• Title/Summary/Keyword: UCP2 expression

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Reduction of Body Weight by Capsaicin is Associated with Inhibition of Glycerol-3-Phosphate Dehydrogenase Activity and Stimulation of Uncoupling Protein 2 mRNA Expression in Diet-induced Obese Rats

  • Ann, Ji-Young;Lee, Mak-Soon;Joo, Hyun-Jin;Kim, Chong-Tai;Kim, Yang-Ha
    • Preventive Nutrition and Food Science
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    • v.16 no.3
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    • pp.210-216
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    • 2011
  • Capsaicin is a pungent component of red pepper, which is widely consumed as food adjuncts. The present study was performed to investigate anti-obesity effects of capsaicin in diet-induced obese rats. Male Sprague-Dawley rats (n=14) were fed with a high-fat diet (Control) or high-fat diet containing 0.016% capsaicin (w/w) (Capsaicin) for 8 weeks. The final body weight and the mass of white adipose tissue were significantly lower in capsaicin supplemented group compared to control. Dietary capsaicin ameliorated lipid profiles with decrease in the plasma concentrations of triglycerides and total cholesterol, and decrease in the levels of total lipids and triglycerides in the liver. Activity of glycerol-3-phosphate dehydrogenase (GPDH), an indicator of triglyceride biosynthesis in white adipose tissue, decreased by 35% in the group supplemented with capsaicin. However, consumption of capsaicin increased the expression of uncoupling protein 2 (UCP2) in white adipose tissue, which is related to energy consumption. Our data suggests that capsaicin may reduce body weight and fat accumulation in high fat diet-induced obese rats. These effects may be mediated, at least partially, by the upregulation of UCP2 gene expression and its ability to inhibit GPDH activity.

Effects of High Fat Diet on Serum Leptin and Insulin Level and Brown Adipose Tissue UCP 1 Expression in Rats (흰쥐에서 고지방식이가 혈중 렙틴 및 인슐린과 갈색지방조직의 UCP 1 발현에 미치는 영향)

  • 홍경희;강순아;김소혜;조여원
    • Journal of Nutrition and Health
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    • v.34 no.8
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    • pp.865-871
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    • 2001
  • The adipose tissue hormone leptin has been proposed to be involved in the regulation of flood intake and energy expenditure via thermogenesis by uncoupling protein(UCP) in brown adipose tissue(BAT). The objective of the study was to examine the effects of high fat diet on the serum leptin levels, BAT UCPl expression and the body fat mass in rats after weaning. During experimental period of 12 weeks, 4 male Sprague-Dawley rats were killed for the baseline experiment at 4 weeks of age while the remaining rats were fed the two different diets: the control diet AIN-76A(n = 20), high fat(beef tallow) diet(n = 20) ad libitum, which provided 11.7% or 40% of calories as fat, respectively. At 16 weeks of age, the increase in the food efficiency ratio(FER) was related to fat mass in rats on high fat diet. Serum leptin level was increased by age and dietary high fat. There was no difference in serum insulin level between groups until 10 weeks of age, but rats fed high fat diet for 12 weeks showed hyperinsulinemia. The amount of body fat pads was increased significantly in high fat group compared to normal diet group. Visceral fat mass affected acutely by high fat diet, as a result, it was higher in rats fed high fat diet for 2 weeks than normal diet. At 16 weeks of age, BAT and visceral fat mass were significantly high in high fat group. Also, the serum leptin levels reflected the amount of body fat mass. BAT UCPI mRNA expression increased with age and dietary high fat. This study demonstrates that dietary high fat increased serum leptin levels, BAT UCPI expression and body fat mass. Futhermore, in rats fed high fat diets, the increases in leptin and UCPI expression counteracts only in part the excess adiposity and obesity.

