• Journal of the Korean Applied Science and Technology
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• v.35 no.2
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• pp.485-491
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• 2018

The purpose of this study was to probe the influences of krill (Euphausia superba) meal supplementation on a dose effect relationship between fluoride levels of krill meal and serum hepatic functional enzyme activity such as alkaline phosphatase (ALP), aspartate aminotransferase (AST), alanine aminotransferase (ALT), and lactate dehydrogenase (LDH) in rats fed experimental diets for 5 weeks. There were no significant differences in the activities of ALP, AST, ALT, and LDH in sera among krill meal diet groups (KM10, KM20, KM30). However, these groups were significantly (p<0.05) lower enzyme activities than control group (CG). The fluoride levels of sera and organ tissues (liver, brain, heart, lung, kidney) in krill meal diet groups (KM10, KM20, KM30) were significantly increased by adding krill meal in comparison with CG. The results indicate that a difficult to found toxicity to the liver from krill meal diet groups.

• Clinical and Experimental Pediatrics
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• v.61 no.1
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• pp.12-16
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• 2018

Purpose: To differentiate adenoviral pharyngoconjunctival fever (PCF) from acute Kawasaki disease (KD) using laboratory tests before results of virus-real time polymerase chain reaction and ophthalmologic examination are obtained. Methods: Baseline patient characteristics and laboratory measurements were compared between 40 patients with adenovirus infection and 123 patients with KD. Results: The patients with adenovirus infection were generally older than those with KD (median: 3.9 years vs. 2 years, P=0.000). White blood cell and, platelet count, and aspartate aminotransferase, alanine aminotransferase, and N-terminal pro-brain natriuretic peptide (NT-proBNP) levels showed significant differences between the 2 groups, but the C-reactive protein (CRP) levels did not ($6.8{\pm}3.0mg/dL$ vs. $8.3{\pm}5.8mg/dL$, P=0.126). In the adenovirus infection group, the CRP levels were <1, <3, <10, and ${\geq}10mg/dL$ in 2 (5%), 3 (7.5%), 30 (75%), and 5 patients (12.5%), respectively. The cutoff NT-proBNP level was 265 pg/mL. Discrepancy was defined as CRP and NT-proBNP levels of ${\geq}3$ or <3 mg/dL, and <265 or ${\geq}265pg/mL$, respectively. Among the 35 patients with adenovirus infection whose CRP levels were ${\geq}3mg/dL$, 29 (82.9%) showed a discrepancy. Conversely, of the 103 patients with KD whose CRP levels were ${\geq}3mg/dL$, 83 (80.6%) showed no discrepancy. Between the groups, a significant difference in discrepancy rate was observed (P=0.000). None of the patients with adenovirus infection had CRP and NT-proBNP levels of <3 mg/dL and ${\geq}265pg/mL$, respectively. Conclusion: With a sensitivity of 82.9% and a specificity of 80.6%, CRP and NT-proBNP levels may differentiate between adenoviral PCF and acute KD.

• Journal of Nutrition and Health
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• v.31 no.2
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• pp.159-165
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• 1998

This study was undertaken to examine relations between obesity and birthweight, parental weight and serum biochemical levels(lipids , glucose, insulin and aminotransferase) in elementary school children aged 10-12 . The weight of obese girls was higher than that of obese boys, while WHR was higher in obese boys than in obese girls. The birth weight of the obese children was significantly higher than that of the non-obese children(p<0.01), and was positively correlated with current weight. The concentrations of serum TG, LDL, VLDL, LDL-cholesterol, glucose, insulin and ALT in obese children were much higher than those in non-obese children . However, the serum HDL -cholesterol concentration of the obese children was significantly lower compared with that of the no-obese children. On the other hand, little differences in these levels were found between genders. The concentrations of PL, TC and AST in the groups showed no significant differences. In the obese children, serum concentrations of TG, LDL-cholesterol , glucose and ALT were more closely associated with GMI than with WHR. No significant correlation was found with serum insulin , glucose and TG levels. These data show that childhood obesity may be related to hyperlipidemia , atherosclerosis, hypertension, diabetes mellitus and fatty liver.

• Nutrition Research and Practice
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• v.9 no.2
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• pp.144-149
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• 2015

BACKGROUND/OBJECTIVE: The aim of this study was to examine the effect of high dietary methionine (Met) consumption on plasma and hepatic oxidative stress and dyslipidemia in chronic ethanol fed rats. MATERIALS/METHODS: Male Wistar rats were fed control or ethanol-containing liquid diets supplemented without (E group) or with DL-Met at 0.6% (EM1 group) or 0.8% (EM2 group) for five weeks. Plasma aminothiols, lipids, malondialdehyde (MDA), alanine aminotransferase (ALT), and aspartate aminotransferase were measured. Hepatic folate, S-adenosylmethionine (SAM), and S-adenosylhomocysteine (SAH) were measured. RESULTS: DL-Met supplementation was found to increase plasma levels of homocysteine (Hcy), triglyceride (TG), total cholesterol (TC), and MDA compared to rats fed ethanol alone and decrease plasma ALT. However, DL-Met supplementation did not significantly change plasma levels of HDL-cholesterol, cysteine, cysteinylglycine, and glutathione. In addition, DL-Met supplementation increased hepatic levels of folate, SAM, SAH, and SAM:SAH ratio. Our data showed that DL-Met supplementation can increase plasma oxidative stress and atherogenic effects by elevating plasma Hcy, TG, and TC in ethanol-fed rats. CONCLUSION: The present results demonstrate that Met supplementation increases plasma oxidative stress and atherogenic effects by inducing dyslipidemia and hyperhomocysteinemia in ethanol-fed rats.

