• Title, Summary, Keyword: UCP2 expression

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The Effect of Conjugated Linoleic Acid Isomers on the Cell Proliferation, Apotosis and Expressions of Uncoupling Protein (Ucp) Genes during Differentiation of 3T3-L1 Preadipocytes (Conjugated Linoleic Acid 이성체가 3T3-L1 지방전구세포 분화중 세포증식, 세포사멸 및 Ucp 유전자 발현에 미치는 영향)

  • Kwon So-Young;Kang Keum-Jee
    • Journal of Nutrition and Health
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    • v.37 no.7
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    • pp.533-539
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    • 2004
  • It has been reported that CLA decreases fat deposition in vivo and in vitro experiments. Among CLA isomers, c9t11 and t10c12 have been shown to exert active biological activities. For example, t10c12 reduces body weight and increases lean body mass, whereas, c9t11 has little effect on body fattness. However, the underlying molecular mechanism for the anti-obesity action of CLA isomers are not well understood. The purpose of this study was to examine the effects of t10c12 and c9t11 on lipid accumulation, cell proliferation, cell death and the expression levels of Ucp genes which are proposed as targets for anti-obesity in 3T3-L1 preadipocytes. Isomers of CLA at 50$\mu$M were added into preadipocyte differentiation medium for 3, 6 and 9days. Control cells received only the vehicle in the differentiation medium. Cytochemical analyses for lipid accumulation, cell proliferation and apotosis were carried out to compare lipidogenesis and cellular activity. RT-PCR analysis of GAPDH, Ucp 2,3 and 4 were also performed to find any modulatory effects of CLA isomers on the metabolic genes. Lipid accumulation indicated by Oil Red-O staining was inhibited in CLA isomers as compared to the control. T10c12 isomer showed less lipidogenesis than c9t11 did. A decrease occurred in CLA isomers as shown by BrdU incorporation. Apotosis has occured at higher level in t10c12 when compared to that of t9c11. Ucp 2, 3 and 4 genes were also upregulated in CLA isomers. T10c12 showed higher level of Ucp gene expressions than the c9t11 did. The biological activities of CLA isomers were also found to be different during differentiation of 3T3-L1 preadipocytes, suggesting that different isomers may be active in certain stage of lipidogenesis. The results indicate that both c9t11 and t10c12 CLA isomers decrease lipidogenesis, inhibit cell proliferation, increase cell death and upregulate in Ucp gene expressions during 3T3-L1 preadipocyte differentiation. T10c12 isomer was more effective than c9t11 in overall anti-obesity activity.

Effects of Sinetrol-XPur on Leptin-Deficient Obese Mice and Activation of cAMP-Dependent UCP-2 (Leptin 유전자 결핍 동물모델을 이용한 시네트롤(Sinetrol-XPur)의 항비만 효과와 cAMP를 통한 UCP-2 활성화 기전 연구)

  • Yoo, Jae Myeong;Lee, Minhee;Kwon, Han Ol;Choi, Sei Gyu;Bae, Mun Hyoung;Kim, Ok-Kyung
    • Journal of the Korean Society of Food Science and Nutrition
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    • v.45 no.4
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    • pp.484-491
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    • 2016
  • The present study investigated the effect of Sinetrol-XPur (polyphenolic Citrus spp. and Paullinia cupana Kunth dry extract) and defined the action mode for cyclic adenosine monophosphate (cAMP)-dependent uncoupling protein (UCP)-2 activation. Leptin-deficient obese mice were treated with two different doses, 100 mg/kg body weight (BW) and 300 mg/kg BW of each AIN93G supplement, for 7 weeks. Treatment of obese mice with both low and high doses of Sinetrol-XPur significantly reduced body weight gain compared to control obese mice. White adipose tissue weight of mice was reduced by 30.96% in high dose-supplemented groups. Serum total cholesterol and triglyceride were reduced by a high dose of Sinetrol-XPur by 20.02% and 30.96%, respectively. Serum level of high density lipoprotein (HDL) was significantly increased by treatment with both doses, as the ratio of HDL to low density lipoprotein increased by 138.78% and 171.49%, respectively. Regarding expression of biochemical factors related to lipid metabolism, fatty acid synthase significantly decreased and UCP-2 increased upon treatment with a high dose of Sinetrol-XPur, but there was no significant difference in lipoprotein lipase and hormone-sensitive lipase. To define cellular mechanism, intracellular cAMP levels in 3T3-L1 adipocytes significantly increased in a dose-dependent manner over the range of $50{\sim}250{\mu}m/mL$. The phosphodiesterase (PDE) inhibitor 3-isobutyl-1-methylxanthine clearly blocked cAMP, suggesting that Sinetrol-XPur promotes lipolysis of adipocytes through inhibition of cAMP-dependent PDE, resulting in induction of cAMP response element binding protein and UCP-2. These results suggest that Sinetrol-XPur supplementation is a viable option for reducing body weight and fat by improving serum lipid profiles and genetic expression of lipid metabolic factors, especially activation of cAMP-dependent UCP-2.

