• Food Science and Biotechnology
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• v.17 no.2
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• pp.336-342
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• 2008

The aim of the present study was to assess the anti-obesity effects of fermented kochujang supplement in C57BL/6J mice. Thirty mice were divided into 3 groups; normal diet control group (ND), high fat diet control group (HD), and high fat diet plus kochujang supplemented group (HDK). Results were as follows: 1. Fennented kochujang supplement in high fat diet decreased body weight and epidydimal and back fat weight compared to non-supplement in HD group. 2. Lipid content and blood glucose level were lower in HDK group than HD group. 3. Fermented kochujang supplement increased mRNA level of lipolytic genes such as acyl-CoA synthetase (ACS), carnitine palmitoyltransferase-1 (CPT-1), and uncoupling proteins-1 (UCP-1) expression, whereas decreased mRNA level of adipogenic genes such as acetyl CoA carboxylase (ACC) expression. These findings suggest that fermented kochujang supplement in high fat diet normalized body weight, epididymal and back fat weight, lipid content, and blood glucose levels through controlling lipid metabolism and provides basic information on the control of obesity.

• 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.

• 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.

• The Korean Journal of Food And Nutrition
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• v.30 no.5
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• pp.1035-1041
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• 2017

(-)-Epigallocatechin-3-gallate (EGCG) is a major catechin found in green tea. It is reported that EGCG possesses various health benefits including anti-cancer, antioxidant, anti-diabetes, and anti-obesity. The objective of this study was to investigate the effects of EGCG on adipogenesis via activation of AMP-activated protein kinase (AMPK) pathway in 3T3-L1 preadipocytes. In order to determine the effects of EGCG on adipogenesis, preadipocyte differentiation was induced in the presence or absence of EGCG ($0{\sim}100{\mu}M$) for a period of 6 days. EGCG significantly inhibited fat accumulation and suppressed the expression of adipogenic specific proteins including peroxisome proliferator-activated receptor (PPAR)-${\gamma}$. Also, EGCG markedly increased the activation of AMPK and acetyl-CoA carboxylase (ACC) and the production of intracellular reactive oxygen species (ROS). However, any pretreatment with a specific AMPK inhibitor, compound C, abolished the inhibitory effects of the EGCG on $PPAR{\gamma}$ expression. This study suggests that EGCG has anti-adipogenic effects through modulation of the AMPK signaling pathway and therefore, may be a promising antiobesity agent.

• The Korean Journal of Food And Nutrition
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• v.22 no.2
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• pp.246-251
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• 2009

This study examined the possible hypoglycemic effects Angelica gigas Naki extracts in streptozotocin-induced diabetic rats(STZ+50%, STZ+100% EtOH and STZ+water). The studies showed that administration of the Angelica gigas Naki extract decreased high blood glucose levels(more than 300 mg/$d{\ell}$) to a normal level(104 mg/$d{\ell}$) in the STZ+50% EtOH group. Liver glucokinase levels were significantly increased in STZ+50% EtOH and STZ+100% EtOH groups compared to the STZ group. Moreover, the liver acetyl CoA carboxylase level was significantly increased in STZ+50% EtOH, STZ+100% EtOH and STZ+water groups compared to the STZ group. These results suggest that the Angelica gigas Naki extract in the STZ+50% EtOH group exerted an ameliorable effect and can be used as an anti-diabetic substance, either as a dietary supplements or as a new drug.

• Herbal Formula Science
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• v.30 no.4
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• pp.225-231
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• 2022

Objectives : Oxidative damage has a variety of mechanism in the human organs including brain and liver. The purpose of this study is to examine the prevention against cellular damage, and the inhibitory effect on lipogenesis of the water extract of Eriobotrya japonica (EJE). Methods : The effect of EJE on cell viability was assessed using the MTT assay. To investigate the mechanism of EJE's inhibition of lipogenesis, we analyzed the relevant proteins using immunoblot analysis. Results : Induction of T0901317, a LXR agonist, significantly increased SREBP-1c expression, which was blocked by the pretreatment of EJE in the dose-dependent manners. This beneficial herb also regulated the genes related with SREBP-1c such as the acetyl-CoA carboxylase. Conclusion : These results suggested that EJE might have a possibility of the treatment of chronic diseases as mediated with the inhibition of LXRα/SREBP-1c pathway.

