid oxidation was examined in fresh homogenates using 1 mM [1–14C] oleic acid (9.9 mBq/mmol) as substrate. Oxidation was measured in the absence or presence of in vitro supplemented L-carnitine (1 mM) and/or malonate (5 mM). Results Clofibrate was not detected in piglet liver or sow milk. Interactions between clofibrate and postnatal age (P &lt; 0.001) on the 14C accumulation in 14CO2, acid soluble products (14C-ASP) and esterified products (14C-ESP) were observed. Accumulation in 14CO2 was not altered by piglet age in control sows; however, accumulation in 14C-ASP was higher at d14 and lower at d19 compared to d1. In contrast, maternal clofibrate increased 14CO2 by 100% and 14C-ASP by 80% in pigs at d1, and the increase was higher in pigs from sows given 0.5% versus 0.25% clofibrate. Accumulation in 14C-ESP in pigs from control sows increased from d1 to d14, but there was no difference detected between d14 and 19. Assessment of pigs from sows fed the 0.25% clofibrate dose revealed no impact on 14C-ESP, but the 0.5% dose increased 14C-ESP by 31%. No interaction was observed between clofibrate and the in vitro treatments (carnitine and malonate; P = 0.5). In vitro supplementation of carnitine increased radiolabel accumulation in CO2 by 60% and in ASP by 120%, but reduced 14C-ESP by 39% compared to control incubations. Supplementation of malonate reduced 14CO2 by 95% and 14C-ESP by 44%, but had no impact on 14C-ASP. Conclusions Maternal clofibrate enhances hepatic fatty acid metabolism in offspring, but the effect fades with postpartum age. The availability of carnitine in the milk could be a key element to support fatty acid oxidation in postnatal pigs. Funding Sources USDA National Institute of Food and Agriculture.

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.

Uteroplacental insufficiency alters hepatic fatty acid-metabolizing enzymes in juvenile and adult rats

2001 ◽  
Vol 280 (1) ◽  
pp. R183-R190 ◽  
Author(s):  
Robert H. Lane ◽  
David E. Kelley ◽  
Elisa M. Gruetzmacher ◽  
Sherin U. Devaskar
Keyword(s):  
Gene Expression ◽  
Fatty Acid ◽  
Fatty Acid Metabolism ◽  
Acid Metabolism ◽  
Female Rats ◽  
Mrna Levels ◽  
Adult Rats ◽  
Serum Triglycerides ◽  
Hepatic Fatty Acid ◽  
Malonyl Coa

Multiple adult morbidities are associated with intrauterine growth retardation (IUGR) including dyslipidemia. We hypothesized that uteroplacental insufficiency and subsequent IUGR in the rat would lead to altered hepatic fatty acid metabolism. To test this hypothesis, we quantified hepatic mRNA levels of acetyl-CoA carboxylase (ACC), carnitine palmitoyltransferase (CPTI), the β-oxidation-trifunctional protein (HADH), fasting serum triglycerides, and hepatic malonyl-CoA levels at different ages in control and IUGR rats. Fetal gene expression of all three enzymes was decreased. Juvenile gene expression of CPTI and HADH continued to be decreased, whereas gene expression of ACC was increased. Serum triglycerides were unchanged. A sex-specific response was noted in the adult rats. In males, serum triglycerides, hepatic malonyl-CoA levels, and ACC mRNA levels were significantly increased, and CPTI and HADH mRNA levels were significantly decreased. In contrast, the female rats demonstrated no significant changes in these variables. These results suggest that uteroplacental insufficiency leads to altered hepatic fatty acid metabolism that may contribute to the adult dyslipidemia associated with low birth weight.

scholarly journals Interrelated effects of dihomo-γ-linolenic and arachidonic acids, and sesamin on hepatic fatty acid synthesis and oxidation in rats

2012 ◽  
Vol 108 (11) ◽  
pp. 1980-1993 ◽  
Author(s):  
Takashi Ide ◽  
Yoshiko Ono ◽  
Hiroshi Kawashima ◽  
Yoshinobu Kiso
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Dietary Fat ◽  
Acid Synthesis ◽  
Acid Oxidation ◽  
Mrna Levels ◽  
Lipogenic Enzymes ◽  
Hepatic Fatty Acid ◽  
Hepatic Fatty Acid Oxidation ◽  
Maize Oil