The Study on the Effect of Acanthopanax Senticocus Herbal Acupuncture on Metabolic Syndrome in High-fat Diet Fed Mice (가시오가피약침(五加皮藥鍼)이 High-fat Diet로 유발(誘發)된 대사증후군(代謝症候群)에 미치는 영향(影響))

  • Yoo, Tae-seop;Koh, Hyung-kyun;Kang, Sung-keel
    • Journal of Acupuncture Research
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    • v.22 no.3
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    • pp.77-92
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    • 2005
  • Objective : The aim of the study was to investigate the effect of Acanthopanax senticocus(AS) herbal acupuncture on the metabolic syndrome in high-fat diet fed mice. Methods : ICR mice were fed with high-fat diet to induce the metabolic syndrome. During the inducement of the metabolic syndrome, the groups were treated with AS herbal acupuncture with different concentrations(125mg/kg, 250mg/kg and 500mg/kg) to the point of Sinsu(BL23) everyday for 5 weeks. Thereafter, body weight, feed efficiency ratio, blood pressure, blood glucose, insulin level, insulin resistance, oral glucose tolerance test(OGTT), lipid profile(TG, TC, HDL-C, LDL-C, NEFA), mass of liver, histology of white adipose tissue(WAT) and brown adipose tissue(BAT), and expression of GLUT-4 and UCP-1 mRNA were measured. Results : The risk factors of metabolic syndrome such as obesity, non-insulin dependent diabetes mellitus(NIDDM), insulin resistance, hypertension, dyslipidemia were aggravated by high-fat diet for 5-weeks. AS herbal acupuncture inhibited the development of weight gain, hyperglycemia, hyperinsulinemia, insulin resistance, hypertension, dylipidemia and expression of GLUT-4 in WAT and UCP-1 mRNA in BAT, and also improved oral glucose intolerance and distribution of adipose tissue.

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Ethyl acetate fraction of GGEx18 modulates fatty acid β-oxidizing enzymes (In vitro 동물세포에서 GGEx18의 ethyl acetate 분획물에 의한 지방산 β-산화효소 유전자 발현의 조절)

