• 대한한방부인과학회지
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• 제34권1호
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• pp.48-65
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• 2021

Objectives: This study was designed to evaluate the efficacy of Changbudodam-tang on obesity by using high-fat diet rats. Methods: Rats were divided into five groups. Normal group: Normal diet, Control group: High-fat diet, Positive control group: High-fat diet+Dietamin 4 mg/kg/day, Changbudodam-tang-Low group: High-fat diet+Changbudodam-tang 250 mg/kg/day, Changbudodam-tang-High group: High-fat diet+Changbudodam-tang 500 mg/kg/day. Weight, food intake were measured every week. After 7 weeks, total cholesterol, high density lipoprotein-cholesterol, low density lipoprotein-cholesterol, Triglyceride, free fatty acid, aspartate aminotransferase, alanine aminotransferase, complete blood count were measured and messenger ribonucleic acid expression of adiponectin, peroxisome proliferator-activated receptor-γ, leptin were observed using Reverse transcription polymerase chain reaction of liver cells. Results: There was no difference in food intake between groups. Body weight tended to decrease compared with the Control group, but it wasn't statistically meaningfull. The total cholesterol, low density lipoprotein-cholesterol, Triglyceride, free fatty acid tended to decrease compared with the Control group. High density lipoprotein-cholesterol tended to decrease compared with the Control group, but it wasn't statistically meaningfull. White blood cell, red blood cell, hemoglobin, platelet, aspartate aminotransferase, alanine aminotransferase were not affected by Changbudodam-tang. The messenger ribonucleic acid expression of Adiponectin, peroxisome proliferator-activated receptor-γ, leptin, which are involved in the differentiation of adipocytes, was decreased compared with the Control group. Conclusions: Based on the results above, it is suggested that Changbudodam-tang can be applied to improving serum lipid levels in obese patients caused by high fat diets.

• 대한한방내과학회지
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• 제30권2호
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• pp.257-269
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• 2009

Objective : Obesity is an important cause of diabetes, and lipotoxicity causes insulin resistance. Recently a lot of research is being done on PPAR-${\alpha}$. TNF-${\alpha}$. adiponectin, and leptin, which are important obesity related factors. In this study, we investigated the effects of Supungsunki-hwan on high fat. high carbohydrate diet-induced obese type 2 diabetic mouse models. Methods: Diabetes was induced in ICR male mouse (30${\pm}$5g) with Surwit's high fat, high sucrose diet. Mice were divided into 4 groups(n=10) of Normal. Control. Supungsunkj-hwan group. and acarbose group. The Supungsunki-hwsn group was given 10% Supungsunkj-hwan in their diet. and the acarbose group was given 0.5% acarbose in their diet. After 6 weeks. body weight. food intake, FBS and OGTT. lipid profile and liver enzymes, epididymal fat weight, and gene expression of leptin, adiponectin, TNF-${\alpha}$ and PPAR-${\alpha}$ were measured. Leptin. adiponectin. tumor necrosis factor(TNF)-${\alpha}$ and peroxisome proliferator-activated receptor (PPAR)-${\alpha}$ were evaluated by reverse transcription-polymerase chain reaction. Results : Supungsunkj-hwan increased the gene expression of PPAR-${\alpha}$, which reduces lipotoxicity and insulin resistance. Supungsunkj-hwan also significantly reduced triglyceride. AST. ALT serum levels. and 1 hour oral glucose tolerance levels. Conclusion : These results show that Supungsunkj-hwan improves insulin resistance in the liver and muscles, by reducing triglyceride levels and lipotoxicity through increased PPAR-${\alpha}$ gene expression. This is supported by the fact that Supungsunkj-hwan significantly reduces 1 hour oral glucose tolerance levels. Therefore we suggest that Supungsunkj-hwan would be an effective treatment for obese type 2 diabetic patients.