• Journal of The Korean Society of Clinical Toxicology
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• v.14 no.2
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• pp.71-77
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• 2016

Purpose: No studies have been conducted to investigate the acute toxicity of aryloxyphenoxypropionate herbicides in humans following ingestion. Therefore, this study was conducted to investigate the clinical characteristics of aryloxyphenoxypropionate herbicide poisoning and provide guidance for physicians treating patients who have ingested these types of herbicides. Methods: A retrospective observational case series was conducted using ten patients with history of aryloxyphenoxy propionate herbicide. Data were collected for clinical manifestation, management and final outcome. Results: The most common symptoms were gastrointestinal irritation and an altered mental state (Glasgow Coma Scale<15). An elevated lactate level was a common laboratory abnormality, and prolonged QTc interval was commonly observed. These clinical features normalized within one day of supportive treatment. Conclusion: The acute toxicity of aryloxyphenoxypropionate herbicides in humans is manageable with supportive treatment. However, physicians should take into account depressed consciousness, the possibility of arrhythmia, and an elevated lactate level when planning their treatment strategy.

• Nutrition Research and Practice
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• v.4 no.5
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• pp.438-442
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• 2010

Rhemannie Radix Preparata (RRP) has been previously employed in traditional oriental medicine as a treatment for diabetic thirst and improving blood flow. The aim of this study was to evaluate its hypoglycemic control by assaying the activities of key enzymes of carbohydrate metabolism in streptozotocin-(STZ)-induced diabetic rats. Further, RRP extracts were prepared in water (RRPW), in 50% ethanol (RRP50), and in 100% ethanol (RRP100), respectively, and compared for their actions in diabetic rats. The oral treatment of RRP (5 mg/kg b.w./d) to diabetic rats for 21 days resulted in a significant decline in blood glucose by 67% compared to diabetic control rats (P < 0.05). The altered activities of glucokinase, glucose-6-phosphate dehydrogenase (G6PD), 6-phosphogluconate dehydrogenase (6PGD), and acetyl CoA carboxylase (ACC) in the livers of diabetic rats were reversed significantly to near-normal levels by the administration of RRP (P < 0.05). Among the three RRP extracts, RRP100 was the most effective in terms of hypoglycemic action. However, the administration of RRP to diabetic rats did not improve insulin production. The modulatory effects of RRP100 on the attenuation of carbohydrate enzyme activities appear to hold promise for widespread use for the treatment of diabetes in the future.

• The Korean Journal of Physiology and Pharmacology
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• v.14 no.5
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• pp.299-304
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• 2010

Losartan is a selective angiotensin II (Ang II) type 1 ($AT_1$) receptor antagonist which inhibits vascular smooth muscle cells (VSMCs) contraction and proliferation. We hypothesized that losartan may prevent cell proliferation by activating AMP-activated protein kinase (AMPK) in VSMCs. VSMCs were treated with various concentrations of losartan. AMPK activation was measured by Western blot analysis and cell proliferation was measured by MTT assay and flowcytometry. Losartan dose- and time-dependently increased the phosphorylation of AMPK and its downstream target, acetyl-CoA carboxylase (ACC) in VSMCs. Losartan also significantly decreased the Ang II- or 15% FBS-induced VSMC proliferation by inhibiting the expression of cell cycle associated proteins, such as p-Rb, cyclin D, and cyclin E. Compound C, a specific inhibitor of AMPK, or AMPK siRNA blocked the losartan-induced inhibition of cell proliferation and the $G_0/G_1$ cell cycle arrest. These data suggest that losartan-induced AMPK activation might attenuate Ang II-induced VSMC proliferation through the inhibition of cell cycle progression.