  • Joo, Byung-Soo;Lee, Hee-Young;Lee, Hye-Rim;Yoon, Mi-Chung;Seo, Bu-Il;Kim, Beom-Hoi;Shin, Soon-Shik
    • The Korea Journal of Herbology
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    • v.27 no.2
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    • pp.53-59
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    • 2012
  • Objectives : This study was undertaken to investigate the effects of the GGEx18 ethyl acetate fraction (EF) on lipid accumulation and gene expression of fatty acid-oxidizing enzymes using 3T3-L1 adipocytes, C2C12 skeletal muscle cells, and NMu2Li liver cells. Methods : PPAR${\alpha}$, AMPK and UCPs transactivation was examined in NMu2Li hepatocytes, C2C12 myocytes, and 3T3-L1 preadipocytes using transient transfection assays. Results : 1. Compared with control, EF significantly increased the mRNA expression of VLCAD in 3T3-L1 adipocytes. 2. Compared with control, EF (0.1 ${\mu}g/ml$) significantly inhibited lipid accumulation in 3T3-L1 adipocytes. 3. EF significantly increased the mRNA expression of AMPK${\alpha}$1, AMPK${\alpha}$2 and PPAR${\alpha}$ in C2C12 skeletal muscle cells compared with control. 4. EF significantly increased the mRNA expression of genes involved in fatty acid ${\beta}$-oxidation, such as thiolase, MCAD, and CPT-1 in C2C12 skeletal muscle cells compared with control. 5. EF significantly increased the mRNA expression of UCP2 involved in energy expenditure in C2C12 skeletal muscle cells compared with control. 6. Compared with control, EF (10 ${\mu}g/ml$) significantly inhibited lipid accumulation in C2C12 skeletal muscle cells. 7. EF (10 ${\mu}g/ml$) significantly increased the mRNA expression of ACOX, HD, VLCAD and MCAD in NMu2Li liver cells compared with control. Conclusions : These results suggest that EF may prevent obesity by increasing the mRNA expression of mitochondrial fatty acid ${\beta}$-oxidizing enzymes in 3T3-L1 adipocytes, by not only regulating the fatty acid oxidation through activation of AMPK and PPAR${\alpha}$, but also increasing the UCP2 mRNA expression in C2C12 skeletal muscle cells, and by stimulating the mRNA expression of fatty acid-oxidizing enzymes in NMu2Li liver cells.

Protein Tyrosine Phosphatase, Receptor Type B (PTPRB) Inhibits Brown Adipocyte Differentiation through Regulation of VEGFR2 Phosphorylation

  • Kim, Ji Soo;Kim, Won Kon;Oh, Kyoung-Jin;Lee, Eun-Woo;Han, Baek Soo;Lee, Sang Chul;Bae, Kwang-Hee
    • Journal of Microbiology and Biotechnology
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    • v.29 no.4
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    • pp.645-650
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    • 2019
  • Brown adipocytes have an important role in the regulation of energy balance through uncoupling protein-1 (UCP-1)-mediated nonshivering thermogenesis. Although brown adipocytes have been highlighted as a new therapeutic target for the treatment of metabolic diseases, such as obesity and type II diabetes in adult humans, the molecular mechanism underlying brown adipogenesis is not fully understood. We recently found that protein tyrosine phosphatase receptor type B (PTPRB) expression dramatically decreased during brown adipogenic differentiation. In this study, we investigated the functional roles of PTPRB and its regulatory mechanism during brown adipocyte differentiation. Ectopic expression of PTPRB led to a reduced brown adipocyte differentiation by suppressing the tyrosine phosphorylation of VEGFR2, whereas a catalytic inactive PTPRB mutant showed no effects on differentiation and phosphorylation. Consistently, the expression of brown adipocyte-related genes, such as UCP-1, $PGC-1{\alpha}$, PRDM16, $PPAR-{\gamma}$, and CIDEA, were significantly inhibited by PTPRB overexpression. Overall, these results suggest that PTPRB functions as a negative regulator of brown adipocyte differentiation through its phosphatase activity-dependent mechanism and may be used as a target protein for the regulation of obesity and type II diabetes.

Effects of Wax Gourd Extracts on Adipocyte Differentiation and Uncoupling Protein Genes(Ucps) Expression in 3T3-Ll Preadipocytes

  • Kang, Keun-Jee;Kwon, So-Young
    • Nutritional Sciences
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    • v.6 no.3
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    • pp.148-154
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    • 2003
  • Although various raw plant materials have been demonstrated to exert anti-obesity effects to a greater or lesser extent in both humans and animals when they are used to supplement the diet, it has not been shown extensively that they influence adipocyte cell differentiation involving lipid metabolic gene expressions. Using a well-established 3T3-L1 preadipocyte differentiation system, we decided to look into molecular and cellular event occurring during adipocyte differentiation when raw plant materials aye included in the process, in an effort to demonstrate the potential use of a screening system to define the functions of traditionally well-known materials. To these ends, the effects of ethanol (EtOH) or EtOH/distilled water (DW) extracts of Wax Gourd were examined using cytochemical and molecular analyses to determine whether components of the extracts modulate adipocyte differentiation of 3T3-Ll preadipocytes in vitro. The cytochemical results demonstrated that EtOH or EtOH/DW extracts did not affect lipid accumulation and cell proliferation, although the degree of lipid accumulation was influenced slightly depending on the extract. EtOH extract was highly effective in apoptotic induction during differentiation of 3T3-Ll preadipocytes (p<0.05). Reverse transcription-polymerase chain reaction (RT-PCR) analysis of lipoprotein lipase (LPL), Uncoupling protein (Ucp) 2, 3 and 4 also showed that while LPL expression was not influenced, Ucp2, 3 and 4 were up regulated in the EtOH extract-treated group and down regulated in the EtOH/DW extract-treated group. These changes in gene expressions suggest that the components in different fractions of Wax Gourd extracts may modulate lipid metabolism by either direct or indirect action. Taking these results together, it was concluded that molecular and cellular analyses of adipocyte differentiation involving lipid metabolic genes should facilitate understanding of cellular events occurring during adipocyte differentiation. Furthermore, the experimental scheme and analytical methods used in this study should provide a screening system for the functional study of raw plant materials in obesity research.

