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Regulasi Adipogenesis oleh mTORC1 melalui lalur STAT3 (Agipogenesis Regulation of mTORC1 through STAT3 Pathway) .—JurnalKedokteranBrawijaya27(3)2014:123-130

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Recently, the processes of adipogenesis become a treatment target for obesity. One of the pathways that allegedly participated in the process of adipogenesis is activated via STAT3. The upstream line of is protein of mammalian targets of rapamycin complex 1 (mTOR). This study aimed to determine the role of STAT3 in adipogenesis through activation of p705681 by mTORC1. This was an experimental study with a post test only with control group design.

Subjects were primary cultured preadipocytes taken from visceral fat white rat (Rattus notvegicus). As cell cultured were at least 70-80% confluent, the induction of differentiation of preadipocytes were initiated. Cell cultures were divided into 4 groups: (K) Control of adipogenesis (A): added a rapamycin 10nM, (B): added α 100 µM inhibitorSTAT3 peptide, (C): added a inhibitor STAT3 peptide and rapomycin 100 pM and 10 nM. The indicator of odipocytes were p70561(1, STAT3 activation, and the activity of Glyserol-3-phospho dehidrogenose (GPDH)and the morphology of odipocytes. Data was analyzed using ANOVA test, Duncan test and Pearson Correlation test with 95% confidence level.

The data indicated that adipogenesis can be blocked as the inhibition of p70561(1 and STAT3 activation by rapamycin and STAT3 inhibitor. The inhibition was strongerat the rapamycini-STAT3 inhibitor group. Statistically, there were a significant correlation between p.70S6K1 and .5 TA 73; STAT3 and GPDH enzyme. it con be concluded that adipogenesis con be regulated by mTORC1 through the activation p70S6K1,STAT3.

Keywords: Adipocytes, obesity, mTORC1, p70S6K1,STAT3

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Jurnal Kedokteran Brawijaya 2 (3) 2013: 123-131

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Malang : Jurnal Kedokteran Brawijaya., 2013

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9p

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2338-0772

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