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Pharmaceutical Biology 2013-Aug

The extract of Cinnamomum cassia twigs inhibits adipocyte differentiation via activation of the insulin signaling pathway in 3T3-L1 preadipocytes.

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Yunkyung Han
Hyo Won Jung
Hyo Sang Bae
Jong-Seong Kang
Yong-Ki Park

Keywords

Abstract

BACKGROUND

Obesity is associated with a number of diseases with metabolic abnormalities such as type 2 diabetes (T2D). Medicinal plants have been widely used for the treatment of obesity and related complications.

OBJECTIVE

In this study, we investigated the antidiabetic properties of the extract of twigs of Cinnamomum cassia Blume (Lauraceae) (Cinnamomi Ramulus; CR) in 3T3-L1 murine preadipocytes.

METHODS

3T3-L1 cells were differentiated into adipocytes for 3 d in insulin-conditioned medium and then treated with CR extract at concentrations of 100 and 500 μg/mL for 6 d. Adipocyte differentiation was measured by Oil Red O staining, and the expression of master transcription factors, peroxisome proliferator-activated receptor-gamma (PPARγ), CCAAT/enhancer binding protein-alpha (C/EBPα), and sterol regulatory element binding protein-1c (SREBP-1c), and lipid metabolism factors were investigated by reverse transcription-polymerase chain reaction (RT-PCR). The activation of the AMP-activated protein kinase (AMPK)/insulin signaling pathway was assessed by western blot analysis.

RESULTS

CR extract significantly reduced lipid accumulation and down-regulated the expression of PPARγ, C/EBPα, and SREBP-1c in 3T3-L1 adipocytes. CR extract also suppressed the expression of fatty acid synthase (FAS), acyl-CoA synthase, and perilipin. Moreover, CR extract markedly up-regulated the phosphorylation of AMPK and acetyl-CoA carboxylase (ACC). In addition, CR extract effectively increased the expression levels of glucose transporter-4 (GLUT-4), phosphatidylinositol 3-kinase (PI3K), and insulin receptor substrate-1 (IRS-1) in 3T3-L1 adipocytes.

CONCLUSIONS

These results suggest that CR extract may have therapeutic potential as a natural agent for the improvement of T2D via regulation of the insulin-dependent signaling pathway.

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