• 한방재활의학과학회지
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• 제26권1호
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• pp.13-31
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• 2016

Objectives In this study, it was investigated whether Gami-Handayeolso-Tang (HDYST) medication has anti-obesity effects in high fat diet (HFD)-fed obese mice. Methods The experimental animals were divided into five groups-normal diet-fed (ND), high fat diet-fed control (HFD), HFD+HDYST 150, HFD+HDYST 300, and HFD+orlistat as a positive drug. The obese markers such as body weight, diet efficiency ratio, serum levels of total cholesterol, triglyceride, lipid contents, leptin, adiponectin, and GOT/GPT were measured. Also, white adipose tissue, liver weight, abdominal fat mass, hepatic lipid contents, and mRNA expression of obese-associating genes were examined in obese mice. Results In high fat diet-fed mice, HDYST administration significantly decreased body weight, diet efficiency ratio, serum levels of total cholesterol, triglyceride, LDL-cholesterol, as well as leptin and GOT/GPT, compared to the HFD group in a dose-dependent manner. HDYST increased significantly the serum levels of HDL-cholesterol and adiponectin. It also reduced the accumulation of lipids, such as total lipid and triglycerides, in organs such as liver and abdominal adipose tissue. Moreover, HDYST administration significantly decreased the expression levels of fatty acid synthetic genes, such as sterol regulatory element-binding protein-1c (SREBP-1c), FAS and Stearoyl-Coenzyme A desaturase 1 (SCD-1), in the liver tissues, while it increased the messenger RAN (mRNA) levels of fatty acid catalytic genes, such as Peroxisome proliferator activated receptor alpha (PPAR-${\alpha}$), acyl-COA oxidase (ACO), and Carnitine palmitoyltransferase-1a (CPT-1a). Conclusions Based on the results above, HDYST reveals anti-obesity effects declining body fat accumulation through the regulation of fatty acid metabolism and leptin/adiponectin serum levels. It therefore suggests that HDYST can be clinically useful for the treatment of obesity.

• Journal of Animal Science and Technology
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• 제63권4호
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• pp.934-953
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• 2021

Ciglitazone is a member of the thiazolidinedione family, and specifically binds to peroxisome proliferator-activated receptor-γ (PPARγ), thereby promoting adipocyte differentiation. We hypothesized that ciglitazone as a PPARγ ligand in the absence of an adipocyte differentiation cocktail would increase adiponectin and adipogenic gene expression in bovine satellite cells (BSC). Muscle-derived BSCs were isolated from six, 18-month-old Yanbian Yellow Cattle. The BSC were cultured for 96 h in differentiation medium containing 5 µM ciglitazone (CL), 10 µM ciglitazone (CM), or 20 µM ciglitazone (CH). Control (CON) BSC were cultured only in a differentiation medium (containing 2% horse serum). The presence of myogenin, desmin, and paired box 7 (Pax7) proteins was confirmed in the BSC by immunofluorescence staining. The CL, CM, and CH treatments produced higher concentrations of triacylglycerol and lipid droplet accumulation in myotubes than those of the CON treatment. Ciglitazone treatments significantly increased the relative expression of PPARγ, CCAAT/enhancer-binding protein alpha (C/EBPα), C/EBPβ, fatty acid synthase, stearoyl-CoA desaturase, and perilipin 2. Ciglitazone treatments increased gene expression of Pax3 and Pax7 and decreased expression of myogenic differentiation-1, myogenin, myogenic regulatory factor-5, and myogenin-4 (p < 0.01). Adiponectin concentration caused by ciglitazone treatments was significantly greater than CON (p < 0.01). RNA sequencing showed that 281 differentially expressed genes (DEGs) were found in the treatments of ciglitazone. DEGs gene ontology (GO) analysis showed that the top 10 GO enrichment significantly changed the biological processes such as protein trimerization, negative regulation of cell proliferation, adipocytes differentiation, and cellular response to external stimulus. Kyoto Encyclopedia of Genes and Genomes pathway analysis showed that DEGs were involved in the p53 signaling pathway, PPAR signaling pathway, biosynthesis of amino acids, tumor necrosis factor signaling pathway, non-alcoholic fatty liver disease, PI3K-Akt signaling pathway, and Wnt signaling pathway. These results indicate that ciglitazone acts as PPARγ agonist, effectively increases the adiponectin concentration and adipogenic gene expression, and stimulates the conversion of BSC to adipocyte-like cells in the absence of adipocyte differentiation cocktail.

