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Aloe emodin glycosides stimulates glucose transport and glycogen storage through PI3K dependent mechanism in L6 myotubes and inhibits adipocyte differentiation in 3T3L1 adipocytes
Author(s) -
Anand S.,
Muthusamy V.S.,
Sujatha S.,
Sangeetha K.N.,
Bharathi Raja R.,
Sudhagar S.,
Poornima Devi N.,
Lakshmi B.S.
Publication year - 2010
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2010.06.004
Subject(s) - glycogen synthase , glucose transporter , glut4 , insulin receptor , glycogen , glucose uptake , insulin , medicine , endocrinology , adipocyte , chemistry , insulin receptor substrate , biochemistry , snf3 , insulin resistance , biology , adipose tissue
The 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 IRβ, insulin receptor substrate1, 85 phosphatidyl inositol 3′ 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 3β. In conclusion, AEG enhances glucose transport by modulating the proximal and distal markers involved in glucose uptake and its transformation into glycogen.