• Toxicological Research
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• v.11 no.2
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• pp.253-259
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• 1995

To investigate an effect of ethanol pretreatment on the bromobenzene metabolism, the brornobenzene (400 mg/kg body wt. i. p.) was given 3 times at intervals of one day to the male rats orally pretreated with 5% ethanol throughout 2 months. In the ethanol pretreated rats, liver injuries were not demonstrated on the basis of the liver weight per body weight, serum levels of alanine aminotransferase (ALT) activity and histopathologic findings. By the bromobenzene treatment, ethanol pretreated rats showed the more decreased levels of serum ALT and liver weight/body weight(%), and decreased degree of liver damage on histopathological observation than the control group. The ethanol pretreated rats showed the more increased activities of hepatic aniline hydroxylase, glutathione Stransf erase (GST) and the more decreased contents of glutathione than the control. Concomitantly the ethanol pretreated rats showed the more decreased contents of hepatic glutathione and increased activities of GST by the bromobenzene treatment. Above results indicate that ethanol pretreatment enhance the metabolizing ability of bromobenzene in rats.

• Mass Spectrometry Letters
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• v.2 no.1
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• pp.20-23
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• 2011

The purpose of this study is to investigate the in vitro metabolism of hesperetin, a bioflavonoid. Hesperetin was incubated with rat liver microsomes in the presence of NADPH and UDP-glucuronic acid for 30 min. The reaction mixture was analyzed by liquid chromatography-ion trap mass spectrometer and the chemical structures of hesperetin metabolites were characterzed based on their MS/MS spectra. As a result, a total of five metabolites were detected in rat liver microsomes. The metabolites were identified as a de-methylated metabolite (eriodictyol), two hesperetin glucuronides, and two eriodictyol glucuronides.

• The Korean Journal of Food And Nutrition
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• v.12 no.1
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• pp.20-25
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• 1999

The study was conducted to investigate the effect of cholesterol and fiber on liver lipid metabolism in rats. Male Sprague Dawley rats were administrated 1% cholesterol and 0.25% sodium cholate to induce hypercholesterolemia and were fed diet containing three levels(0%, 5% and 10%) of cellulose and pec-tin respectively. The rats were sacrified after 5 weeks of feeding period. Net weight gain and feed ef-ficiency ratio were increased in 10% fiber groups as compared to those of 5% fiber groups. Feed intake did not show significancy by fiber kinds and levels. Liver and kidney weights tended to be decreased in proportion to level of fiber. Heart weight was lowered in 10% fiber groups as compared to that of 5% fi-ber groups. Liver triglyceride concentration was significantly increased in pectin groups. Total-free-cholesterol and cholesteryl ester concentrations in liver were significantly decreased by fiber and were decreased in proportion to level of fiver. Phospholipid concentration was significantly decreased by fiber and were decreased in proportion to level of fiber. Phospholipid concentration was significantly decreased in 5% cellulose group. the results indicate that 10% pectin may have beneficial roles in hypercholester-olemia.

• Journal of Biomedical Engineering Research
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• v.43 no.1
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• pp.1-10
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• 2022

Non-alcoholic fatty liver disease(NAFLD) is excessive hepatic lipid accumulation mainly caused by obesity. This study aimed to evaluate whether micro-current stimulation(MCS) could modulate lipid metabolism regarding the Sirt1/AMPK pathway, fatty acid β-oxidation pathway, and lipolysis and lipogenesis-related factors in FL83B cells. For the NAFLD cell model, FL83B cells were treated with oleic acid for lipid accumulation. MCS were stimulated for 1 hr and used frequency 10 Hz, duty cycle 50%, and biphasic rectangular current pulse. The intensity of MCS was divided into 50, 100, 200, and 400 ㎂. Through the results of Oil red O staining, it was confirmed that MCSs with the intensity of 200 ㎂ and 400 ㎂ significantly reduced the degree of lipid droplet formation. Thus, these MCS intensities were applied to western blot analysis. Western blot analysis was performed to analyze the effects of MCS on lipid metabolism. MCS with the intensity of 400 ㎂ showed that significantly activated the Sirt1/AMPK pathway, a key pathway for regulating lipid metabolism in hepatocytes, and fatty acid β-oxidation-related transcription factors. Moreover, it activated the lipolysis pathway and suppressed lipogenesis-related transcription factors such as SREBP-1c, FAS, and PPARγ. In the case of MCS with the intensity of 200 ㎂, only PGC1α and SREBP-1c showed significant differences compared to cells treated only with oleic acid. Taken together, these results suggested that MCS with the intensity of 400 ㎂ could alleviate hepatic lipid accumulation by modulating lipid metabolism in hepatocytes.

