• Journal of Nutrition and Health
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• v.32 no.6
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• pp.628-636
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• 1999

There is a marked increase in geriatric disease, especially liver disease, due to the continuous increase in alcohol and fat consumption. Since the fatty liver, induced by alcohol or fat, is basically from abnormalities in the lipid metabolism, it is possible that fatty acid binding protein(FABP) which is related to the fatty acid metabolism may also be abnormal in these livers. FABP is a small molecular weight protein family present in cytosol in high concentration. It has been proposed as a fatty acid transfer protein and as a binding protein responsible for controlling intracellular free fatty acid concentration. In this research, we have examined the relationship between liver FABP and fatty liver induced by alcohol or high cholesterol diet. Rats were fed one of either semipurified liquid diets; control diet containing 65% carbohydrate, 20% protein, and 15% fat or high cholesterol diet containing 1%(w/w) cholesterol or alcohol diet containing 37% of alcohol instead of carbohydrate. After 5 weeks of feeding period, all rats received commercial chow diet for 5 weeks to examine recovery effect. Liver and blood samples were collected at 0, 1, 3, 5 and 10 weeks to analyze lipid compositions. FABP was purified from liver cytosol and injected to rabbit to obtain antiserum. Liver FABP amount was determined by SDS-PAGE and western blotting methods. Fatty acid binding capacity was determined by binding of 14Cpalmitate with the delipidated liver cytosol. Consumption of alcohol increased serum cholesterol, triglyceride concentration and decreased HDL-cholesterol concentration after 5 weeks. Serum apolipoprotein B concentration increased after 3 weeks and LDL-cholesterol and apolipoprotein A concentration changed after 1 week. Liver cholesterol and triglyceride concentration increased after 3 weeks. Consumption of high cholesterol diet changed liver and serum lipid composition after 3 weeks. Swiching to normal diet for 5 weeks did not normalize most of lipid composition in serum and liver except serum and liver except serum cholesterol, triglyceride and liver cholesterol. Liver cytosol FABP content and the fatty acid binding capacity decreased dramatically after 1 week with alcohol consumption. This results indicate that FABP content changes before the changes before the changes of blood or liver lipid composition, suggesting changes of FABP may cause development of the fatty liver induced by alcohol and can be used as an index of detecting a early development of fatty liver.

• Asian-Australasian Journal of Animal Sciences
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• v.15 no.1
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• pp.66-71
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• 2002

We investigated the effect of fish oil (FOS) on growth performance, ruminal metabolism and fatty acid composition and physical characteristics of longissimus muscle in 10 steers and 10 bulls of Korean cattle. Concentrates diet was supplemented with FOS at 5% of the diet. FOS contained 3.34% eicosapentaenoic acid (EPA) and 24.87% docosahexaenoic acid (DHA) of total fatty acids by weight. Average daily weight gain and feed efficiency were not affected (p>0.871) by FOS, but feed intake was decreased. FOS had lower (p<0.003) pH and higher (p<0.001) $NH_3$-N than that of control. There was a treatment effect (p<0.001) for serum cholesterol concentrations. FOS increased (p<0.009) concentrations of n-3 fatty acids, including linolenic, EPA and DHA in longissimus muscle. Physical traits were significantly (p<0.015) changed by feeding FOS except for pH and lightness (L). We concluded that the fatty acid composition and physical properties of the muscle in fattening Korean cattle can be altered by feeding 5% FOS.

• 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).

• Journal of Nutrition and Health
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• v.31 no.8
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• pp.1315-1323
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• 1998

