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Proteomic analysis for inhibitory effect of chitosan oligosaccharides on 3T3‐L1 adipocyte differentiation
Author(s) -
Rahman Md. Atiar,
Kumar Suresh G.,
Kim Sang Woo,
Hwang Hye Jin,
Baek Yu Mi,
Lee Sung Hak,
Hwang Hee Sun,
Shon Yun Hee,
Nam Kyung Soo,
Yun Jong Won
Publication year - 2008
Publication title -
proteomics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.26
H-Index - 167
eISSN - 1615-9861
pISSN - 1615-9853
DOI - 10.1002/pmic.200700888
Subject(s) - adipogenesis , adipocyte , adipocyte protein 2 , intracellular , biochemistry , cytoskeleton , microbiology and biotechnology , context (archaeology) , cellular differentiation , glucose transporter , chemistry , lipid droplet , biology , fatty acid , cell , in vitro , insulin , gene , endocrinology , adipose tissue , paleontology
In the present study, we performed a differential proteomic analysis using 2‐DE combined with MS to clarify the molecular mechanism for the suppressive effect of chitosan oligosaccharides (CO) during differentiation of adipocyte 3T3‐L1. Cell differentiation was significantly inhibited by CO at the concentration of 4 mg/mL. Protein mapping of adipocyte homogenates by 2‐DE revealed that numerous protein spots were differentially altered in response to CO treatment. Out of 50 identified proteins showing significant alterations, six were up‐regulated and 44 were down‐regulated by CO treatment in comparison to control mature adipocytes. Among them, most of the proteins are associated with lipid metabolism, cytoskeleton, and redox regulation, in which the levels of farnesyl diphosphate synthetase (FDS), dedicator of cytokinesis 9 (DOCK9), and chloride intracellular channel 1 (CLIC1) were significantly reduced (>two‐fold) with CO treatment. These results have not previously been examined in the context of adipogenesis, and thus can be used as novel biomarkers. Taken together with immunoblot analysis, it was concluded that the inhibitory effect of CO on adipocyte differentiation was mediated by C/EBPα and PPARγ pathway through significant downregulations of important adipogenic molecules such as fatty acid binding protein and glucose transporter 4.