• 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.

• Proceedings of the Korea Environmental Mutagen Society Conference
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• 2004.05a
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• pp.90-90
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• 2004

• Current Research on Agriculture and Life Sciences
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• v.24
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• pp.29-35
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• 2006

In this study we evaluated the anti-diabetic potential of Puerariae Radix and its isoflavone (puerarin) by investigating their inhibitory activities against digestive enzymes, ${\alpha}$-amylase, ${\alpha}$-glucosidase and lipase and effect on glucose uptake and PPAR ${\gamma}$ expression. The activities of carbohydrate digestive enzymes were not inhibited by puerarin. Glucose uptake in differentiated adipocytes was stimulated by puerarin. Furthermore, puerarin enhanced the differentiation of preadipocytes as evaluated by triacylglycerol (TG) accumulation, which is specific for differentiated adipocytes. The effect of puerarin on expression of peroxisome proliferator-activated receptor ${\gamma}$ (PPAR-${\gamma}$) gene, which is associated with obesity and dyslipidemia, was examined by both real-time PCR and reverse transcriptase PCR. The study demonstrated that puerarin increased the expression of PPAR-${\gamma}$. In conclusion, puerarin showed potential to exert anti-diabetic action by enhancing cellular glucose uptake and thereby TG accumulation in adipocyte tissue.

• Journal of Microbiology and Biotechnology
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• v.28 no.10
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• pp.1645-1653
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• 2018

The genus Acer contains several species with various bioactivities including antioxidant, antitumor and anti-inflammatory properties. However, Acer okamotoanum Nakai, one species within this genus has not been fully studied yet. Therefore, in this study, we investigated the anti-adipogenic activities of leaf extract from A. okamotoanum Nakai (LEAO) on 3T3-L1 preadipocytes. Adipogenesis is one of the cell differentiation processes, which converts preadipocytes into mature adipocytes. Nowadays, inhibition of adipogenesis is considered as an effective strategy in the field of anti-obesity research. In this study, we observed that LEAO decreased the accumulation of lipid droplets during adipogenesis and down-regulated the expression of key adipogenic transcription factors such as peroxisome proliferator-activated receptor ${\gamma}$ (PPAR ${\gamma}$) and CCAAT/enhancer binding protein ${\alpha}$ (C/EBP ${\alpha}$). In addition, LEAO inactivated PI3K/Akt signaling and its downstream factors that promote adipogenesis by inducing the expression of PPAR ${\gamma}$. LEAO also activated ${\beta}$-catenin signaling, which prevents the adipogenic program by suppressing the expression of PPAR ${\gamma}$. Therefore, we found that treatment with LEAO is effective for attenuating adipogenesis in 3T3-L1 cells. Consequently, these findings suggest that LEAO has the potential to be used as a therapeutic agent for preventing obesity.

• Korean Journal of Veterinary Service
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• v.28 no.2
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• pp.91-98
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• 2005

Green tea was known which regulated adipocyte differentiation metabolism. The mechanism on the lipid decreased contents of TAG in the plasma. In addition, green tea increased the expression leptin mRNA, PPAR $\delta$ mRNA and TGF $\beta$. The tea tested was korean powdered green tea. In this experiment, Sprague-Dawley (SD) rats were fed $3\%$ green tea(powdered) for 3 weeks on the basal diet and obese diet and green tea grouts-fed pork meats. duck meats. The expression of leptin mRNA and PPAR $\delta$ mRNA were up-regulated in the green tea-fed groups compared with those of the not green tea-fed groups. There were no significantly difference on the expression of leptin mRNA and PPAR $\delta$ mRNA in green tea grouts-fed pork meats, duck meats as compared with the not fed green tea grouts meats. TGF $\beta$ mRNA. TNF $\alpha$ mRNA and adipsin mRNA were not expressed in the pork meats, duck meats. The expression of TGF $\beta$ mRNA, TNF $\alpha$ mRNA and adipsin mRNA were observed in the experimental rats but no significantly difference on the contents. Physiologic regulated genes were not expressed In the green tea grout-fed pork meats and duck meats.