• Animal Bioscience
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• v.37 no.3
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• pp.437-450
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• 2024

Objective: Vanin-1 (VNN1) is a pantetheinase that catalyses the hydrolysis of pantetheine to produce pantothenic acid and cysteamine. Our previous studies have shown that the VNN1 is specifically expressed in chicken liver which negatively regulated by microRNA-122. However, the functions of the VNN1 in lipid metabolism in chicken liver haven't been elucidated. Methods: First, we detected the VNN1 mRNA expression in 4-week chickens which were fasted 24 hours. Next, knocked out VNN1 via CRISPR/Cas9 system in the chicken Leghorn Male Hepatoma cell line. Detected the lipid deposition via oil red staining and analysis the content of triglycerides (TG), low-density lipoprotein-C (LDL-C), and high-density lipoprotein-C (HDL-C) after VNN1 knockout in Leghorn Male Hepatoma cell line. Then we captured various differentially expressed genes (DEGs) between VNN1-modified LMH cells and original LMH cells by RNA-seq. Results: Firstly, fasting-induced expression of VNN1. Meanwhile, we successfully used the CRISPR/Cas9 system to achieve targeted mutations of the VNN1 in the chicken LMH cell line. Moreover, the expression level of VNN1 mRNA in LMH-KO-VNN1 cells decreased compared with that in the wild-type LMH cells (p<0.0001). Compared with control, lipid deposition was decreased after knockout VNN1 via oil red staining, meanwhile, the contents of TG and LDL-C were significantly reduced, and the content of HDL-C was increased in LMH-KO-VNN1 cells. Transcriptome sequencing showed that there were 1,335 DEGs between LMH-KO-VNN1 cells and original LMH cells. Of these DEGs, 431 were upregulated, and 904 were downregulated. Gene ontology analyses of all DEGs showed that the lipid metabolism-related pathways, such as fatty acid biosynthesis and long-chain fatty acid biosynthesis, were enriched. KEGG pathway analyses showed that "lipid metabolism pathway", "energy metabolism", and "carbohydrate metabolism" were enriched. A total of 76 DEGs were involved in these pathways, of which 29 genes were upregulated (such as cytochrome P450 family 7 subfamily A member 1, ELOVL fatty acid elongase 2, and apolipoprotein A4) and 47 genes were downregulated (such as phosphoenolpyruvate carboxykinase 1) by VNN1 knockout in the LMH cells. Conclusion: These results suggest that VNN1 plays an important role in coordinating lipid metabolism in the chicken liver.

• Journal of Nutrition and Health
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• v.35 no.2
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• pp.171-182
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• 2002

This study wa performed to investigate the effect of dired powder of chestnut and acorn on lipid metabolism, antioxidative capacity and antithrombotic effect in rats. Fifty-four male Sprague-Dawley rats weighing 199$\pm$17g were blocked into nine groups according to their body weight. Rats were raised with diets containing only flesh or flesh with inner skin of 5% and 10% dried nut powders for four weeks. Food intake, body weight gain, food efficiency ratio and organ weight were no different among the experimental groups. The plasma and liver lipid levels of all the nut diet groups were lover than those of the control group. The nut diets showed hypolipidenic effect in the plasma and liver. Plasma and liver thiobarbituric acid reactive substance (TBARS) concentrations were significantly decreased in all the nut diet groups. The plasma TBARS levels of the inner skin groups were significantly different from the control group dose-dependently. Superoxide dismutase(SOD) activity was significantly different among the experimental groups, and all the nut groups showed higher activity than the control group. There were significant differences in SOD activity between the chestnut and acorn groups and the chestnut groups showed higher erythrocyte SOD activity and the acorn groups showed higher liver SOD activity than the other groups. Whereas catalase and GSH-Px activities in the erythrocyte and liver of both nut groups showed a tendency to increase, they were not significantly different among the experimental groups. The bleeding time and whole blood clotting time tended to be extended by feeding both types of nut but they were not significantly different among the experimental groups. Production of TX $B_2$ and PG $F_{1{\alpha}}$ was no different among the experimental groups. These results suggest that chestnut and acorn diets have the effect of lowering plasma and liver lipid levels, inhibiting lipid peroxide formation and increasing antioxidative enzymes activity. Thus, it is plausible that chestnut and acorn could be recommended in the treatment and prevention of cardiovascular diseases.