• 한국식품저장유통학회지
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• 제30권3호
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• pp.502-513
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• 2023

본 연구에서는 영지버섯 균사체 발효 꾸지뽕 잔가지 추출물의 지방세포 분화 억제 및 염증 억제 효과를 확인하고자 하였다. 세포독성을 확인한 결과, 최대 1,000 ㎍/mL 농도까지 세포에 처리하여도 세포 생존율이 감소하지 않음을 확인되었다. 분화과정 동안 발효 꾸지뽕 잔가지 추출물을 처리하였을 때, 세포 내 지방 축적이 감소되었다. 분화과정에 관여하는 대표적인 adipokine인 leptin과 adiponectin의 생성량을 확인한 결과, 발효 꾸지뽕나무 잔가지 추출물에 의해 adiponectin의 생성 증가와 leptin의 생성 감소를 확인하였다. 지방세포 분화 관련 유전자의 발현은 분화 유도인자만 처리한 군에 비해 발효 꾸지뽕나무 잔가지 추출물이 함께 처리된 군에서 추출물의 농도가 높아질수록 지방분화 전사인자인 PPARγ와 C/EBPα의 발현량이 감소하는 것을 확인하였다. 분화된 3T3-L1 세포에서 LPS에 의해 분비되는 염증성 사이토카인(TNF-α, IL-6, MCP-1)의 생성량 변화를 측정한 결과, LPS 처리로 증가된 염증성 사이토카인의 생성을 억제하였으며 염증 관련 유전자인 iNOS, COX-2의 발현도 감소되었다. 또한, 발효 꾸지뽕나무 잔가지 추출물과 발효되지 않은 꾸지뽕나무 잔가지 추출물을 비교하였을 때, 발효 꾸지뽕나무 잔가지 추출물이 지방세포 분화 및 염증 억제 효과에서 더 높은 활성을 보였으며, 이들 결과를 종합적으로 볼 때, 영지버섯 균사체를 이용한 발효가 꾸지뽕나무 잔가지의 활성 증가에 기여하는 것으로 보인다. 따라서 발효 꾸지뽕나무 잔가지 추출물은 항비만, 항염증 소재로서 비만뿐만 아니라 대사성 질환 개선을 위한 기능성 소재로서 활용이 가능할 것으로 판단되며, 향후 발효 꾸지뽕나무 추출물의 명확한 항비만, 항염증 효능을 확인하기 위해서는 유용 물질 분리 및 작용기전 등 추가적인 연구가 필요할 것으로 판단된다.

• 동의생리병리학회지
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• 제28권3호
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• pp.288-295
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• 2014

Bojungchiseub-tang (BJCST) has been used in symptoms and signs of edema, dampness-phlegm, kidney failure, and so on. BJCST is also expected to have strong anti-obesity activities. However, little is known about the mechanisms of its inhibitory effects on adipocyte differentiation and adipogenesis. In the present study, we examined the effects and mechanism of BJCST on transcription factors and adipogenic genes of 3T3-L1 preadipocytes to understand its inhibitory effects on adipocyte differentiation and adipogenesis. Our results showed that BJCST significantly inhibited differentiation and adipogenesis of 3T3-L1 preadipocytes in a dose-dependent manner. To elucidate the mechanism of the effects of BJCST on lowering lipid content in 3T3-L1 adipocytes, we examined whether BJCST modulate the expressions of transcription factors to induce adipogenesis and adipogenic genes related to regulate accumulation of lipids. As a result, the expression of steroid regulatory element-binding protein (SREBP)1, cytidine-cytidine-adenosine-adenosine-thymidine (CCAAT)/enhancer binding proteins ${\alpha}$ ($C/EBP{\alpha}$), $C/EBP{\beta}$, $C/EBP{\delta}$, and peroxisome proliferator-activated receptor ${\gamma}$ ($PPAR{\gamma}$) genes, which induce the adipose differentiation, liver X receptor $(LXR){\alpha}$ and fatty acid synthase (FAS) genes, which induce lipogenesis and adipose-specific aP2, Adipsin, lipoprotein lipase (LPL), CD36, TGF-${\beta}$, leptin and adiponectin genes, which compose fat formation were decreased. BJCST also reduced the expression of acyl CoA oxidase (ACO) and uncoupling protein (UCP) genes related to lipid oxidation. In conclusion, BJCST could regulate transcript factor related to induction of adipose differentiation and inhibited the accumulation of lipids and expression of adipogenic genes.

• Animal cells and systems
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• 제13권2호
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• pp.127-132
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• 2009

We have examined the hypothesis that the Gly972Arg variant of the insulin receptor substrate 1 (IRS1) gene is associated with the components contributing to overweight (obesity) and metabolic syndrome. We describe IRS1 genotype frequencies in 274 Korean men. The frequencies of Gly972Gly (GIG) and Gly972Arg (G/A variant) of the IRS1 gene were 88.3% and 11.7%, respectively, and the differences in frequencies between the overweight (BMI$\geq$25kg/m$^2$) group and non-overweight (BMI<25kg/m$^2$) group were statistically significant. The subjects with G/A variant of IRS1 gene in non-overweight had significantly higher level of visceral fat thickness and adiponectin/leptin ratio than those with GIG alleles. In overweight group, the subjects with G/A variant of IRS1 gene also showed significantly higher level of insulin than those with GIG alleles. These results suggest that the IRS1 genetic polymorphism is involved in the occurrence of overweight, as well as metabolic syndrome.