• Korean Journal of Food Science and Technology
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• v.47 no.4
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• pp.499-503
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• 2015

We investigated the anti-obesity effects of ethanolic extract (ID1216) of Polygonatum sibiricum rhizome and its potential underlying mechanism in an animal model. ID1216 treatment decreased body weight gain and white adipose tissue weight in the prevention study. The mRNA levels of sirtuin-1 (SIRT1), peroxisome proliferator-activated receptor ${\gamma}$ coactivator-$1{\alpha}$ ($PGC1{\alpha}$), and peroxisome proliferator-activated receptor ${\alpha}$ ($PPAR{\alpha}$) significantly increased in the epididymal white adipose tissue of ID1216-administered mice. The stimulation effects of ID1216 on these gene expressions were also observed in a cell-based assay using differentiated 3T3-L1 adipocytes. In addition, similar to orlistat, ID1216 treatment improved weight gain and reduced epididymal fat in the treatment model. These results suggest that ID1216 has potential as an anti-obesity agent by modulating the expression of genes related to thermogenesis, lipid metabolism and fatty acid oxidation.

• Journal of the Society of Cosmetic Scientists of Korea
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• v.42 no.4
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• pp.393-401
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• 2016

Ultraviolet (UV) irradiation from the sun is the primary environmental factor that causes skin damages including skin cancer and premature skin aging. Because, even the most powerful sunscreen can't always afford enough protection, it is necessary to enhance the defensive power of skin against UV. Recently, constitutive photomorphogenic protein-1 (COP1) has shown to contribute to the regulation of UVB response of keratinocytes. In this study, we represent that COP1 and its associated protein, de-etiolated 1 (DET1), might participate in photoaging process in human skin as Arabidopsis COP1 does sun-protective function in plants. After UVB irradiation, the decrease of COP1 and DET1 mRNA expression was followed by the increase of c-Jun total protein. Moreover, transfection with DNA vectors expressing COP1 and DET1 down-regulated the c-Jun total protein. We found that Zanthoxylum piperitum extract (ZE) up-regulated the expression of COP1 and DET1 on human keratinocytes, and inhibited the expression of MMP1 which is one of the genes regulated by c-Jun signal. In addition, ZE has been reported to stimulate PPAR-${\alpha}$ and strengthen the skin barrier. We found that ZE decreased the UVB-induced IL-6 and IL-8 in NHEK cells. In human study, ZE protected skin against UV-B induced erythema and erythema-induced pigmentation. These results indicate that ZE could be useful for the protection against the adverse effects of UV irradiation through various mechanisms.

• Nutrition Research and Practice
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• v.8 no.2
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• pp.158-164
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• 2014

BACKGROUD/OBEJECTIVES: This study aims to find out the effects of peanut sprout extracts on weight controls and protein expressions of transcription factors related to adipocyte differentiation and adipocytokine in rats under high-fat diets. MATERIALS/METHODS: Four week-old Sparague-Dawley (SD) were assigned to 4 groups; normal-fat (NF) diets (7% fat diet), high-fat (HF) diets (20% fat diet), high fat diets with low peanut sprout extract (HF + PSEL) diet (20% fat and 0.025% peanut sprout extract), and high fat diets with high peanut sprout extract (HF + PSEH) diet (20% fat and 0.05% peanut sprout extract). Body weight changes, lipid profiles in adipose tissue, and the mRNA protein expressions, such as peroxisome proliferator-activated receptor ${\gamma}$ ($PPAR{\gamma}$), CCAAT element binding protein ${\alpha}$ (C/EBP ${\alpha}$), leptin, and adiponectin, were determined. RESULTS: After 9 weeks of feeding, the HF + PSEH group had significantly less weight gains than the HF group (P < 0.05). However, the total dietary intakes or food efficiency ratios among groups were not significantly different. The weight of epididymal fat in HF + PSEH group, $3.61{\pm}0.5g$, or HF + PSEL group, $3.80{\pm}0.7g$, was significantly lower than the HF group, $4.39{\pm}0.4g$, (P < 0.05). Total lipids and total cholesterol in adipose tissue were significantly decreased in HF + PSEH group compared to those in the HF group, respectively (P < 0.05). PSEH supplementation caused AST and ALT levels to decrease when it compared to HF group, but it was not statistically significant. The protein expression of $PPAR{\gamma}$ in HF + PSEH group was significantly lower than the HF group (P < 0.05). Comparing with the HF group, the protein expression of adiponectin in HF + PSEH group was significantly increased (P < 0.05). The protein expressions of C/EBP ${\alpha}$ and leptin in HF + PSEH group were lower than the HF group, but it was not statistical significant. CONCLUSIONS: In conclusion, peanut sprout extract has anti-obesity effect by lowering the expressions of $PPAR{\gamma}$ which regulates the expression of adiponectin.

