• Nutrition Research and Practice
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• v.7 no.4
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• pp.287-293
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• 2013

This study determined the effects of fucoxanthin on gene expressions related to lipid metabolism in rats with a high-fat diet. Rats were fed with normal fat diet (NF, 7% fat) group, high fat diet group (HF, 20% fat), and high fat with 0.2% fucoxanthin diet group (HF+Fxn) for 4 weeks. Body weight changes and lipid profiles in plasma, liver, and feces were determined. The mRNA expressions of transcriptional factors such as sterol regulatory element binding protein (SREBP)-1c, Carnitine palmitoyltransferase-1 (CPT1), Cholesterol $7{\alpha}$-hydroxylase1 (CYP7A1) as well as mRNA expression of several lipogenic enzymes were determined. Fucoxanthin supplements significantly increased plasma high density lipoprotein (HDL) concentration (P < 0.05). The hepatic total lipids, total cholesterols, and triglycerides were significantly decreased while the fecal excretions of total lipids, cholesterol, and triglycerides were significantly increased in HF+Fxn group (P < 0.05). The mRNA expression of hepatic Acetyl-CoA carboxylase (ACC), Fatty acid synthase (FAS), and Glucose-6-phosphate dehydrogenase (G6PDH) as well as SREBP-1C were significantly lower in HF+Fxn group compared to the HF group (P < 0.05). The hepatic mRNA expression of Hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) and Acyl-CoA cholesterol acyltransferase (ACAT) were significantly low while lecithin-cholesterol acyltransferase (LCAT) was significantly high in the HF+Fxn group (P < 0.05). There was significant increase in mRNA expression of CPT1 and CYP7A1 in the HF+Fxn group, compared to the HF group (P < 0.05). In conclusion, consumption of fucoxanthin is thought to be effective in improving lipid and cholesterol metabolism in rats with a high fat diet.

• The Korean Journal of Physiology and Pharmacology
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• v.22 no.1
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• pp.23-33
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• 2018

Cushing's syndrome (CS) is a collection of symptoms caused by prolonged exposure to excess cortisol. Chronically elevated glucocorticoid (GC) levels contribute to hepatic steatosis. We hypothesized that histone deacetylase inhibitors (HDACi) could attenuate hepatic steatosis through glucocorticoid receptor (GR) acetylation in experimental CS. To induce CS, we administered adrenocorticotropic hormone (ACTH; 40 ng/kg/day) to Sprague-Dawley rats by subcutaneous infusion with osmotic mini-pumps. We administered the HDACi, sodium valproate (VPA; 0.71% w/v), in the drinking water. Treatment with the HDACi decreased steatosis and the expression of lipogenic genes in the livers of CS rats. The enrichment of GR at the promoters of the lipogenic genes, such as acetyl-CoA carboxylase (Acc), fatty acid synthase (Fasn), and sterol regulatory element binding protein 1c (Srebp1c), was markedly decreased by VPA. Pan-HDACi and an HDAC class I-specific inhibitor, but not an HDAC class II a-specific inhibitor, attenuated dexamethasone (DEX)-induced lipogenesis in HepG2 cells. The transcriptional activity of Fasn was decreased by pretreatment with VPA. In addition, pretreatment with VPA decreased DEX-induced binding of GR to the glucocorticoid response element (GRE). Treatment with VPA increased the acetylation of GR in ACTH-infused rats and DEX-induced HepG2 cells. Taken together, these results indicate that HDAC inhibition attenuates hepatic steatosis through GR acetylation in experimental CS.