• Natural Product Sciences
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• v.20 no.4
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• pp.262-268
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• 2014

Rutaecarpine is one of the major alkaloids present in the fruits of Evodia rutaecarpa. In this study, rutaecarpine was evaluated, both in vitro and in vivo, for its hepatoprotective properties against thioacetamide (TAA)-induced hepatic fibrosis. The results showed that rutaecarpine inhibited TAA-induced cytotoxicity, reduced the expression of the fibrogenic cytokine transforming growth factor ${\beta}1$ ($TGF-{\beta}1$), and induced the expression of bcl-2. To evaluate its in vivo effects, animal models with TAA-induced hepatic fibrosis were utilized. Levels of liver tissue injury-associated enzymes, including alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were monitored. $TGF-{\beta}1$ and the ${\alpha}$-smooth muscle actin (${\alpha}$-SMA) were measured as markers of the protective effects on hepatic fibrosis. The AST and ALT levels in blood were greatly enhanced by TAA and completely blunted by rutaecarpine. Rutaecarpine led to the down-regulation of $TGF-{\beta}$ and Bax mRNA expression, as well as the up-regulation of Bcl-2 and $Bcl-X_L$ mRNA levels. In conclusion, rutaecarpine inhibited TAA-induced hepatic fibrosis and apoptosis by inducing the expression of Bcl-2 while blocking $TGF-{\beta}1$ in our TAA-intoxicated model.

• Archives of Pharmacal Research
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• v.26 no.5
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• pp.351-357
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• 2003

Five kinds of allylthiopyridazine derivatives were synthesized and their chemoprotective activities examined in rats exposed to aflatoxin $B_1$-toxicant. Rats were pretreated with five allylthiopyridazine derivatives at daily oral doses of 50 mg/kg for 10 consecutive days, and during this period with one or three repeated doses of the potent hepatotoxin, aflatoxin $B_1$. The hepatoprotective effects of the allylthiopyridazine derivatives against aflatoxin $B_1$ (1 mg/kg, three times at intervals of 3 days, i.p., or at 3 mg/kg, once at final days, i.p.) administration were showed the significantly normal as compared with control in body and liver weights. Aspartate aminotransferase and alanine aminotransferase levels were markedly elevated after aflatoxin $B_1$ administration, and pretreatment with allylthiopyridazine derivatives, before aflatoxin $B_1$ administration, resulted in decreased levels of these enzymes. In addition, the allylthiopyridazine derivatives, K6 (3-methoxy-), K8 (3-chloro-), K16 (3-ethoxy-) and K17 (3-n-propoxy), induced elevated hepatic GSH levels. Four kinds of allylthiopyridazine derivatives investigated were effective against aflatoxin $B_1$ -induced hepatotoxicity.

• Food Science and Biotechnology
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• v.17 no.6
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• pp.1207-1213
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• 2008

The possible protective effects of highly zinc-containing yeast Saccharomyces cerevisiae, FF-10 strain, isolated from tropical fruit rambutan on acute alcoholic liver injury in rats were evaluated. Zinc concentration in this strain was 30.6mg%. The activities of serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), and $\gamma$-glutamyl transpeptidase ($\gamma$-GTP) were highly increased when alcohol was treated, relative to the normal rats. Also, a highly significant increase in the blood alcohol and acetaldehyde levels by alcohol treatment was observed. Administration of FF-10 strain markedly prevented alcohol-induced elevation of the activities of serum ALT, AST, and $\gamma$-GTP, and the levels of blood alcohol and acetaldehyde, and these reduced levels reached to that of normal rats. As compared with alcohol treated control rats, the FF-10 strain supplementation showed highly decreased the triglyceride concentration in serum. Alcohol treatment induced the marked accumulation of small lipid droplets, hepatocytes necrosis, and inflammation, but FF-10 strain administration attenuated to alcohol-induced accumulation of small lipid droplets and hepatocyte necrosis in the liver. Therefore, the current finding suggests that zinc-enriched yeast FF-10 strain isolated from tropical fruit rambutan may have protective effect against alcohol-induced hepatotoxicity.