• Biomedical Science Letters
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• v.14 no.3
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• pp.131-137
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• 2008

Adipogenesis is a complex sequence of events that culminates in the differentiation of fibroblast-like preadipocytes into specialized lipid-filled adipocytes and also involves a cascade of expression of many transcription factors such as peroxisome proliferator-activated receptor ${\gamma}(PPAR{\gamma})$ and CCAAT/enhancer-binding proteins (C/EBPs). $PPAR{\gamma}$ and C/EBPs transcriptionally transactivate adipocyte specific genes, including fatty acid transport protein (FAT/CD36) and leptin. To determine whether $17{\beta}$-estradiol modulates $C/EBP{\alpha}$ actions on adipogenesis in high fat diet-fed female ovariectomized (OVX) C57BL/6 mice, mice were treated with $17{\beta}$-estradiol for 7 days and the effects of $17{\beta}$-estradiol on adipose tissue mass and expression of adipocyte specific gene as well as $C/EBP{\alpha}$ were measured. Compared to vehicle-treated OVX control mice, OVX mice treated with $17{\beta}$-estradiol for 7 days had lower adipose tissue weights that were similar to weights in high fat diet-fed sham-operated (Sham) mice. OVX mice showed the increased expression of $C/EBP{\alpha}$ mRNA compared with Sham mice. However, $17{\beta}$-estradiol treatment in OVX mice inhibited OVX induced-$C/EBP{\alpha}$ activation, indicating that $17{\beta}$-estradiol may act as an inhibitor of $C/EBP{\alpha}$ action. Moreover, $17{\beta}$-estradiol decreased mRNA levels of adipocyte marker genes, such as lipoprotein lipase, FAT/CD36 and leptin, to levels in Sham mice. These results suggest that down-regulation of adipogenesis by $17{\beta}$-estradiol may be due to reduced adipose $C/EBP{\alpha}$ activities in female OVX C57BL/6 mice.

• Asian Pacific Journal of Cancer Prevention
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• v.14 no.11
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• pp.6761-6767
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• 2013

The nuclear receptor, peroxisome proliferator-activated receptor gamma ($PPAR{\gamma}$), is expressed in various cancer cells including breast, prostate, colorectal and cervical examples. An endogenous ligand of $PPAR{\gamma}$, 15-deoxy-${\Delta}^{12,14}$ prostaglandin $J_2$ (PGJ2), is emerging as a potent anticancer agent but the exact mechanism has not been fully elucidated, especially in breast cancer. The present study compared the anticancer effects of PGJ2 on estrogen receptor alpha ($ER{\alpha}$)-positive (MCF-7) and $ER{\alpha}$-negative (MDA-MB-231) human breast cancer cells. Based on the reported signalling cross-talk between $ER{\alpha}$ and $ER{\alpha}$, the effect of the $ER{\alpha}$ ligand, $17{\beta}$-estradiol (E2) on the anticancer activities of PGJ2 in both types of cells was also explored. Here we report that PGJ2 inhibited proliferation of both MCF-7 and MDA-MB-231 cells by inducing apoptotic cell death with active involvement of mitochondria. The presence of E2 potentiated PGJ2-induced apoptosis in MCF-7, but not in MDA-MB-231 cells. The $ER{\alpha}$ antagonist, GW9662, failed to block PGJ2-induced activities but potentiated its effects in MCF-7 cells, instead. Interestingly, GW9662 also proved capable of inducing apoptotic cell death. It can be concluded that E2 enhances $ER{\alpha}$-independent anticancer effects of PGJ2 in the presence of its receptor.