Literature DB >> 23627464

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

Yunkyung Han1, Hyo Won Jung, Hyo Sang Bae, Jong-Seong Kang, Yong-Ki Park.   

Abstract

CONTEXT: 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.
MATERIALS AND 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. DISCUSSION AND
CONCLUSION: 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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Year:  2013        PMID: 23627464     DOI: 10.3109/13880209.2013.772211

Source DB:  PubMed          Journal:  Pharm Biol        ISSN: 1388-0209            Impact factor:   3.503


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