• The Korean Journal of Physiology and Pharmacology
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• v.9 no.3
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• pp.173-177
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• 2005

The purpose of this study was to discern the critical point in skeletal muscle fatty acid oxidation by changing plasma free fatty acids (FFA) level in rat. In the study, 3 key steps in lipid oxidation were examined after changing plasma FFA level by acipimox. The rates of both palmitate and palmitoylcarnitine oxidation were decreased by decrease of plasma FFA level, however, carnitine palmitoyl transferase (CPT) 1 activity was not changed, suggesting CPT1 activity may not be involved in the fatty acid oxidation at the early phase of plasma FFA change. In the fasted rats, ${\beta}-hydroxy$ acyl-CoA dehydrogenase (${\beta}$-HAD) activity was depressed to a similar extent as palmitate oxidation by a decrease of plasma FFA level. This suggested that ${\beta}-oxidation$ might be an important process to regulate fatty acid oxidation at the early period of plasma FFA change. Citrate synthase activity was not altered by the change of plasma FFA level. In conclusion, the critical step in fatty acids oxidation of skeletal muscles by the change of plasma FFA level by acipimox in fasting rats might be the ${\beta}-oxidation$ step rather than CPT1 and TCA cycle pathways.

• Biomedical Science Letters
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• v.12 no.4
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• pp.319-327
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• 2006

This study aimed to determine whether troglitazone stimulates genes related to fatty acid ${\beta}$-oxidation, leading to modulation of white adipose tissue (WAT) metabolism in high fat diet-fed mice. Female C57BL/6J mice were randomly divided into two groups (n=10/group). After they received either a high fat diet or the same high fat diet supplemented with troglitazone for 4 weeks, the effects of troglitazone on gene expression and physiology of WAT were measured using Northern, histological and serological analyses. Administration of troglitazone induced the expression of genes involved in mitochondrial and peroxisomal fatty acid ${\beta}$-oxidation in mesenteric WAT. Troglitazone also significantly increased uncoupling protein 2 mRNA levels. The changes in WAT gene expression were accompanied by reductions in circulating levels of free fatty acids and triglycerides as well as glucose and insulin. Histological studies showed that troglitazone treatment decreased the average size of adipocytes in mesenteric WAT. These results suggest that troglitazone-stimulated WAT expression of genes associated with fatty acid ${\beta}$-oxidation regulates WAT metabolism of high fat diet-fed mice, contributing to improvement of insulin sensitivity.

• Proceedings of the Botanical Society of Korea Conference
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• 1999.07a
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• pp.37-40
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• 1999

cDNAs for long- and short-chain acyl-CoA oxidases in fatty acid $\beta$-oxidation were isolated and were characterized their enzymatical and molecular properties. Both oxidases were exclusively localized in glyoxysomes, indicating that glyoxysomes can completely metabolize fatty acids to acyl-CoA by their cooperative action. In order to clarify the regulatory mechanisms underlying degradation of storage oil, we tried to obtain glyoxysome-deficient mutants of Arabidopsis. We screened 2,4-dichlorophenoxybutyric acid (2,4-DB) mutants of Arabidopsis which have defects in glyoxysomal fatty acid $\beta$-oxidation. Four mutants can be classified as carrying alleles at three independent loci, which we designated pedl, ped2, and ped3, respectively (where ped stands for peroxisome defective). The characteristics of these ped mutants are described.

• Journal of Nutrition and Health
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• v.30 no.9
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• pp.1067-1072
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• 1997

One known effect of long chain n-3 polyunsaturated fatty acids is their ability to decrease plasma triglycerides. However, identification of the specific n-3 fatty acids and the underlying mechanisms responsible for this change remains uncertain. This present study was designed to evaluate the effects of moderate levels of dietary docosahexaenoic acid (22 :6(n-3)) on modulating plasma triglyderides. Male CD-1 mice were maintained for 15 days on identical diets containing either docosahexahexaenoic acid ethyl ester(1.5%, w/w) or linoleic acid(18 : 2(n-6)) ethyl ester (1.5%, w/w) . Plasma triglycerides were 40% lower in the docosahexaenoic acid group than in the linoleic acid group. Hepatic carnitine palmitoyltransferase activity (a key regulatory enzyme for mitocondria $\beta$-oxidation) was not significantly different between the dietary groups. However, plasma acid soluble acylcarnitine levels (which increase with increasing $\beta$-oxidation )were significantly higher in the decosahexaenoic acid group. This data suggests that plasma triglyceride levels are lower in mice fed diets containing moderate levels of docosahexaenoic acid compared to linoleic acid, but this effect on plasma triglycerides is not modulated through an augmentation of mitochondrial $\beta$-oxidation.