Interrelated effects of dihomo-γ-linolenic acid (DGLA) and arachidonic acid (ARA), and sesamin, a sesame lignan, on hepatic fatty acid synthesis and oxidation were examined in rats. Rats were fed experimental diets supplemented with 0 or 2 g/kg sesamin (1:1 mixture of sesamin and episesamin), containing 100 g/kg of maize oil or fungal oil rich in DGLA or ARA for 16 d. Among the groups fed sesamin-free diets, oils rich in DGLA or ARA, especially the latter, compared with maize oil strongly reduced the activity and mRNA levels of various lipogenic enzymes. Sesamin, irrespective of the type of fat, reduced the parameters of lipogenic enzymes except for malic enzyme. The type of dietary fat was rather irrelevant in affecting hepatic fatty acid oxidation among rats fed the sesamin-free diets. Sesamin increased the activities of enzymes involved in fatty acid oxidation in all groups of rats given different fats. The extent of the increase depended on the dietary fat type, and the values became much higher with a diet containing sesamin and oil rich in ARA in combination than with a diet containing lignan and maize oil. Analyses of mRNA levels revealed that the combination of sesamin and oil rich in ARA compared with the combination of lignan and maize oil markedly increased the gene expression of various peroxisomal fatty acid oxidation enzymes but not mitochondrial enzymes. The enhancement of sesamin action on hepatic fatty acid oxidation was also confirmed with oil rich in DGLA but to a lesser extent.

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 The PPARβ/δ Activator GW501516 Prevents the Down-Regulation of AMPK Caused by a High-Fat Diet in Liver and Amplifies the PGC-1α-Lipin 1-PPARα Pathway Leading to Increased Fatty Acid Oxidation

Endocrinology ◽  
2011 ◽  
Vol 152 (5) ◽  
pp. 1848-1859 ◽  
Author(s):  
Emma Barroso ◽  
Ricardo Rodríguez-Calvo ◽  
Lucía Serrano-Marco ◽  
Alma M. Astudillo ◽  
Jesús Balsinde ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
High Fat Diet ◽  
Plasma Lipoproteins ◽  
Acid Oxidation ◽  
Mrna Levels ◽  
High Fat ◽  
Hepatic Fatty Acid ◽  
Lipin 1 ◽  
Hepatic Fatty Acid Oxidation

Metabolic syndrome-associated dyslipidemia is mainly initiated by hepatic overproduction of the plasma lipoproteins carrying triglycerides. Here we examined the effects of the peroxisome proliferator-activated receptors (PPAR)-β/δ activator GW501516 on high-fat diet (HFD)-induced hypertriglyceridemia and hepatic fatty acid oxidation. Exposure to the HFD caused hypertriglyceridemia that was accompanied by reduced hepatic mRNA levels of PPAR-γ coactivator 1 (PGC-1)-α and lipin 1, and these effects were prevented by GW501516 treatment. GW501516 treatment also increased nuclear lipin 1 protein levels, leading to amplification in the PGC-1α-PPARα signaling system, as demonstrated by the increase in PPARα levels and PPARα-DNA binding activity and the increased expression of PPARα-target genes involved in fatty acid oxidation. These effects of GW501516 were accompanied by an increase in plasma β-hydroxybutyrate levels, demonstrating enhanced hepatic fatty acid oxidation. Moreover, GW501516 increased the levels of the hepatic endogenous ligand for PPARα, 16:0/18:1-phosphatidilcholine and markedly enhanced the expression of the hepatic Vldl receptor. Interestingly, GW501516 prevented the reduction in AMP-activated protein kinase (AMPK) phosphorylation and the increase in phosphorylated levels of ERK1/2 caused by HFD. In addition, our data indicate that the activation of AMPK after GW501516 treatment in mice fed HFD might be the result of an increase in the AMP to ATP ratio in hepatocytes. These findings indicate that the hypotriglyceridemic effect of GW501516 in HFD-fed mice is accompanied by an increase in phospho-AMPK levels and the amplification of the PGC-1α-lipin 1-PPARα pathway.

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.

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