Sinapic acid induces the expression of thermogenic signature genes and lipolysis through activation of PKA/CREB signaling in brown adipocytes

  • Hossain, Monir;Imran, Khan Mohammad;Rahman, Md. Shamim;Yoon, Dahyeon;Marimuthu, Vignesh;Kim, Yong-Sik
    • BMB Reports
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    • v.53 no.3
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    • pp.142-147
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    • 2020
  • Lipid accumulation in white adipose tissue is the key contributor to the obesity and orchestrates numerous metabolic health problems such as type 2 diabetes, hypertension, atherosclerosis, and cancer. Nonetheless, the prevention and treatment of obesity are still inadequate. Recently, scientists found that brown adipose tissue (BAT) in adult humans has functions that are diametrically opposite to those of white adipose tissue and that BAT holds promise for a new strategy to counteract obesity. In this study, we evaluated the potential of sinapic acid (SA) to promote the thermogenic program and lipolysis in BAT. SA treatment of brown adipocytes induced the expression of brown-adipocyte activation-related genes such as Ucp1, Pgc-1α, and Prdm16. Furthermore, structural analysis and western blot revealed that SA upregulates protein kinase A (PKA) phosphorylation with competitive inhibition by a pan-PKA inhibitor, H89. SA binds to the adenosine triphosphate (ATP) site on the PKA catalytic subunit where H89 binds specifically. PKA-cat-α1 gene-silencing experiments confirmed that SA activates the thermogenic program via a mechanism involving PKA and cyclic AMP response element-binding protein (CREB) signaling. Moreover, SA treatment promoted lipolysis via a PKA/p38-mediated pathway. Our findings may allow us to open a new avenue of strategies against obesity and need further investigation.

Fermented Kochujang Supplement Shows Anti-obesity Effects by Controlling Lipid Metabolism in C57BL/6J Mice Fed High Fat Diet

  • Koo, Bon-Sun;Seong, So-Hui;Kown, Dae-Young;Sohn, Hee-Sook;Cha, Youn-Soo
    • 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.

Molecular biologic mechanism of obesity by GGEx18 (경신강지환(輕身降脂丸)18의 분자생물학적인 비만조절 기전에 관한 연구)