• Journal of the East Asian Society of Dietary Life
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• v.16 no.3
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• pp.281-291
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• 2006

This study investigated the effect of the powder of the small water dropwort(PSWD) and brewer's yeast(BY) on the liver function and serum lipid metabolism in alcohol-consuming rats. Male Sprague-Dawley rats were fed an AIN-93 diet(control), ethanol plus control(A), ethanol plus PSWD(AS), ethanol plus BY(AB), ethanol plus PSWD and BY(ABS) diet for seven weeks. The feed intake, body weight gain and feed efficiency ratio were the lowest and in the alcohol-consuming groups. The weight of the liver, kidney, spleen and epididymis of the anatomized rats showed positive correlation with the body weight gain. Compared with group A, the content of the lipid in the serum was significantly low in the AS and AB groups. In particular, it was the most effective in the AB group. The GOT, GPT and ALP level in the serum showed a significant difference in the alcohol-consuming groups. Compared with the A group, they showed a significantly low difference in the AS and AB groups. The total cholesterol and triglyceride levels in the liver were similar in all groups. The weight of the feces was significantly different but there was no significant difference in the content of total cholesterol and triglyceride levels in the AS and AB groups. These results suggest that BY and PSWD improve the liver function, and had an effect on reducing the lipid content of the serum and feces of alcohol-consumed rats. In particular, the effect of BY which contained protein, dietary fiber and vitamin B was higher than that of PSWD.

• Toxicological Research
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• v.11 no.2
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• pp.267-271
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• 1995

A single large dose of ethanol as well as chronic ethanol consumption produces alcoholic fatty liver in human and experimental animals. We examined the effects of YH439, a potential hepatoprotective agent, on alcoholic fatty liver generation in adult female rats. In rats treated with YH439 (250 mg/kg, po) 4 hr prior to a single dose of ethanol (6 g/kg, po), a significant decrease in hepatic triglyceride accumulation was observed. YH439 also has an inhibitory effect on hepatic triglyceride and cholesterol accumulation induced by repeated ethanol treatments for one week. Because it has been known that induction of alcoholic fatty liver is associated with lipid peroxidation and/or hepatic glutathione depression, the effect of YH439 on these parameters was determined in the livers of rats treated with ethanol. Coadministration with YH439 inhibited MDA formation and gIutathione depression induced by acute or repeated ethanol administration. In order to determine the effect of YH439 on ethanol metabolism in vivo, disappearance of ethanol from blood was measured. In rats treated with a single dose of ethanol (6 g/kg, po), the ethanol concentration in blood reached a peak approximately 120 min following the treatment which declined linearly for 18 hrs. YH439 had no effect on the decline of blood ethanol concentration regardless of the dose of ethanol given to rats. These results in this study suggest that YH439 has an inhibitory effect on fatty liver generation induced by acute or repeated ethanol consumption through a mechanism not directly related to the rate of ethanol metabolism in vivo.

• Toxicological Research
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• v.35 no.4
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• pp.403-410
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• 2019

Curcumin, a hydrophobic polyphenol isolated from the Curcuma longa L. plant, has many pharmacological properties, including antioxidant, anti-inflammatory, and chemo-preventive activities. Curcumin has been shown to have potential in preventing nonalcoholic fatty liver disease (NAFLD). However, the low bioavailability of curcumin has proven to be a major limiting factor in its clinical adoption. Theracurmin, a highly bioavailable curcumin that utilizes micronized technology showed improved biological absorbability in vivo. The aim of this study was to investigate the role of theracurmin in modulating hepatic lipid metabolism in vivo. A fatty liver mouse model was produced by feeding mice a high fat diet (HFD; 60% fat) for 12 weeks. We found that treatment for 12 weeks with theracurmin significantly lowered plasma triacylglycerol (TG) levels and reduced HFD-induced liver fat accumulation. Theracurmin treatment lowered hepatic TG and total cholesterol (T-CHO) levels in HFD-fed mice compared to controls. In addition, theracurmin administration significantly reduced lipid peroxidation and cellular damage caused by reactive oxygen species in HFD-fed mice. Overall, these results suggest that theracurmin has the ability to control lipid metabolism and can potentially serve as an effective therapeutic remedy for the prevention of fatty liver.

• Clinical Nutrition Research
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• v.12 no.2
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• pp.154-167
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• 2023

Hepatic encephalopathy (HE) associated with liver failure is accompanied by hyperammonemia, severe inflammation, depression, anxiety, and memory deficits as well as liver injury. Recent studies have focused on the liver-brain-inflammation axis to identify a therapeutic solution for patients with HE. Lipocalin-2 is an inflammation-related glycoprotein that is secreted by various organs and is involved in cellular mechanisms including iron homeostasis, glucose metabolism, cell death, neurite outgrowth, and neurogenesis. In this study, we investigated that the roles of lipocalin-2 both in the brain cortex of mice with HE and in Neuro-2a (N2A) cells. We detected elevated levels of lipocalin-2 both in the plasma and liver in a bile duct ligation mouse model of HE. We confirmed changes in cytokine expression, such as interleukin-1β, cyclooxygenase 2 expression, and iron metabolism related to gene expression through AKT-mediated signaling both in the brain cortex of mice with HE and N2A cells. Our data showed negative effects of hepatic lipocalin-2 on cell survival, iron homeostasis, and neurite outgrowth in N2A cells. Thus, we suggest that regulation of lipocalin-2 in the brain in HE may be a critical therapeutic approach to alleviate neuropathological problems focused on the liver-brain axis.