• Journal of Life Science
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• v.5 no.2
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• pp.70-75
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• 1995

The effect of lipoxygenase (LOX) on the oxidation and co-oxidation of lipid fraction was studied in the model system of rainbow trout. For the reaction in model system 1 g of lipid fraction and 50mL of enzyme extract(LOX, 140 unit in 50mL phosphate buffer solution at pH 7, 4)), which were obtained from rainbow trout, were homoginized in the presence of Tween 20 and kept at 23$\circ$C for 3 days. The activity of LOX was decreased to 43% of initial level during the reaction in the model system. The initial composition of rainbow trout lipid was showed to be consisted of trigliceride(TG;82%) and free fatty acid(FFA;0.1%), while this converted to 59% of TG and 20% of FIFA, respectively after reaction in model system. Change of fatty acid composition was also observed and the content of linoleic acid, one of the major fatte acids, was decreased to 13% from 54% in the content of total fatty acids after reaction. The carotenoids in rainbow trout were composed of 0.4% $\alpha$-carotene, 1.6% $\beta$ -carotene, 80% canthaxanthin, 7% lutein and 11% zeaxanthin, thus the canthaxanthin was the major component. This canthaxanthin was the most degraded carotenoid by lipoxygenase catalyzed co-oxidation during the reaction. On the other hand the tocopherol isomers found in the rainbow trout were $\alpha$ and $\beta$ -tocopherol, and $\alpha$-tocopherol had a higher degradation rate by the lipoxygenase catalyzed co-oxidation than of $\beta$-tocopherol in the reaction of model system.

• Biomedical Science Letters
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• v.17 no.1
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• pp.13-20
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• 2011

The peroxisome proliferator-activated receptor ${\alpha}$ ($PPAR{\alpha}$) is a nuclear transcription factor that plays a central role in lipid and lipoprotein metabolism. To investigate whether swim training improves obesity and lipid metabolism through $PPAR{\alpha}$ activation in female sham-operated (Sham) and ovariectomized (OVX) mice, we measured body weight, visceral adipose tissue mass, serum free fatty acid at 6 weeks as well as the expression of hepatic $PPAR{\alpha}$ target genes involved in fatty acid oxidation. Swim-trained mice had decreased body weight, visceral adipose tissue mass and serum free fatty acid levels compared to high fat diet fed control mice in both female Sham and OVX mice. These reductions were more prominent in OVX than in Sham mice. Swim training significantly increased hepatic mRNA levels of $PPAR{\alpha}$ target genes responsible for mitochondrial fatty acid ${\beta}$-oxidation, such as carnitine palmitoyltransgerase-1 (CPT-1), very long chain acyl-CoA dehydrogenase (VLCAD), and medium chain acyl-CoA dehydrogenase (MCAD) in OVX mice. However, swim trained female Sham mice did not increase hepatic mRNA levels of $PPAR{\alpha}$ target genes responsible for mitochondrial fatty acid ${\beta}$-oxidation compared to Sham control mice. These results indicate that swim training differentially regulates body weight and adipose tissue mass between OVX and Sham mice, at least in part due to differences in liver $PPAR{\alpha}$ activation.

• Nutrition Research and Practice
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• v.7 no.4
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• pp.294-301
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• 2013

