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Glucose transporter 4 Phosphatidyl inositol 30 kinase Glycogen synthesis a b s t r a c tThe present study discusses the efficacy of Aloe emodin-8-O-glycoside (AEG), a plant derived anthroquinone, on alleviating insulin resistance and augmenting glycogen synthesis in L6 myotubes and 3T3L1 adipocytes. Dose-dependent increase in glucose uptake activity (GUA) was observed in both cell lines. Immunoblot analysis revealed an insulin-like glucose transporting mechanism of AEG by activating key markers involved in the insulin signaling cascade such as insulin receptor beta IRb, insulin receptor substrate1, 85 phosphatidyl inositol 3 0 kinase (PI3K) and PKB. Glucose transporter 4 translocation was confirmed by determining the uptake of glucose in the presence of insulin receptor tyrosine kinase and PI3K inhibitors. AEG was found to enhance glycogen synthesis through the inhibition of glycogen synthase kinase 3b. In conclusion, AEG enhances glucose transport by modulating the proximal and distal markers involved in glucose uptake and its transformation into glycogen.

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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.