Effect of oral taurine supplementation on plasma total and phospholidpid -fatty acid profiles and their metabolism were evaluated in healthy female adults. Among twenty five female volunteers(23.6$\pm$0.3 years old ) participated in the taruine supplementation program(6g taurine /day), twenty four subjects succesfully completed the 2 week program , and only nine subjects continued to take taurine for another 2 weeks. Levels of plasma fatty acids and taruine were measured by gas-liquid chromatobraphy and an automated amino acid analyzer based on ion exchange chromatography, respectively. Plasma taurine concentration s of the subjects were 108. 7$\pm$3.4 , 184.2$\pm$8.2 and 235.9$\pm$77.0$\mu$emol/L at 0 , 2 and 4 weeks of taurine supplementation. Fatty acid compositions and elongation and desaturation indices of polyunsaturated fatty acids (PUFA) in plasma total lipids were not influenced by oral taurine supplementation. However, fatty acid compositions and their metabolism in plasma phospholipids were significantly affected by taurine supplementation in female adults. Compared to the values for 0 week, the percentage of saturated fatty acids (SFA) in plasma phospholipid was significantly lowered at 2 weeks, but elevated at 4 weeks of taurine supplementation. In contrast , the percentage of phospholipid PUFA significantly increased at 2 weeks and decreased at 4 weeks of taurine supplementation from to the values for 0 weeks. Foru weeks of oral taurine supplementation signifinatly elevated the eongation index(20 : 4$\omega$6 ⇒22 : 4 $\omega$6, p<0.01), and decreased the desaturation index (20 : 3 $\omega$6 ⇒20 : 4 $\omega$6 , p<0.01) of $\omega$6 fatty acids in plasma phospholipids. Plasma taurine concentration was positively correlated with the percentage of 14 : 0 fatty acids and the enlongation index o f$\omega$3 fatty acids(20 : 5 $\omega$3 ⇒22 : 5 $\omega$3), and thenegatively correlated with the percentage of 20 : 0 in plasma phospholipids. These results indicate that oral taurine supplementation for 4 weeks signidicantly elelvated the percentage of SFA, and lowered the percentage of PUFA in plasma phospholipids with no influence on plasm total fatty aicd composition in healthy female adults.

• Biomolecules & Therapeutics
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• v.27 no.2
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• pp.134-144
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• 2019

The prevalence of nonalcoholic fatty liver disease (NAFLD) has increased with the incidence of obesity; however, the underlying mechanisms are unknown. In this study, high-resolution metabolomics (HRM) along with transcriptomics were applied on animal models to draw a mechanistic insight of NAFLD. Wild type (WT) and catalase knockout (CKO) mice were fed with normal fat diet (NFD) or high fat diet (HFD) to identify the changes in metabolic and transcriptomic profiles caused by catalase gene deletion in correspondence with HFD. Integrated omics analysis revealed that cholic acid and $3{\beta}$, $7{\alpha}$-dihydroxy-5-cholestenoate along with cyp7b1 gene involved in primary bile acid biosynthesis were strongly affected by HFD. The analysis also showed that CKO significantly changed all-trans-5,6-epoxy-retinoic acid or all-trans-4-hydroxy-retinoic acid and all-trans-4-oxo-retinoic acid along with cyp3a41b gene in retinol metabolism, and ${\alpha}/{\gamma}$-linolenic acid, eicosapentaenoic acid and thromboxane A2 along with ptgs1 and tbxas1 genes in linolenic acid metabolism. Our results suggest that dysregulated primary bile acid biosynthesis may contribute to liver steatohepatitis, while up-regulated retinol metabolism and linolenic acid metabolism may have contributed to oxidative stress and inflammatory phenomena in our NAFLD model created using CKO mice fed with HFD.

• Asian-Australasian Journal of Animal Sciences
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• v.32 no.1
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• pp.137-143
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• 2019

Objective: The aim of this study was to compare male and female geese of two contrasting genotypes in terms of fatty acid composition, indexes related to human health, lipid metabolism and oxidative stability of the meat. Methods: The experiment was carried out on total of 120 geese of two different genotypes; the native breed Czech goose (CG) and commercial hybrid Novohradska goose (NG). One-d-old goslings were divided into 4 groups according to genotype and sex, and 8 birds from each group were slaughtered at 8 weeks of age. Results: The effects of the interactions between genotype and sex were observed on growth performance and carcass traits. Final body weight (p<0.001), daily weight gain (p<0.001), daily feed intake (p<0.001), slaughter weight (p<0.001), and cold carcass weight (p<0.001) were highest in NG males and lowest in CG females. The meat fatty acid composition results showed effects of both genotype and sex on the total n-6 and the total polyunsaturated fatty acid (PUFA) content, as well as the PUFA n-6/PUFA n-3 ratio. Regarding genotype, the total n-6, the total PUFA content and the PUFA n-6/PUFA n-3 ratio were higher in CG, and higher values were found in females. In terms of the lipid metabolism, ${\Delta}^5-{\Delta}^6$ desaturase (p = 0.006) was higher in males. The meat oxidative stability results revealed an interaction between genotype, sex and storage time (p<0.001). The highest (13.85 mg/kg) malondialdehyde content was measured in the meat of CG females after 5 days of storage and was presumably related to a higher PUFA content. Conclusion: NG had a relatively higher growth rate and meat oxidative stability, whereas the advantage of CG meat is its favourable fatty acid profile characterized by a higher PUFA content.

• 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.

