• Korean Journal of Veterinary Pathology
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• v.5 no.1
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• pp.9-16
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• 2001

To investigate the effects of safflower seed supplementation diet on the hepatic injury of rats administered with carbon tetrachloride (CCI$_4$), histopathological changes were assessed following acute and chronic administration in rats. In acute cases, all rats in group fed with 10% safflower seed supplementation diet survived despite the administration of lethal doses of $CCl_4$. However, most rats in group fed with control diet died. The hepatic injuries of survived rats, in the histopathological findings, were mild compared to those of dead rats. In the chronic cases, livers of group 2 fed with control diet were more progressive in fatty changes and centrilobular necrosis than those of group 3 fed with 20%safflower seed diet. However, after six weeks, livers of group 2 and 3 showed severe necrosis and mild fibrosis at the same time. Group 5 fed with 10% safflower seed supplementation diet and water containing 0.05% phenobarbital sodium showed mild fatty changes and necrosis compared with group 4 fed with control diet and water containing 0.05% phenobarbital sodium at sixth week. At 8 to 10 wee71s after the administration of $CCl_4$, severe fibrosis. fatty changes and marked necrosis were observed in group 4, but hepatic injuries were less severe in group 5. The present results suggested that safflower seed has some protective effect in hepatic lesions and consequently delay the progression of hepatic fibrosis.

• Journal of Microbiology and Biotechnology
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• v.23 no.3
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• pp.405-413
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• 2013

Monocyte chemotactic protein-3 (MCP-3), a chemokine that is in a superfamily of structurally related small chemotactic cytokines involved in leukocyte trafficking, is regarded as a key factor in atherogenesis. In this study, we examined the changes in atherogenic parameters including hepatic lipid accumulation and oxidative balance in MCP- 3-overexpressing transgenic mice (MCP-3 mice) under atherogenic conditions. To induce an extreme atherogenic condition, mice were fed a high-fat, high-cholesterol (HFHC) diet for 12 weeks. The body weight and food intake were not changed by MCP-3 overexpression in the aorta. On a HFHC diet, the MCP-3 mice had higher plasma levels of total cholesterol and a higher atherogenic index compared with wild-type mice, although there were no differences in the plasma HDL-cholesterol and triglyceride levels. Furthermore, an increase in lipid accumulation was observed in the aortas as well as the livers of the HFHC diet-fed MCP-3 mice compared with wild-type mice. The activities of antioxidant enzymes increased in the livers of the HFHC diet-fed MCP-3 mice, whereas supplementation with antioxidants, naringin and hesperidin, reversed the activities of the hepatic antioxidant enzymes in HFHC diet-fed MCP-3 mice, indicating that there might be more oxidative damage to the tissues in the HFHC diet-fed MCP-3 mice leading to progression towards atherosclerosis and hepatic steatosis. Microarray analyses of the aorta revealed atherosclerosis-, PPARs-, lipoprotein receptor, and apolipoprotein-related genes that were affected by the HFHC diet in MCP-3 mice. These findings suggest that aortic MCP-3 overexpression may contribute to the development of atherosclerosis and hepatic steatosis under atherogenic conditions.

• Journal of Environmental Health Sciences
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• v.10 no.2
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• pp.79-87
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• 1984

The purpose of the study is to determine the effects of Zn in lead poisoning rats by way of examining interaction mechanism of Pb and Zn. The fifty-five rats were Pb divided into four groups such as Zn group, group, Pb and Zn group, and control group. The rats of Zn group and of Zn and Pb group were subdivided into four groups by dose of Zn respectively 250mg/l, 500mg/l, 1, 000mg/l and 2, 000 mg/l. The rats having been fed the above mentioned chemicals, were weighed every five days for fifty-five days, and the subjects were slaughtered for measuring $\delta$-ALAD activities in blood and the accumulation amount of the chemicals in livers and kidneys. The results of the study are summarized as following 1. As for body weight gains, those of the control group rats were the highest, and those of Pb group the lowest. 2. $\delta$-ALAD activities of Pb group showed the tendency of decrease in comparison with those of control group. In Zn group, the subgroups of 250mg/l and 500mg/l showed higher activities than control group, whereas the subgroups of 1, 000mg/l and 2.000mg/l showed lower. 3. Hb value of Pb group was lower than that of control group. In Zn group, Hb value of the groups of 250mg/l and 500mg/l was a little higher than that of control group, while that of the groups of 1, 000mg/l and 2, 000mg/l was lower. 4. The amount of Pb and Zn accumulated in liver was much higher than in kidney. The amount of Pb accumulated in organs of Zn and Pb group decreased gradually in contrast to high concentration of Zn.

