• Journal of Sasang Constitutional Medicine
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• v.22 no.1
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• pp.34-40
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• 2010

1. Objectives: Leptin is ob-gene originated hormone that is concerned with energy metabolism, obesity and asthma which features are supposed to related with Sasangin's 4 viscera physiological theory of Sasang constitutional medicine(SCM). This study aims to investigate whether serum leptin concentration is associated with Sasangin. 2. Methods: Two Way ANOVA analysis was used on the constitution and serum leptin concentration corresponding with BMI among 1054 cases drawn from the Constitutional Information Bank, which was a database with clinically confirmed constitution cases collected from 21 oriental medical institutes in Korea starting from November 2007 to May 2009. The measurement of serum leptin concentration is implemented through radioimmunoassay by request to SCL. 3. Results: Male subjects showed notable difference(p=0.033) in the comparison between constitution and serum leptin concentration corresponding to BMI levels. Tae-eumins showed the highest serum leptin concentration levels in the normal and overweight groups, followed by Soyangin and Soeumin. As the groups changed from overweight to obese, there was an interaction phenomenon in the order of serum leptin concentration levels(p=0.040). As a result, Soeumins showed the highest serum leptin concentration levels and Tae-eumins and Soyangins followed in place. Female subjects did not show statistically notable differences in comparison between constitution and serum leptin concentration corresponding to BMI levels(p=0.239). Serum leptin concentration levels among overweight and obese groups, resulted in the order of Soeumins, Tae-eumins, and Soyangins. But in the as groups changed from overweight to normal the order resulted in Tae-eumin, Soyangin, and Soeumin(p=0.660). 4. Conclusion: Due to a number of limitations in this study, the examination of the relation between constitution and leptin, a main hormone responsible for the digestion, appetite, and energy metabolism, resulted to be uncertain. But statistically notable differences were confirmed in male Tae-eumins with the consideration of BMI. Further examination of the relation between constitution and leptin is necessary through prospective studies with the restriction of confusion variables in the future.

• Food Science of Animal Resources
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• v.33 no.3
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• pp.411-416
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• 2013

This study aimed to examine the mechanisms underlying the effects of Garcinia cambogia extract on the adipogenic differentiation of 3T3-L1 cells and long-chain saturated fatty acid-induced lipotoxicity of HepG2 cells. 3T3-L1 preadipocytes, mouse embryonic fibroblast-adipose like cell line, were treated with MDI solution (0.5 mM IBMX, 1 ${\mu}M$ dexamethasone, 10 ${\mu}g/mL$ insulin) to generate a cellular model of adipocyte differentiation. Using this cellular model, the anti-obesity effect of Garcinia cambogia extract was evaluated. MDI-induced lipid accumulation and expression of adipogenesis-related genes were detected by Oil red O staining, Nile Red staining, and Western blot analysis. Effects Garcinia cambogia extract on palmitate-induced lipotoxicity was also analyzed by MTT assay, LDH release, and DAPI staining in HepG2 cells. Garcinia cambogia extract significantly suppressed the adipogenic differentiation of preadipocytes and intracellular lipid accumulation in the differentiating adipocytes. Garcinia cambogia extract also markedly inhibited the expression of peroxisome proliferator- activated receptor ${\gamma}2$ ($PPAR{\gamma}2$), CCAT/enhancer-binding protein ${\alpha}$ ($C/EBP{\alpha}$), and adipocyte protein aP2 (aP2). In addition, Garcinia cambogia extract significantly attenuated palmitate-induced lipotoxicity in HepG2 cells. Palmitateinduced cellular damage and reactive aldehydes were also significantly reduced in the presence of Garcinia cambogia extract. These findings suggest that the Garcinia cambogia extract inhibits the adipogenic differentiation of 3T3-L1 preadipocytes, probably by regulating the expression of multiple genes associated with adipogenesis such as $PPAR{\gamma}2$, $C/EBP{\alpha}$, aP2, and thereby modulating fatty acid-induced lipotoxicity to reduce cellular injury in hepatocytes.

• Journal of Life Science
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• v.19 no.11
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• pp.1637-1643
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• 2009

Shikonin, a component of Lithospermum erythrorhizon Sieb. et Zucc, exerts various characteristics such as anti-inflammatory, anti-cancer and anti-obesity functions. To elucidate the molecular mechanism of shikonin-induced inhibition of adipogenesis, we analyzed the mRNA expression level of various adipogenesis-related factors including C/EBPs (CCAAT/enhancerbinding proteins) and $PPAR{\gamma}$ (peroxisome proliferator-activated receptor $\gamma$). The data showed that mRNA expressions of C/$EBP{\beta}$ and C/$EPB{\delta}$ were only slightly changed by shikonin treatment, but mRNA expressions of $PPAR{\gamma}$ and C/$EPB{\alpha}$ were significantly down-regulated. Then, we tested whether upstream regulators of C/$EBP{\beta}$ and $PPAR{\gamma}$ were involved in anti-adipogenesis of shikonin. C/$EBP{\gamma}$ and CHOP (C/EBP homologous protein), which are upstream regulators of C/$EBP{\beta}$, were not affected by shikonin treatment. On the contrary, the mRNA level of KROX20 was markedly down-regulated by shikonin treatment. These results suggest that KROX20 might regulate downstream factors of adipogenesis through C/$EBP{\beta}$-independent pathway. The expression of KLF15 (Kruppel-like factor15), which is a member of KLF family and is a upstream regulator of $PPAR{\gamma}$, was dramatically decreased by shikonin treatment, but KLF2 was not changed. Shikonin had no impact on the expression of KLF5 in the early stage of adipogenesis, but shikonin increased expression of KLF5 in the late stage of adipogenesis. Even though mRNA expression of KLF5 was moderately changed by shikonin treatment, its effect may be small compared with the effect of KLF15, which was markedly inhibited. Taken together, these results suggest that shikonin inhibits adipogenesis through the down-regulation of $PPAR{\gamma}$ and C/$EPB{\alpha}$, which is mediated by the down-regulation of two pro-adipogenic factors, KROX20 and KLF15.