• The Korean Journal of Physiology and Pharmacology
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• v.10 no.5
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• pp.283-287
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• 2006

Although estrogen is known to playa role in fatty acid metabolism, it remains unclear whether fatty acid oxidation in mature female rats differs from fatty acid oxidation in peri-pubertal young rats. In this study, we measured fatty acid metabolism in the skeletal muscles and livers of 5 and 50 weeks old male and female rats. The rate of palmitate oxidation in the liver and gastrocnemius red in the 50-week-old female rats were elevated as compared to the 5-week-old females, whereas there were no differences in the male rats. The rate of palmitate oxidation in the gastrocnemius red was correlated inversely with intra-abdominal fat mass in the 5-week-old male and female rats, whereas the palmitate oxidation rate was positively correlated with fat mass in the liver and gastrocnemius red in the 50-week-old rats. HOMA-IR and plasma insulin levels were positively correlated with intra-abdominal fat mass in the pooled 50-week-old male and female rats, but this correlation was not apparent in 5-week-old rats. In summary, the rate of fatty acid oxidation measured in the middle-aged adult female rats was significantly higher than those measured in the peri-pubertal young female rats. This difference may be attributed to the influence of ovarian hormones.

• Journal of Nutrition and Health
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• v.33 no.1
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• pp.13-22
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• 2000

Effects of high fat diet and/or endurance exercise training on hepatic total and phospholipid(PL) fatty acid compositions were evaluated in rats fed one of the following diets for 31 days. control diet(CD, 5 wt% corn oil) or high fat diet(HFD, 35 wt% corn oil). Half of the rats in each group were exercise-trained regularly on a treadmill for 90 minutes/day during the entire feeding period. Total and PL fatty acid compositions of hepatic lipid extracts were determined by a gas-liquid chromatograph),. Endurance exercise training did not change the daily food intake, but significantly reduced body weight gain and feed efficiency ratio of rats, which were most prominent in animals fed HFD. Exercise training did not significantly change the percentages of ∑saturated fatty acids (SFA) and ∑polyunsaturated fatty acids(PUEA), but decreased the percentage of ∑monounsaturated fatty acids(MUFA) in hepatic total fatty acids, which might be associated with the decrease in (equation omitted) 9-desaturation index of hepatic total fatty acid metabolism. Exercise training significantly lowered the percentages of 16 : 0 and 22 : 5$\omega$3, and increased the percentages of 20 : 1 and 20 : 3$\omega$3 in both total and PL fatty acid compositions in rat liver. Both total fatty acid and PL fatty acid compositions of rat liver responded more sensitively to changes in dietary fat content than to endurance exercise training in this study. Feeding HFD, whoch contains high level of linoleic acid(LA, 18 : 2$\omega$6), significantly decreased the percentages of ∑SFA and $\Sigma$MUFA, and increased the percentages of ∑PUFA and ∑$\omega$6 fatty acids of hepatic total fatty acids. Hepatic total fatty acid composition was affected by dietary fat content and dietary fatty acid composition more sensitively than those found in hepatic PL fatty acid composition. HFD significantly decreased most of desaturation indices, while exercise training significantly decreased elongation index(20 : 5$\omega$3⇒22 : 5$\omega$3) of hepatic total and PL fatty acid metabolism in rats. (Korean J Nutrition 33(1) : 13-22, 2000)

• Korean Journal of Exercise Nutrition
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• v.16 no.1
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• pp.1-9
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• 2012

Long chain fatty acids (LCFAs) are transported into cells via plasma transporters, are activated to fatty acyl-CoA by fatty acyl-CoA synthase (ACS), and enter mitochondria via the carnitine system (CPT1/CACT/CPT2). The mitochondrial carnitine system plays an obligatory role in β-oxidation of LCFAs by catalyzing their transport into the mitochondrial matrix. Fatty acyl-CoAs are oxidized via the β-oxidation pathway, which results in the production of acetyl-CoA. The acetyl-CoA can be imported into the tricarboxylic acid (TCA) cycle for oxidation in the mitochondrial matrix or can be used for malonyl-CoA synthesis by acetyl-CoA carboxylase 2 (ACC2) in the cytoplasm. In skeletal muscle, ACC2 catalyzes the carboxylation of acetyl-CoA to form malonyl-CoA, which is a potent endogenous inhibitor of carnitine palmitoyltransferase 1 (CPT1). Thus, ACC2 indirectly inhibits the influx of fatty acids into the mitochondria. Fatty acid metabolism can also be regulated by malonyl-CoA-mediated inhibition of CPT1.