• Environmental Analysis Health and Toxicology
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• v.23 no.4
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• pp.325-335
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• 2008

The protective effects of the Naringin, on carbon tetrachloride ($CCl_4$)-induced hepatotoxicity and the possible mechanisms involved in this protection were investigated in mice. Pretreatment with Naringin prior to the administration of $CCl_4$ significantly prevented an increase in serum alanine, aspartate aminotransferase activity and hepatic lipid peroxidation in a dose-dependent manner. In addition, pretreatment with Naringin also significantly prevented the depletion of glutathione (GSH) content in the livers of $CCl_4$-induced mice. However, reduced hepatic glutathione levels was unaffected by treatment with Naringin alone. In addition, Naringin prevented $CCl_4$-induced apoptosis and necrosis, as indicated by a liver DNA laddering. To determine whether caspase-8,-3 pathway involved in $CCl_4$-induced acute liver injury, caspase-8, -3 activities were tested by ELISA. Naringin attenuated $CCl_4$induced caspase-8, -3 activities in mouse livers. $CCl_4$-induced hepatotoxicity was also prevented, as indicated by a liver histopathologic study. The effects of Naringin on the cytochrome P450 (CYP) 2E1, the major isozyme involved in $CCl_4$ were also investigated. Treatment of mice with Naringin resulted in a significant decrease of the CYP2E1-dependent hydroxyl at ion and aniline in a dose-dependent manner. These findings suggest that protective effects of Naringin against the $CCl_4$-induced hepatotoxicity may be due to its ability to block CYP2E1-mediated $CCl_4$ bioactivation and that is also protects against caspase-8, -3 pathway mediated apoptosis.

• Journal of Korean Society of Occupational and Environmental Hygiene
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• v.21 no.2
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• pp.82-89
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• 2011

Methylcyclohexane is frequently used in industrial sites (2,592tons/year) as rubber adhesives, ink, paint thinners, organic solvents, and so on. However, there are limited data on the toxic evaluation of methylcyclohexane. This study aims to predict the hazards and neurological effects of methylcyclohexane using SD rats in order to prevent health disorders of workers. The OECD Guideline for Testing of Chemicals (OECD, 2001) was used as a reference during the tests. For 13 weeks (once a day, five days per week) 0, 10, 100 and 1,000mg/kg/day of methylcyclohexane was injected to SD rats to observe any changes in the body or organ weight, hematology, histopathology, mobility, blood pressure, and neurotransmitter. As a result, some male and female SD rats injected with 1,000mg/kg/day of methylcyclohexane died. On the other hand, surviving rats showed significant changes such as hematological changes involving the decrease in the number of red blood corpuscles, and the decrease or increase in the weight of the lungs, kidneys, spleens, and livers (p< 0.05, p<0.01). Also histopathological lesions were observed in the hearts and kidneys. In the test for the effect on the nervous system, SD rats injected with 100mg/kg/day of methylcyclohexane had higher blood pressure levels compared to the control group. However, no abnormal effects was observed in the mobility, serotonin, neurotransmitter, and the biopsy of the brain and coronary arteries. The study results revealed that the livers, hearts, and kidneys were affected by methylcyclohexane. The absolute toxic dose of methylcyclohexane is 1,000mg/kg/day, NOAEL is 100 mg/kg/day, and it is not a toxic substance to the nervous system.