• Journal of Microbiology and Biotechnology
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• v.27 no.11
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• pp.1925-1931
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• 2017

Korean red pine (Pinus densiflora) bark extract, PineXol (PX), was investigated for its potential antioxidant and anti-inflammation effects in vitro. It was hypothesized that PX treatment ($25-150{\mu}g/ml$) would reduce the lipid synthesis in HepG2 hepatocytes as well as lipid accumulation in 3T3-L1 adipocytes. Hepatocytes' intracellular triglycerides and cholesterol were decreased in the PX $150{\mu}g/ml$ treatment group compared with the control (p < 0.05). Consequently, de novo lipogenic proteins (acetyl-CoA carboxylase 1, stearoyl-CoA desaturase 1, elongase of very long chain fatty acids 6, glycerol-3-phosphate acyltransferase 1, and sterol regulatory element-binding protein 1) were significantly decreased in hepatocytes by PX $150{\mu}g/ml$ treatment compared with the control (p < 0.05). In differentiated 3T3-L1 adipocytes, the lipid accumulation was significantly attenuated by all PX treatments (p < 0.01). Regulators of adipogenesis, including CCAAT-enhancer-binding proteins alpha, peroxisome proliferatoractivated receptor gamma, and perilipin, were decreased in PX $100{\mu}g/ml$ treatment compared with the control (p < 0.05). In conclusion, PX might have anti-obesity effects by blocking hepatic lipogenesis and by inhibiting adipogenesis in adipocytes.

• Journal of Nutrition and Health
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• v.56 no.6
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• pp.641-654
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• 2023

Purpose: Sour cherry (Prunus cerasus L.) contains abounding phytochemicals, such as polyphenols and anthocyanins, and has antioxidative effects. Adenosine monophosphate-activated protein kinase (AMPK) is a crucial regulator in enhancing the lipid metabolism. This study hypothesized that the intake of sour cherry affects AMPK signaling. Therefore, this study examined whether sour cherry regulates AMPK to balance the hepatic lipid metabolism and exert ameliorating effects. Methods: Male C57BL/6J mice had obesity induced with a 45% fat diet. The mice were divided into four groups: control (CON), high-fat diet (HFD), low percentage sour cherry powder (LSC), and high percentage sour cherry powder (HSC). The mice in the sour cherry groups were fed 1% sour cherry or 5% sour cherry in their respective diets for 12 weeks. Results: The body weight, visceral fat weight, and lipid droplet size significantly decreased in the treatment groups. The serum and hepatic triglyceride and total cholesterol levels improved significantly in the HSC group. The low-density lipoprotein cholesterol levels were also reduced significantly, whereas the high-density lipoprotein cholesterol levels were increased significantly in both treatment groups. The sterol regulator binding protein-1c and fatty acid synthase expression levels as fatty acid synthesis-related enzymes were significantly lower in the treatment groups than in the high-fat diet group. Furthermore, the adipose triglyceride lipase and hormone-sensitive lipase expression levels as lipolytic enzyme activity and AMPK/acetyl-CoA carboxylase/carnitine palmitoyltransferase-1 as fatty acid β-oxidation-related pathway were upregulated significantly in both sour cherry groups. Conclusions: These results show that sour cherry intake improves hepatic lipid synthesis and chronic diseases by activating AMPK signaling. Therefore, this study suggests that phytochemical-rich sour cherry can be developed as a healthy functional food.

• Asian-Australasian Journal of Animal Sciences
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• v.13 no.12
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• pp.1758-1763
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• 2000

The effect of tu-chung (Eucommia ulmoides, Oliver) leaf meal on reducing lipid accumulation in chickens fed 1% cholesterol containing diet was studied. Forty male White Leghorn chickens aged 56 days were weighed and divided into four groups of ten chickens, and fed diets with or without 1% dietary cholesterol which were supplemented with 0 and 5% tu-chung. Tu-chung supplementation to the diet without cholesterol increased acetyl-CoA carboxylase (p<0.01) but decreased 3-hydroxy-3-methylglutaryl-CoA reductase activities (p<0.01) with no effect on fatty acid synthetase activities. However, its supplementation to the diet with cholesterol had no effect on these three enzyme activities as compared with the cholesterol containing diet without tu-chung. Tu-chung supplementation to the diet without cholesterol increased hepatic triglyceride (p<0.01), whereas its supplementation to the diet with cholesterol decreased it (p<0.01). Tu-chung supplementation to the diet with cholesterol decreased plasma cholesterol ester, free cholesterol, phospholipids (p<0.05) and triglyceride (p<0.01) as compared with the cholesterol containing diet without tu-chung. Supplementation of tu-chung to the diet without cholesterol decreased plasma free cholesterol (p<0.05). It is concluded that tu-chung leaf meal reduced an increase in lipid accumulation in chickens stimulated by 1% cholesterol feeding.