In this study, we examined the hepatic anti-steatosis activity of carnosic acid (CA), a phenolic compound of rosemary (Rosmarinus officinalis) leaves, as well as its possible mechanism of action, in a high-fat diet (HFD)-fed mice model. Mice were fed a HFD, or a HFD supplemented with 0.01% (w/w) CA or 0.02% (w/w) CA, for a period of 12 weeks, after which changes in body weight, blood lipid profiles, and fatty acid mechanism markers were evaluated. The 0.02% (w/w) CA diet resulted in a marked decline in steatosis grade, as well as in homeostasis model assessment of insulin resistance (HOMA-IR) index values, intraperitoneal glucose tolerance test (IGTT) results, body weight gain, liver weight, and blood lipid levels (P < 0.05). The expression level of hepatic lipogenic genes, such as sterol regulating element binding protein-1c (SREBP-1c), liver-fatty acid binding protein (L-FABP), stearoyl-CoA desaturase 1 (SCD1), and fatty acid synthase (FAS), was significantly lower in mice fed 0.01% (w/w) CA and 0.02% (w/w) CA diets than that in the HFD group; on the other hand, the expression level of ${\beta}$-oxidation-related genes, such as peroxisome proliferator-activated receptor ${\alpha}$ (PPAR-${\alpha}$), carnitine palmitoyltransferase 1 (CPT-1), and acyl-CoA oxidase (ACO), was higher in mice fed a 0.02% (w/w) CA diet, than that in the HFD group (P < 0.05). In addition, the hepatic content of palmitic acid (C16:0), palmitoleic acid (C16:1), and oleic acid (C18:1) was significantly lower in mice fed the 0.02% (w/w) CA diet than that in the HFD group (P < 0.05). These results suggest that orally administered CA suppressed HFD-induced hepatic steatosis and fatty liver-related metabolic disorders through decrease of de novo lipogenesis and fatty acid elongation and increase of fatty acid ${\beta}$-oxidation in mice.

• Journal of the Korean Society of Food Science and Nutrition
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• v.24 no.1
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• pp.67-73
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• 1995

Effects of tocopherols and $\beta$-carotene on the oxidation of the solid model system of a free fatty acid mixture (64.5% of linolic acid ; 26.4% of oleic acid ; 5.0% of palmitic acid) with tocopherols and $\beta$-carotene were studied. $\alpha$-tocopherol revealed an antioxidant activity at the concentration below 0.05%, however, it showed a prooxidant activity when the concentration was higher than 0.05%. The antioxidant activity of ${\gamma}$ -tocopherol was not affected by the concentrations in the range of 0.01~0.10% in the model and ${\gamma}$-tocopherol showed higher antioxidant activity than that of $\alpha$-tocopherol. It seemed that $\alpha$-tocopherol was unstable compared to ${\gamma}$-tocopherol during oxidation. $\beta$-carotene showed a weak antioxidative activity at the initial stage of this system while $\beta$-carotene showed a prooxidant activity in the presence of tocopherol. $\beta$ -carotene was highly susceptible to autoxidative degradation during oxidation.

• Asian-Australasian Journal of Animal Sciences
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• v.23 no.3
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• pp.312-317
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• 2010

Complete oxidation of fatty acid in the liver of ketotic cows was investigated. Serum non-esterified fatty acid (NEFA), beta-hydroxybutyric acid (BHBA) and glucose concentrations were measured using biochemical techniques. Carnitine palmitoyl transferase II (CPT II), 3-hydroxy acyl-CoA dehydrogenase (HAD) and oxaloacetic acid (OAA) concentrations in the liver were detected by ELISA. Serum glucose was lower in ketotic cows than controls (p<0.05). Serum BHBA and NEFA concentrations were higher in ketotic cows than controls (p<0.05). OAA, CPT II, and HAD contents in the liver of ketotic cows were lower than in controls (p<0.05). There were negative correlations between serum NEFA concentration and OAA, CPT II and HAD, but no correlation between serum BHBA concentration and capacity for complete oxidation of fatty acid. Overall, the capacity for complete fatty acid oxidation in the liver of ketotic cows might have been decreased. High serum NEFA concentrations may be unfavorable factors for the pathway of complete oxidation of fatty acid in the liver.

• Asian-Australasian Journal of Animal Sciences
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• v.16 no.3
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• pp.403-408
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• 2003

The study investigated the lipid metabolism of Tsaiya ducks under fasting and ad libitum feeding conditions. Sixty Tsaiya ducks in their growing period (8-12 wk-old) and sixty Tsaiya ducks in their laying period (26-30 wk-old, 10-14 weeks after the onset of laying) were randomly divided into ad libitum feeding and 3-day fasting groups. The activities of lipid metabolism related enzymes were determined. Experimental results indicated that fasting depressed the activities of lipogenesis related enzymes such as fatty acid synthetase and NADP-malic dehydrogenase in both periods (p<0.05). Fasting also increased the activities of liver fatty acid $\beta$-oxidation enzymes (p<0.05). However, the activities of lipoprotein lipase in adipose tissue, heart and ovarian follicle in both periods and the hormone-sensitive lipase of adipose tissue in the growing period were decreased by fasting (p<0.01).