• Korean Journal of Community Nutrition
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• v.3 no.4
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• pp.622-629
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• 1998

This study was performed to investigate the effect of dietary intakes and nutritional status for fatty liver male patients with fatty livers. General characteristics, nutritional knowledge, and dietary intakes were obtained from fatty liver male patients aged 20-60yr living in Seoul and Kyunggi province by individual interview and blood samples. The Results were as follows : the mean age of the subjects was 39yrs. Old and over half the subjects were overweight. Although nutritional knowledge, recognition, and accuracy scores were good, these did not affect the subject's health. The average alcohol intake of subjects was 79.8g/day and the drinking duration was 5-40yrs(average : 17yrs). The subjects drank alcohol over 4tiles/week and preferred Soju. Most side dishes taken with alcohol drinking by the subjects were foods from animal sources. Half of the subjects also drank alcohol the next day for breakfast as a hangover-chaser. The reasons for drinking were due to social relationships and by habit. Vitamin D and folate were lower than the RDA for Koreans, and other nutrient amounts were higher than the RDA. The amounts of aspartate amino-transferase(AST), Alanine amino-transferase(ALT), ${\gamma}$-glutamyl transpeptidase(${\gamma}$-GTP), Triglyceride(TG) for the subjects were higher. In conclusion, fatty liver patients drank excessively and frequently. It seems that heavy alcohol drinking is more prone to overweight or obese people and contributes to fatty livers. Therefore, the subjects need to be taken effectively educated about alcohol-induced liver damage and the importance of a balanced diet for on healthy liver.

• Animal Bioscience
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• v.34 no.11
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• pp.1766-1775
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• 2021

Objective: The oxidative stress status and changes of chicken ovary tissue after shading were studied, to determine the mechanism of the effect of shading on follicular development. Methods: Twenty healthy laying hens (40 weeks old) with uniform body weight and the same laying rate were randomly divided into two groups (the shading group and normal light group). In the shading group, the cage was covered to reduce the light intensity inside the cage to 0 without affecting ventilation or food intake. The normal lighting group received no additional treatment. After 7 days of shading, oxidative stress related indicators and gene expression were detected. Results: Analysis of paraffin and ultrathin sections showed that apoptosis of ovarian granulosa cells (GCs) increased significantly after light shading. Enzyme linked immunosorbent assay results revealed that the levels of total antioxidant capacity, malondialdehyde, superoxide dismutase (SOD), glutathione, catalase (CAT), and other substances in the sera, livers, ovaries, and follicular GCs of laying hens increased significantly after shading for 7 days; and reactive oxygen species (ROS) levels in the livers of laying hens also increased significantly. ROS in the serum, ovarian and GCs also increased. After shading for 7 days, the levels of 8-hydroxy-2 deoxyguanosine in the sera and ovarian tissues of laying hens increased significantly. Cell counting kit-8 detection showed that the proliferation activity of GCs in layer follicles decreased after shading for 7 days; the expression level of the anti-apoptotic gene B-cell lymphoma-2 in ovarian tissue and follicular GCs was significantly reduced, and the expression levels of pro-apoptotic caspase 3 (casp3), and SOD, glutathione peroxidase 2 (GPX2), and CAT were all significantly increased. Conclusion: Oxidative stress induced by shading light has a serious inhibitory effect on follicular development during reproduction in laying hens.

• Animal Bioscience
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• v.34 no.5
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• pp.922-930
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• 2021

Objective: Tibetan pigs, predominantly originating from the Tibetan Plateau, have been subjected to long-term natural selection in an extreme environment. To characterize the metabolic adaptations to hypoxic conditions, transcriptomic and proteomic expression patterns in the livers of Tibetan and Yorkshire pigs were compared. Methods: RNA and protein were extracted from liver tissue of Tibetan and Yorkshire pigs (n = 3, each). Differentially expressed genes and proteins were subjected to gene ontology and Kyoto encyclopedia of genes and genomes functional enrichment analyses. Results: In the RNA-Seq and isobaric tags for relative and absolute quantitation analyses, a total of 18,791 genes and 3,390 proteins were detected and compared. Of these, 273 and 257 differentially expressed genes and proteins were identified. Evidence from functional enrichment analysis showed that many genes were involved in metabolic processes. The combined transcriptomic and proteomic analyses revealed that small molecular biosynthesis, metabolic processes, and organic hydroxyl compound metabolic processes were the major processes operating differently in the two breeds. The important genes include retinol dehydrogenase 16, adenine phosphoribosyltransferase, prenylcysteine oxidase 1, sorbin and SH3 domain containing 2, ENSSSCG00000036224, perilipin 2, ladinin 1, kynurenine aminotransferase 1, and dimethylarginine dimethylaminohydrolase 1. Conclusion: The findings of this study provide novel insight into the high-altitude metabolic adaptation of Tibetan pigs.