• Asian-Australasian Journal of Animal Sciences
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• v.14 no.4
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• pp.535-539
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• 2001

The present study was conducted to evaluate the effect of fermented chub mackerel extract (FCME) on lipid metabolism in rats fed diets without cholesterol. Four week-old male rats were divided into three groups of 10 rats with 0, 1% or 2% FCME supplementation to the diets. Purified diets were used in the present study. Feed and water were fed ad libitum. FCME supplementation had no effect on the activities of acetyl-CoA carboxylase, fatty acid synthetase, and the content of free cholesterol, triglyceride and phospholipid in the liver (p>0.05). 1% FCME supplementation significantly increased serum triglyceride (p<0.05) and hepatic 3-hydroxy-3-methylglutaryl-CoA reductase activity (p<0.05) with no effect on serum total cholesterol, free cholesterol and phospholipid concentration. FCME supplementation significantly reduced serum LDL+VLDL-cholesterol (p<0.01) and atherogenic index (p<0.01) with no effect on HDL-cholesterol. The current study showed that FCME inclusion might reduce the risk of atherosclerosis in rats fed diet without cholesterol.

• The Journal of Korean Medicine
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• v.27 no.3 s.67
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• pp.14-25
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• 2006

Objectives: Samjunghwan has been known to be effective for the treatment of obesity. To show the effectiveness of Samjunghwan in a more scientific way, Samjunghwan extract was prepared and evaluated in high-fat diet rats by measuring the changes of body weight and lipid metabolism as described below. Methods: 245 g of crushed Samjunghwan was extracted with methyl alcohol. The extract was evaporated under reduced pressure to give 21.8 g. For 30 days, the control group rats were given a high fat diet, while the test group rats were given a high fat diet plus Samjunghwan extract. The normal group rats were given a normal diet. 50 mg of Samjunghwan extract per 1 kg of body weight was added to the diet for the test group rats. Results: The control group rats on a high fat diet gained weight by about 27-28% as compared to the normal group, whereas the test group rats on a high fat diet plus Samjunghwan extract lost weight about 6-8% as compared to the control group. A significant increase of liver weight caused by a high fat diet was also inhibited by the same Samjunghwan extract administration. Similar inhibitory effects on the food intake and on the epididymal adipose tissue weight were observed in the high fat diet rats by the administration of Samjunghwan extract. Serum and liver total lipid levels in the control group on a high fat diet increased significantly as compared to the normal group, whereas their serum and liver levels increased less on a high fat diet plus Samjunghwan extract administered test group than the control group. Impressively, serum leptin levels in the test group decreased almost to the level of the normal group, which was well in accordance with the decreased fat contents in the test group rats. Furthermore, the activities of hepatic acetyl-CoA carboxylase and fatty acid synthetase were increased in the control group, while their activities in the test group on a high fat diet plus Samjunghwan extract decreased nearly to the levels of normal group rats on a normal diet. Conclusions: These results showed that the obesity caused by a high fat diet was effectively inhibited the administration of Samjunghwan extract. Our results also showed that the abnormal lipid metabolism caused by a high fat diet was effectively cured by the administration of Samjunghwan extract.

