Vanillin induces adipocyte differentiation in 3T3-L1 cells by activating extracellular signal regulated kinase 42/44

To investigate the effect of vanillin, a dietary component, on adipocyte differentiation and the mechanism involved in the process using 3T3-L1 murine preadipocytes. The effect of vanillin on adipocyte differentiation was detected by Oil Red O analysis. The activation of extracellular signal regulat...

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Published in:Life sciences (1973) Vol. 88; no. 15; pp. 675 - 680
Main Authors: Haridas Nidhina, Pachakkil A., Poulose, Ninu, Gopalakrishnapillai, Anilkumar
Format: Journal Article
Language:English
Published: Netherlands Elsevier Inc 11-04-2011
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Summary:To investigate the effect of vanillin, a dietary component, on adipocyte differentiation and the mechanism involved in the process using 3T3-L1 murine preadipocytes. The effect of vanillin on adipocyte differentiation was detected by Oil Red O analysis. The activation of extracellular signal regulated kinase 42/44 (ERK 42/44), Akt, expression of the key regulator of adipocyte differentiation peroxisome proliferators-activated receptor (PPARγ) and its target gene glucose transporter 4 (GLUT4) were detected by western blotting. Glucose uptake assay was used to determine the insulin sensitivity of adipocytes differentiated by vanillin treatment. To confirm the role of ERK 42/44 and Akt, Oil Red O analysis was performed with cells differentiated in the presence or absence of ERK inhibitor U0126 or Akt kinase 1/2 inhibitor. Vanillin induced adipocyte differentiation in 3T3-L1 cells in a dose dependent manner and also increased the expression levels of PPARγ and its target gene GLUT4. The adipocytes differentiated by vanillin exhibited insulin sensitivity as demonstrated by a significant increase in glucose uptake. Vanillin treatment activated the phosphorylation of ERK 42/44 during the initial phase of adipocyte differentiation but there was no significant change in the Akt phosphorylation status. The data show that vanillin induces adipocyte differentiation in 3T3-L1 cells by activating ERK42/44 and these adipocytes are insulin sensitive in nature.
Bibliography:http://dx.doi.org/10.1016/j.lfs.2011.02.001
ObjectType-Article-1
SourceType-Scholarly Journals-1
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ISSN:0024-3205
1879-0631
DOI:10.1016/j.lfs.2011.02.001