  • Lee, Hee-Young;Yoon, Ki-Hyeon;Seo, Bu-Il;Park, Gyu-Ryeol;Yoon, Mi-Chung;Shen, Zhi-Bin;Cui, Hong-Hua;Shin, Soon-Shik
    • The Korea Journal of Herbology
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    • v.26 no.1
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    • pp.65-74
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    • 2011
  • Objectives : This study was undertaken to verify the modulation mechanism of Gyeongshingangjeehwan18 (GGEx18) in ob/ob male mice. Methods : Eight-week old mice (wild-type C57BL/6J and ob/ob) were used for all experiments. Wild-type C57BL/6J mice were used as lean control and obese ob/ob mice were randomly divided into 5 groups : obese control, GGEx15 (Ephedra sinica Stapf + Rheum palmatum L.), GGEx16 (Ephedra sinica Stapf + Laminaria japonica Aresch), GGEx17 (Rheum palmatum L. + Laminaria japonica Aresch), and GGEx18 (Ephedra sinica Stapf + Laminaria japonica Aresch + Rheum palmatum L.). After mice were treated with several kinds of GGEx for 11 weeks, the mRNA expression of peroxisome proliferator-activated receptor (PPAR) target genes and uncoupling protein (UCP) were measured. In addition, $PPAR{\alpha}$ and $PPAR{\beta}$ transactivation was examined in NMu2Li hepatocytes, C2C12 myocytes, and 3T3-L1 preadipocytes using transient transfection assays. Results : 1. Hepatic $PPAR{\alpha}$ target genes, such as ACOX and VLCAD mRNA levels were significantly increased by GGEx18 compared with obese controls. In skeletal muscle, LCAD mRNA expression was stimulated by GGEx16, GGEx17, and GGEx18, whereas MCAD mRNA expression by GGEx17 and GGEx18. $PPAR{\beta}$ target LPL mRNA levels were also increased by GGEx16, GGEx17, and GGEx18 in skeletal muscle, but adipose LPL mRNA levels were decreased. In addition, GGEx18 upregulated UCP mRNA expression in skeletal muslce. 2. $PPAR{\alpha}$ reporter gene expression was increased by GGEx18 in NMu2Li cells compared with vehicle. $PPAR{\alpha}$ and $PPAR{\beta}$ reporter activities were also increased by all GGEx treatments in C2C12 and 3T3-L1 cells. Conclusions : These results suggest that GGEx can act as $PPAR{\alpha}$ and $PPAR{\beta}$ activators, and that GGEx may regulate obesity by stimulating $PPAR{\alpha}$, $PPAR{\beta}$, and UCP activity. Of the 4 compositions, GGEx18 seems to be most effective in improving obesity and lipid disorders.

Anti-obesity Effects of SBY-III in High Fat Diet-Fed Obese Rats Continued by High Fat Diet and Regulated by Normal Diet (SBY-III이 비만 및 비만 후 식이조절 흰쥐에 미치는 영향)

  • Woo, Kyung-Ha;Chung, Seok-Hee;Lee, Jong-Su;Kim, Sung-Soo;Shin, Hyun-Dae
    • Journal of Korean Medicine Rehabilitation
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    • v.15 no.2
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    • pp.117-117
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    • 2005
  • Objectives : This experimental study was designed to investigate the effect of SBY-III extract on the weight, cell size of epididymal fat-pad, fat accumulation area in liver, serum lipid level and UCP1 mRNA in brown adipose tissue of high fat diet-fed obese rats continued by high fat diet and regulated by normal Diet. Methods : The body weight gain, weight of the internal organs(epididymis, liver, brown adipose tissue), insulin, triglyceride, total cholesterol, total lopod, free fatty acid, expression of UCP1 mRNA were measured in high fat diet-fed obese rats continued by high fat diet and regulated by normal diet. The experimental study are divided into exp-I and exp-II. Each study was administered normal diet, high fat diet and SBY-III according to each situation. Normal group is normal diet for 8 weeks. Exp-I are divided into control group(high fat diet for 8 weeks) and sample group(high fat diet for 8 weeks and SBY-III for last 2 weeks). Exp-II are divided into control group(high fat diet for 6 weeks and normal diet for 2 weeks) and sample group(high fat diet for 6 weeks and normal diet with SBY-III for 2 weeks). These were then compared mutually. Results : 1. Irrespective of diet control, sample group taken SBY-III showed the more effective decrease of weight gain than control group and diet control-fed sample group with SBY-III showed the more effective decrease of weight loss including weight gain than control group. 2. Irrespective of diet control, sample group taken SBY-III showed the more effective decrease cell size of epididymal fat-pad, fat accumulation area in liver than control group. 3. Non diet control-fed sample group taken SBY-III showed the more effective decrease of serum triglyceride, total lipid, free fatty acid than control group and diet control-fed sample group taken SBY-III showed the decrease of serum triglyceride, free fatty acid than control group. 4. Only diet control-fed sample group taken SBY-III showed the decrease of UCP1 volume. Conclusions : These results shows that SBY-III has effects on anti-obesity, especially keeping pace with diet control.