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Effect of Probiotics-Fermented Samjunghwan on Differentiation in 3T3-L1 Preadipocytes (3T3-L1 전지방세포에서 발효 삼정환의 지방 분화 억제 효과)

  • Song, Mi-Young;Bose, Shambhunath;Kim, Ho-Jun
    • Journal of the Korean Society of Food Science and Nutrition
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    • v.42 no.1
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    • pp.1-7
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    • 2013
  • Samjunghwan (SJH) was fermented using five different probiotic bacterial strains (Lactobacillus plantarum, Enterococcus faecium, Pediococcus pentosaceus, Lactobacillus acidophilus or Bifidobacterium longum) separately. We examined the inhibition of preadipocyte differentiation through Oil Red O staining and analyzed the expression of CCAAT/enhancer-binding protein ${\alpha}$ ($C/EPB{\alpha}$), peroxisome proliferator-activated receptor ${\gamma}$ ($PPAR{\gamma}$), uncoupling protein (UCP)-2, and 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase which are adipogenic transcription factors. Both Lactobacillus plantarum and Enterococcus faecium-fermented SJH reduced Oil Red O dye staining compared with the same dose of non-fermented SJH. Only Lactobacillus plantarum-fermented SJH inhibited all adipogenic transcription factors and showed the best down-regulation of $PPAR{\gamma}$, UCP-2, and HMG-CoA reductase compared with the same dose of non-fermented SJH. The effect of SJH on the inhibition of preadipocyte differentiation was more prominent from the fermented SJH. Lactobacillus plantarum-fermented SJH, in particular, blocks the expression of $PPAR{\gamma}$, UCP-2, HMG-CoA reductase.

Nelumbo nucifera Leaf Extract Regulates Lipid Metabolism and Differentiation in 3T3-L1 Adipocytes and db/db Mice

  • Chul-Min Park;Oh Jin Min;Min-Seok Kim;Bhesh Raj Sharma;Dong Wook Kim;Dong Young Rhyu
    • Natural Product Sciences
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    • v.28 no.4
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    • pp.161-167
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    • 2022
  • Obesity is a complex metabolic disorder that increases the risk for type 2 diabetes, hyperlipidemia, hypertension, and atherosclerosis. In this study, we evaluated the anti-obesity effects of Nelumbo nucifera leaf (NL) extract in 3T3-L1 adipocytes and obese db/db mice. NL extract among various parts (leaf, seed, and root) of N. nucifera most effectively reduced adipogenesis via inhibiting CCAAT enhancer binding protein α (C/EBPα) and peroxisome proliferator activated receptor γ (PPARγ) expression in 3T3-L1 adipocytes. The addition of NL extract enhanced the protein expression of uncoupling protein 2 (UCP2) as compared to untreated 3T3-L1 adipocytes. The oral administration of NL extract (100 mg/kg BW) significantly reduced food efficacy ratio, body weight, and face or total cholesterol level in obese db /db mice. Also, administration of NL extract significantly decreased adipocyte size and C/EBPα or PPARγ expression in the adipose tissues as compared with control (obese db/db mice). Therefore, our results suggest that NL extract among various parts of N. nucifera could be used as a functional food ingredient for the prevention and treatment of metabolic diseases including obesity and diabetes.

Fenofibrate Inhibits Visceral Adiposity by Inhibiting UCPs in C57BL/6J Mice Fed on a High Fat Diet

  • Oh, Jaeho;Yoon, Michung
    • Biomedical Science Letters
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    • v.18 no.4
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    • pp.355-361
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    • 2012
  • We investigated to verify whether the $PPAR{\alpha}$ agonist fenofibrate regulates adipose tissue metabolism and to determine the molecular mechanism involved in this regulation. After male mice (C57BL/6J) received a high fat diet with or without fenofibrate for 6 weeks, the effects of fenofibrate on not only adipose tissue weight, visceral adipocyte size, serum lipid and glucose levels, but also the expression of uncoupling proteins (UCPs). Mice given a fenofibrate-supplemented high fat diet showed reduced both visceral and subcutaneous adipose tissue weights versus high fat diet-fed animals. The size of visceral adipocytes was significantly decreased by fenofibrate treatment. The administration of fenofibrate resulted in decreased serum levels of triglycerides, free fatty acids, and glucose. Moreover, fenofibrate up-regulated mRNA levels of visceral adipose tissue UCP2 and skeletal muscle UCP3. Therefore, our results suggest that the increases in the expression of UCPs by fenofibrate seem to suppress diet-induced visceral adiposity as well as severe hypertriglyceridemia and hyperglycemia in male mice.

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.

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.

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.