• Asian-Australasian Journal of Animal Sciences
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• v.8 no.4
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• pp.379-385
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• 1995

Ninety Wistar male rats were used to study the effects of vitamin E and Se supplementation to diets containing aflatoxin $B_1$ on the contents of liver lipids and various blood parameters. Two levels of dietary aflatoxin (0 and 1 ppm), 3 levels of vitamin E (30, 60 and 120 IU/kg), and 3 levels of Se (0.1, 1 and 2 ppm) were used to design a $2{\times}3{\times}3$ factorial experiment. Rats, weighing about 200 g, were randomly allotted to 18 cages, 5 rats per cage. The aflatoxin significantly (p < .05) decreased growth rate, feed intake and feed efficiency. Aflatoxin increased the glucose level and decreased the cholesterol level in blood significantly. Levels of blood triglyceride, total protein, and albumin were not affected by aflatoxin, vitamin E or Se. Activities of blood alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were significantly increased by aflatoxin; however, the glutathione peroxidase (GSH-Px) activity in the blood was decreased by aflatoxin even in the presence of Se. The vitamin E supplementation decreased the AST activity significantly, while GSH-Px activity increased significantly as the levels of dietary Se increased. The levels of total cholesterol and free cholesterol in the liver were significantly lower in rats receiving aflatoxin, while the extra vitamin E supplementation increased these hepatic cholesterol levels. It was concluded that the extra dietary vitamin E or Se supplementation might partially alleviate some of the harmful effects of aflatoxin in rats.

• Preventive Nutrition and Food Science
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• v.21 no.3
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• pp.171-180
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• 2016

Non-alcoholic fatty liver disease (NAFLD) is one of the most prevalent liver diseases associated with an altered lifestyle, besides genetic factors. The control and management of NAFLD mostly depend on lifestyle modifications, due to the lack of a specific therapeutic approach. In this context, we assessed the effect of carrot juice on the development of high fructose-induced hepatic steatosis. For this purpose, male weanling Wistar rats were divided into 4 groups, fed either a control (Con) or high fructose (HFr) diet of AIN93G composition, with or without carrot juice (CJ) for 8 weeks. At the end of the experimental period, plasma biochemical markers, such as triglycerides, alanine aminotransferase, and ${\beta}$-hydroxy butyrate levels were comparable among the 4 groups. Although, the liver injury marker, aspartate aminotransferase, levels in plasma showed a reduction, hepatic triglycerides levels were not significantly reduced by carrot juice ingestion in the HFr diet-fed rats (HFr-CJ). On the other hand, the key triglyceride synthesis pathway enzyme, hepatic stearoyl-CoA desaturase 1 (SCD1), expression at mRNA level was augmented by carrot juice ingestion, while their protein levels showed a significant reduction, which corroborated with decreased monounsaturated fatty acids (MUFA), particularly palmitoleic (C16:1) and oleic (C18:1) acids. Notably, it also improved the long chain n-3 polyunsaturated fatty acid, docosahexaenoic acid (DHA; C22:6) content of the liver in HFr-CJ. In conclusion, carrot juice ingestion decreased the SCD1-mediated production of MUFA and improved DHA levels in liver, under high fructose diet-fed conditions. However, these changes did not significantly lower the hepatic triglyceride levels.

• Asian-Australasian Journal of Animal Sciences
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• v.27 no.12
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• pp.1744-1748
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• 2014

A dose-response experiment with seven supplemental pyridoxine levels (0, 0.66, 1.32, 1.98, 2.64, 3.30, and 3.96 mg/kg) was conducted to investigate the effects of pyridoxine on growth performance and plasma aminotransferases and homocysteine of White Pekin ducks and to estimate pyridoxine requirement for these birds. A total of 336 one-day-old male White Pekin ducks were divided to 7 experimental treatments and each treatment contained 8 replicate pens with 6 birds per pen. Ducks were reared in raised wire-floor pens from hatch to 28 d of age. At 28 d of age, the weight gain, feed intake, feed/gain, and the aspartate aminotransferase, alanine aminotransferase, and homocysteine in plasma of ducks from each pen were all measured. In our study, the pyridoxine deficiency of ducks was characterized by growth depression, decreasing plasma aspartate aminotransferase activity and increasing plasma homocysteine. The ducks fed vitamin $B_6$-deficient basal diets had the worst weight gain and feed/gain among all birds and this growth depression was alleviated (p<0.05) when pyridoxine was supplemented to basal diets. On the other hand, plasma aspartate aminotransferase and homocysteine may be the sensitive indicators for vitamin $B_6$ status of ducks. The ducks fed basal diets had much lower aspartate aminotransferase activity and higher homocysteine level in plasma compared with other birds fed pyridoxine-supplemented diets (p<0.05). According to quadratic regression, the supplemental pyridoxine requirements of Pekin ducks from hatch to 28 days of age was 2.44 mg/kg for feed/gain and 2.08 mg/kg for plasma aspartate aminotransferase and the corresponding total requirements of this vitamin for these two criteria were 4.37 and 4.01 mg/kg when the pyridoxine concentration of basal diets was included, respectively. All data suggested that pyridoxine deficiency could cause growth retardation in ducks and the deficiency of this vitamin could be indicated by decreasing plasma aspartate aminotransferase activity and increasing plasma homocysteine.