• Journal of Nutrition and Health
• /
• v.26 no.7
• /
• pp.887-898
• /
• 1993

In order to determine the effect of iron depletion and subsequent supplementation on the muscle capacity for peroxisomal (PO) and mitochondrial(MO) $\beta$-oxidation during high fat feeding, weanling rats were fed a 44% (HF) or 2.5% (LF) fat diet with (+Fe) or without (-Fe) iron for 6 or 9 weeks. After 1 week rats fed HF+Fe or HF-Fe had 50-100% more PO and MO in heart, soleus, psoas and gastrocnemius than did rats fed low fat, but after 3 weeks rats fed HF-Fe had lower muscle PO and MO. In muscles of iron depleted rats PO and MO were not increased by supplementation with iron for 3 weeks. After 6 weeks MO and PO in skeletal muscles of rats fed HF+Fe were lower than after 3 weeks. It is concluded that adequate iron is necessary for miaximum response of muscle PO and MO to high fat feeding. However, after 6 weeks both PO and MO have returned to levels similar to those of rats fed low fat diets, hence, the elevated catalase activities seen at this time do not reflect peroxisomal $\beta$-oxidation.

• Toxicological Research
• /
• v.14 no.3
• /
• pp.285-291
• /
• 1998

This study was designed to examine the effects of polyundaturated fatty acid(PUFA) from different sourecs on hepatic lipogenic enzyme and peroxisomal ${\beta}$-oxidation in murine hepatocarcinogenesis initiated by diethylnitrodamine (DEN). Male Sprague-Dawley rats were fed one of three diets containing 10%(w/w)fat; fish oil-corn oil blended(FO), corn oil-beef tallow-fish oil blended(CF), or corn oil-beef tallow-perilla oil blended (CP), from the gestation period. At 10 weeks, animals were received a single inraperitoneal injection of DEN (200mg/kg body weight), were subjected to two-thirds partial hepatectomy 3 weeks later and were sacrificed 8 weeks after DEN initiation. The areas of placental glutathione S-transferase (GST-P) positive foci were significantly smaller in rats fed fish oil containing diets (FO and CF) than those fed CP diet. Fish oil feeding significantly decreased th activities of lipogenic enzyme. Rats fed fish oil containing diets (FO, CF) exhibited the lower fatty acid synthase (FAS) activity than those fed CP diet and FAS activity was positively correlated with areas of GSP-P positivie foci. Glucose-6-phophate dehydrogenase activity was the lowest and peroxisomal ${\beta}$-oxidation was stimulated in rats fed FO diet compared to other groups. It was also found that serum cholesterol was decreased in FO group. Therefore, the preventive effect against hepatocarcinogenesis and hypolipidemic effect of fish oil can be explained partly by suppression of the hepatic lipogenesis and by increase of peroxisomal ${\beta}$-oxidation.

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

• Environmental Mutagens and Carcinogens
• /
• v.17 no.2
• /
• pp.78-91
• /
• 1997

Peroxisome is a single membrane-bounded organelle found in hepatic parenchymal cells and kidney tubular epithelial cells. A number of enzymes exist in peroxisome contributing to anabolic and catabolic peroxisomal functions. Extramitochontriai $\beta$-oxidation of fatty acid is a major function of peroxisome. Peroxisomes can be proliferated by many structually unrelated compounds such as hypolipidemic drugs, plasticizers, pesticides, some pharmaceutical agents and high fat diet. These chemicals, called peroxisome proliferators, act via the peroxisome proliferator activated receptor, to induce peroxisome proliferation, hepatomegaly and hepatocellular carcinoma in rodent. The clear mechanisms of peroxisome proliferator-induced hepatocarcinogenesis have been not demonstrated. Since they are not genotoxic, biochemical changes or changes in gene expressions may be involved. A free radical theory has been suggested based on the finding of oxidative damages of macromolecules by hydrogen peroxide released in the peroxisomal $\beta$-oxidation of fatty acid. Increased cell proliferation by a peroxisome proliferator has been also thought to be an important factor in the hepatocarcinogenesis as suggested in other cases of nongenotoxic carcinogenesis. The alternation of eicosanoid concentrations by peroxisome proliferators may be important in the peroxisome proliferator-induced hepatocarcinogenesis since peroxisome proliferators decrease the concentration of eicosanoids, and the peroxisome proliferator ciprofibrate-eicosanoid combination is comitogenic and costimulates some mitogenic signals in hepatocytes. All of proposed mechanisms should be considered in the peroxisome prolifrator-induced hepatocarcinogenesis.