• 대한본초학회지
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• 제31권1호
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• pp.1-5
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• 2016

Objectives : The purpose of this study was to investigate inhibitory effects of steamed Polygonatum odoratum extract (POE) on insulin resistance in rat skeletal muscle cells, L6 cells.Methods : Polygonatum odoratum (P. odoratum) extract was extracted with ethyl acetate. Activity of α-glucosidase in POE was measured for blood glucose regulation. MTT assay was examined for cell toxicity. Western blot analysis for measurement of adiponectine, peroxisome proliferator-activated receptorγ (PPARγ), insulin receptor substrate (IRS), glucose transporter 4 (Glut-4) and phosphorylation of serine/threonine-specific protein kinase (Akt) expressions were performed. Akt signaling pathway were analyzed with LY294002, which is a specific PI3K/Akt inhibitor.Results : The results revealed that POE inhibited α-glucosidase activity. Treatment of POE in L6 cells inhibited the differentiation of L6 cells compared to those of vehicl control. Additionally, protein expressions of adiponectine, PPARγ, IRS and Glut-4 were significantly regulated compared to those of vehicle control (p < 0.05), respectively. Futhermore, phosphorylation of Akt was increased in L6 cells treated with POE compared to that of vehicle control (p < 0.05). pAkt expression was significantly accentuated with Akt inhibitor (LY294002).Conclusions : These results suggest that POE may have potential as a natural agent for prevention/improvement of diabetes, especially, regulation of blood glucose. Therefore, further additional study should be conducted to elucidate in depth the pharmaceutical efficacy of these.

• Journal of Ginseng Research
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• 제35권1호
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• pp.45-51
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• 2011

Wild ginseng has been used as a traditional medicine for thousands of years and for increase physical strength in Korea, China and Japan. This study reports that cultivated wild ginseng (CWG) inhibits adipocyte differentiation of 3T3-L1 pre-adipocytes in a concentration-dependent manner. Inhibition of adipocyte differentiation is one possible anti-obesity strategy. CWG inhibits the expression of the adipocyte differentiation regulator peroxisome proliferators-activated receptor (PPAR)${\gamma}$ and CCAAT/enhancer-binding protein ${\alpha}$mRNA. It also inhibited the expression of PPAR${\gamma}$ and adiponectin at the protein level during the differentiation of pre-adipocytes into adipocytes. Additionally, CWG blocked the cell cycle at the sub-$G_1$ phase transition, causing cells to remain in the pre-adipocyte state. These results indicate that CWG inhibits adipocyte differentiation and adipogenesis through pre-adipocyte cell cycle arrest in cultured 3T3-L1 cells.

• 한국자원식물학회:학술대회논문집
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• 한국자원식물학회 2018년도 춘계학술발표회
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• pp.80-80
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• 2018

Chlorogenic acid is a phenolic compound found in Cudrania tricuspidata fruits. In the present study, the effect of chlorogenic acid on the inhibition of adipogenesis in 3T3-L1 adipocytes was investigated. Cells were stained with Oil red O reagent to detect lipid droplets in adipocytes. The 3T3-L1 cells were lysed and measured for intracellular triglyceride and adipokine by ELISA kit. The protein expression of adipogenesis-related gene was evaluated by Western blot analysis. Chlorogenic suppressed lipid droplet and intracellular triglyceride accumulation in a concentration manner and also decreased secretion of adipokines such as leptin and adiponectin, compared with fully differentiated adipocytes. Treatment of 3T3-L1 cells with chlorogenic acid reduced the protein levels of peroxisome proliferator-activated receptor gamma ($PPAR{\gamma}$) and, CCAAT/enhancer binding proteins alpha ($C/EBP{\alpha}$). This indicates that chlrogenic acid was effective as an anti-obesity agent by repressing the differentiation of 3T3-L1 into adipocytes and inhibiting triglyceridef formation in adipocyte and that it exerts its role mainly through the significant down-regulation of $PPAR{\gamma}$ and $C/EBP{\alpha}$.