Open AccessCinnamic acid, from the bark of Cinnamomum cassia , regulates glucose transport via activation of GLUT4 on L6 myotubes in a phosphatidylinositol 3‐kinase‐independent manner
Author(s) -
LAKSHMI Baddireddi Subhadra,
SUJATHA Sundaresan,
ANAND Singaravelu,
SANGEETHA Kadapakkam Nandhabalan,
NARAYANAN Rangarajan Badri,
KATIYAR Chandrakanth,
KANAUJIA Anil,
DUGGAR Rajeev,
SINGH Yogendra,
SRINIVAS Konasubrahmanya,
BANSAL Vinay,
SARIN Simi,
TANDON Ruchi,
SHARMA Suchitra,
SINGH Suchita
Publication year - 2009
Publication title -
journal of diabetes
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.949
H-Index - 43
eISSN - 1753-0407
pISSN - 1753-0393
DOI - 10.1111/j.1753-0407.2009.00022.x
Subject(s) - glut4 , cinnamomum , cinnamic acid , cassia , glucose transporter , glucose uptake , insulin receptor , biochemistry , pharmacology , insulin , chemistry , medicine , insulin resistance , alternative medicine , traditional chinese medicine , pathology
Background: Cinnamomum cassia (Family: Lauraceae) is an Ayurvedic medicinal plant used traditionally for the treatment of a number of diseases, including diabetes. The hypoglycemic effect of this plant has been established in vivo . However, the effects of cinnamic acid, isolated from C. cassia , on the insulin signaling cascade in an in vitro model have not been elucidated. Hence, the aim of the present study was to evaluate the anti‐diabetic effect of cinnamic acid on glucose transport by L6 myotubes. Methods: The mechanism of action of cinnamic acid was determined using specific targets in the insulin signaling pathway, including protein tyrosine phosphatase (PTP) 1B, phosphatidylinositol 3‐kinase (PI3‐K) and the glucose transporter GLUT4. After differentiation of myoblast to myotubes, the cells were serum deprived for 5 h and then treated with 1 ng/mL cinnamic acid and 50 μmol/L rosiglitazone for 18 h and 100 nmol/L insulin for 20 min for gene expression studies. Results: Expression of GLUT4 mRNA was increased following treatment of L6 myotubes with 1 ng/mL cinnamic acid. Furthermore, cinnamic acid inhibited PTP1B activity (by 96.5%), but had no significant effect on PI3‐K activity. Conclusion: On the basis of the results of the present study, we postulate that cinnamic acid isolated from the hydro‐alcoholic extract of Cinnamomum cassia activates glucose transport by a PI3‐K‐independent pathway. However, the detailed mechanism of action requires further analysis.