• Asian-Australasian Journal of Animal Sciences
• /
• v.10 no.4
• /
• pp.402-407
• /
• 1997

This study was conducted to investigate the effects of effects of enprostil, a prostaglandin $E_2$, analogue, on liver triacylglycerol content and factors that regulate liver lipid metabolism in mice. Mice received vehicle or $10{\mu}g$ enprostil/kg body weight intraperitoneally every 6 h, and were killed at 0, 6, 12, 18 and 24 h after the first injection. Enprostil significantly lowered liver triacylglycerol content after 12 h of the first injection. However, the peroxisomal ${\beta}$-oxidation activity was inconsistent with the result of liver triacylglycerol content, because its activity was lovered by enprosil. In another experiment, the effect of enprostil on lipid metabolism in mice was investigated in a short period. Mice received $10{\mu}g$ enprostil/kg body weight intraperitoneally, and were killed after 0, 5, 10, 30 and 60 min. After 30 min, malic enzyme activity was significantly increased by the administration of enprostil compared with the activity at 5 min after. No significant changes in liver carnitine palmitoyltransferase and peroxisomal ${\beta}$-oxidation activities were observed. Plasma free fatty acid concentrations were markedly reduced from 5 through 60 min after the administration of enprostil. Consequently, enprostil suppressive effect on liver triacylglycerol concentration might result from the decreased entry of free fatty acid into liver.

• Journal of Nutrition and Health
• /
• v.29 no.9
• /
• pp.925-933
• /
• 1996

This study intended to compare the hypolipidemic effects among six experimental groups fed by three different dietary carbohydrates on hyperlipodemic rats. Sixty experimental animals were divided into 6 groups, SB, ST, SP and CB, CT, CP after production of hyperlipidemia fed by SB diet on Sprague-Dawley rats for 4 weeks. Rats were fed by six experimental diets for eight weeks. Hyjperlipidemic rats showed three times higher in plasma TG level not in cholesterol content compare to control group fed by stock diet. Two different dietary carbohydrates seem to be effective in body weight gain and fat cumulation as weight of epididymal fat pad. In comparison of S and C groups, C fed groups showed lowering effect in plasma TG and total lipid contents, but among S fed groups, ST and SP group showed lower than SB in this respects. Dietary carbohydrates seem to be more effective than fat in plasma lipid contents. When we compare among three different fat groups, only T groups with different carbohydrates increased in peroxisomal lipid oxidation and decreased in lipogenic enzyme activites. As same token, sucrose fed group with three fat sources seem to increase activiteies enzyme activities. In epididymal fat pad and Heart, SP and CP effect more in LPL activites than other groups. In conclusion, we can recommed to consume polysaccharides rather than disaccharide and n-3 fatty acids such as perilla and tuna oils to alleviate hypertringlycemic condition.

• Journal of The Korean Society of Inherited Metabolic disease
• /
• v.12 no.1
• /
• pp.49-53
• /
• 2012

X-linked adrenoleukodystrophy (ALD) is a rare inherited metabolic disease which results in impaired peroxisomal ${\beta}$-oxidation and the accumulation of very long chain fatty acids (VLCFA) in the adrenal cortex, the myelin of the central nervous system, and the testes. X-linked ALD is caused by mutations in the ABCD1 gene encoding an ATP-binding cassette transporter superfamily located in the peroxisomal membrane. This disease is characterized by a variety of phenotypes. The classic childhood cerebral ALD is a rapidly progressive demyelinating condition affecting the cerebral white matter before the age of 10 years in boys. We report the case of a 8-year-old with childhood cerebral X-linked ALD who developed inattention, hyperactivity, motor incoordination and hemiparesis. We diagnosed ALD with elevated plasma very long chain fatty acid level and diffuse high signal intensity lesions in both parieto-occipital white matter and cerebellar white matter in brain MRI. We identified a novel c.983delT (p.Met329CysfsX7) mutation of the ABCD1 gene. There is no correlation between X-ALD phenotype and mutations in the ABCD1 gene. Further studies for searching additional non-genetic factor which determine the phenotypic variation will be needed.