• Nutrition Research and Practice
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• v.15 no.2
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• pp.160-172
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• 2021

BACKGROUND/OBJECTIVES: Nutritional status and food intake during pregnancy and lactation can affect fetal programming. In the current metabolic syndrome epidemic, high-fructose diets have been strongly implicated. This study investigated the effect of maternal high-fructose intake during pregnancy and lactation on the development of metabolic syndrome in adult offspring. SUBJECTS/METHODS: Drinking water with or without 20% fructose was administered to female C57BL/6J mice over the course of their pregnancy and lactation periods. After weaning, pups ate regular chow. Accu-Chek Performa was used to measure glucose levels, and a tail-cuff method was used to examine systolic blood pressure. Animals were sacrificed at 7 months, their livers were excised, and sections were stained with Oil Red O and hematoxylin and eosin (H&E) staining. Kidneys were collected for gene expression analysis using quantitative real-time Polymerase chain reaction. RESULTS: Adult offspring exposed to maternal high-fructose intake during pregnancy and lactation presented with heavier body weights, fattier livers, and broader areas under the curve in glucose tolerance test values than control offspring. Serum levels of alanine aminotransferase, aspartate aminotransferase, glucose, triglycerides, and total cholesterol and systolic blood pressure in the maternal high-fructose group were higher than that in controls. However, there were no significant differences in mRNA expressions of renin-angiotensin-aldosterone system genes and sodium transporter genes. CONCLUSIONS: These results suggest that maternal high-fructose intake during pregnancy and lactation induces metabolic syndrome with hyperglycemia, hypertension, and dyslipidemia in adult offspring.

• Molecules and Cells
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• v.45 no.4
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• pp.180-192
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• 2022

Nuclear receptor coactivator 6 (NCOA6) is a transcriptional coactivator of nuclear receptors and other transcription factors. A general Ncoa6 knockout mouse was previously shown to be embryonic lethal, but we here generated liver-specific Ncoa6 knockout (Ncoa6 LKO) mice to investigate the metabolic function of NCOA6 in the liver. These Ncoa6 LKO mice exhibited similar blood glucose and insulin levels to wild type but showed improvements in glucose tolerance, insulin sensitivity, and pyruvate tolerance. The decrease in glucose production from pyruvate in these LKO mice was consistent with the abrogation of the fasting-stimulated induction of gluconeogenic genes, phosphoenolpyruvate carboxykinase 1 (Pck1) and glucose-6-phosphatase (G6pc). The forskolin-stimulated inductions of Pck1 and G6pc were also dramatically reduced in primary hepatocytes isolated from Ncoa6 LKO mice, whereas the expression levels of other gluconeogenic gene regulators, including cAMP response element binding protein (Creb), forkhead box protein O1 and peroxisome proliferator-activated receptor γ coactivator 1α, were unaltered in the LKO mouse livers. CREB phosphorylation via fasting or forskolin stimulation was normal in the livers and primary hepatocytes of the LKO mice. Notably, it was observed that CREB interacts with NCOA6. The transcriptional activity of CREB was found to be enhanced by NCOA6 in the context of Pck1 and G6pc promoters. NCOA6-dependent augmentation was abolished in cAMP response element (CRE) mutant promoters of the Pck1 and G6pc genes. Our present results suggest that NCOA6 regulates hepatic gluconeogenesis by modulating glucagon/cAMP-dependent gluconeogenic gene transcription through an interaction with CREB.