• Asian-Australasian Journal of Animal Sciences
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• v.24 no.9
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• pp.1274-1281
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• 2011

Dietary protein restriction affects lipid metabolism in rats. This study was performed to determine the effect of a low protein diet on hepatic lipid metabolism and insulin sensitivity in growing male rats. Growing rats were fed either a control 20% protein diet or an 8% low protein diet. Feeding a low protein diet for four weeks from 8 weeks of age induced a fatty liver. Expression of acetyl-CoA carboxylase, a key lipogenic enzyme, was increased in rats fed a low protein diet. Feeding a low protein diet decreased very low density lipoprotein (VLDL) secretion without statistical significance. Feeding a low protein diet down-regulated protein expression of microsomal triglyceride transfer protein, an important enzyme of VLDL secretion. Feeding a low protein diet increased serum adiponectin levels. We performed glucose tolerance test (GTT) and insulin tolerance test (ITT). Both GTT and ITT were increased in protein-restricted growing rats. Our results demonstrate that dietary protein restriction increases insulin sensitivity and that this could be due to low-protein diet-mediated metabolic adaptation. In addition, increased adiponectin levels may influences insulin sensitivity. In conclusion, dietary protein restriction induces a fatty liver. Both increased lipogenesis and decreased VLDL secretion has contributed to this metabolic changes. In addition, insulin resistance was not associated with fatty liver induced by protein restriction.

• Asian-Australasian Journal of Animal Sciences
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• v.25 no.8
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• pp.1145-1152
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• 2012

This experiment was conducted with male chicks to investigate the influence of hormones and nutrients on the development of fatty liver syndrome (FLS) as well as the effects of dietary lipotropic factors on hepatic fat accumulation and lipogenic enzyme gene expression. A total of two-hundred sixteen 4-wk-old Hy-Line male chicks were divided into six groups and fed an experimental diet (T1, low-energy diet with low levels of lipotropic factors; T2, high-energy diet with low levels of lipotropic factors; T3 and T5, low-energy diet with high levels of lipotropic factors; T4 and T6, high-energy diet with high levels of lipotropic factors) for six weeks. The chicks in T5 and T6 groups were treated with intramuscular injections of estradiol benzoate for three days prior to biopsy and clinical analysis of FLS. Chicks treated with estrogen had significantly greater liver weights than untreated chicks. The abdominal fat contents were increased in chicks consuming high-energy diets as compared to those consuming low-energy diets. Treatment with estrogen significantly increased the concentrations of serum cholesterol, triacylglycerol and phospholipid (p<0.05). The hepatic triacylglycerol levels were tenfold higher in the estrogen treated chicks than in the untreated chicks. There were no significant differences in malondialdehyde levels between the treatment groups. Estrogen treatment dramatically increased the levels of fatty acid synthetase, acetyl-CoA carboxylase and ApoB mRNA. The results indicated that treatment with exogenous estrogen in growing male chicks induced hepatic fat accumulation, which might be partially due to increased lipogenic enzyme gene expression.

• The Journal of Internal Korean Medicine
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• v.37 no.3
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• pp.442-452
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• 2016

Objectives: This study was performed to investigate the anti-lipogenic effect and the mechanism of Jungmanbunso-hwan extract (JMBSH) on a cellular model of non-alcoholic fatty liver disease (NAFLD) caused by palmitate in HepG2 cells.Methods: The JMBSH was prepared, andHepG2 cells were treated with various concentrations of JMBSH in order to perform an MTT assay. The HepG2 cells were cultivated in palmitate-containing media with or without extract of JMBSH. The intracellular lipid content in the HepG2 cells was examined. The effects of JMBSH on sterol regulatory element-binding transcription factor-1c (SREBP-1c), acetyl-CoA carboxylase (ACC), fatty acid synthase (FAS), stearoyl-CoA desaturase-1 (SCD-1), and AMP-activated protein kinase (AMPK) activation in HepG2 cells were measured.Results: JMBSH did not reduce HepG2 cell viability under 1,000 μg/mL. JMBSH considerably decreased intracellular lipid accumulation caused by palmitate in HepG2 cells. JMBSH repressed expression of SREBP-1c, which mediates the induction of lipogenic genes (ACC, FAS, and SCD-1). JMBSH also activated AMPK, which plays animportant role in the regulation of hepatic lipid metabolism.Conclusions: This study suggested that JMBSH relieves hepatic steatosis by repressing SREBP-1c, which mediates the induction of lipogenic genes. The anti-lipogenic effect of JMBSH may also be related to the activation of AMPK. Therefore, JMBSH could potentially be applied to NAFLD treatment after further clinical studies.