• Journal of Microbiology and Biotechnology
• /
• v.28 no.4
• /
• pp.597-605
• /
• 2018

Acyl-CoA oxidases (ACOXs) play important roles in lipid metabolism, including peroxisomal fatty acid ${\beta}$-oxidation by the conversion of acyl-CoAs to 2-trans-enoyl-CoAs. The yeast Yarrowia lipolytica can utilize fatty acids as a carbon source and thus has extensive biotechnological applications. The crystal structure of ACOX3 from Y. lipolytica (YlACOX3) was determined at a resolution of $2.5{\AA}$. It contained two molecules per asymmetric unit, and the monomeric structure was folded into four domains; $N{\alpha}$, $N{\beta}$, $C{\alpha}1$, and $C{\alpha}2$ domains. The cofactor flavin adenine dinucleotide was bound in the dimer interface. The substrate-binding pocket was located near the cofactor, and formed at the interface between the $N{\alpha}$, $N{\beta}$, and $C{\alpha}1$ domains. Comparisons with other ACOX structures provided structural insights into how YlACOX has a substrate preference for short-chain acyl-CoA. In addition, the structure of YlACOX3 was compared with those of medium- and long-chain ACOXs, and the structural basis for their differences in substrate specificity was discussed.

• Journal of Nutrition and Health
• /
• v.29 no.7
• /
• pp.703-712
• /
• 1996

This study planned to compare the effects of source and amount of dietary n-3 fatty acid, tuna oil and perilla oil, on lipid metabolism and eicosanoids production in Spargue-Dawley strain male rats. Weaning rats were fed 5 different experimantal diets for 4 weeks. (S : beef tallow 50%+sesame oil 50%, T1 : beef tallow 50%+sesame oil 40%+tuna oil 10%, T2 : beef tallow 50%+sesame oil 25%+tuna oil 25%, P1 : beef tallow 50%+sesame oil 40%+perilla oil 10%, P2 : beef tallow 50%+sesame oil 25%+perilla oil 25%) Food intake was higher in T2 group than in other groups, but body weight gain and food efficiency tate were not different among groups. Plasma total lipid and triglyceride were significantly lower in groups fed perilla oil as much as groups fed tuna oil than in S. But tuna oil reduced plasma cholesterol level more than perilla oil. Liver total lipid per unit, cholesterol and triglyceride were not affected by dietary fat sources. Peroxisomal $\beta$-oxidation was higher in T1 and T2 than in P1 and P2. Activities of glucose 6 phosphate dehydrogenase and malic enzyme were lower in T1 and T2 than in group fed sesame oil only. Plasma TXB2 was affected by n-3 fatty acid consumption, and it was lower in perilla oil groups as much as tuna oil groups than in S. But 6-keto PGF1$\alpha$ was not different among experimental groups. The results of this study indicated that tuna oil and perilla oil both decreased plasma lipids, however, the mechanism may be different. And tuna oil and perilla oil had a similar effects on eicosanoids production.

• Journal of the Korean Chemical Society
• /
• v.37 no.12
• /
• pp.1068-1075
• /
• 1993

Catalase activities were assayed on the leaves and roots of Tomato (Lycopersicum esculentum) as a function of age for 1 year after germination. The enzyme activities of root tissue demonstrated to be insignificant through all stages of development. On the other hand, the catalase activities of leaf peroxisomal fractions showed remarkable changes with peak value of 76 ${\mu}mol$/ml/min at germination stage within 2 weeks growth, 7.2 ${\mu}mol$/ml/min at adult stage around 4∼5 months growth and very small activities at aged period around 11∼12 months growth. It is suggested that there may be two factors concerning such catalase activities in relation with age, firstly the glyoxisomal reactions including glyoxylate cycle and $\beta$-oxidation at germination stage and secondly photosynthesis hereafter seemed to affect age dependent changes of catalase activity by producing coincident amount of $H_2O_2$. In addition, NADPH coenzyme was found to have ability to restore catalytic acitivity of inactivated catalase (compound II) at all stages of development except old age, indicating NADPH would play a role as catalase protector against deleterious substrate,$H_2O_2$.