Publication Type:

Journal Article


Biochemical and Biophysical Research Communications, Volume 380, Number 1, p.39-43 (2009)



3T3-L1 Cells, 7 dirhamnoside, adipocyte, Adipocytes, animal cell, Animals, article, controlled study, drug binding, drug inhibition, drug isolation, flavonoid, Glucose, glucose transport, glucose transporter 4, Glucose Transporter Type 4, high performance liquid chromatography, insulin, Insulin Antagonists, kaempferol 3, Kaempferols, Mice, molecular docking, mouse, nonhuman, priority journal, protein kinase B, protein transport, Proto-Oncogene Proteins c-akt, translocation line, unclassified drug


<p>Insulin stimulated GLUT4 (glucose transporter 4) translocation and glucose uptake in muscles and adipocytes is important for the maintenance of blood glucose homeostasis in our body. In this paper, we report the identification of kaempferitrin (kaempferol 3,7-dirhamnoside), a glycosylated flavonoid, as a compound that inhibits insulin stimulated GLUT4 translocation and glucose uptake in 3T3-L1 adipocytes. In the absence of insulin, we observed that addition of kaempferitrin did not affect GLUT4 translocation or glucose uptake. On the other hand, kaempferitrin acted as an inhibitor of insulin-stimulated GLUT4 translocation and glucose uptake in 3T3-L1 adipocytes by inhibiting Akt activation. Molecular docking studies using a homology model of GLUT4 showed that kaempferitrin binds directly to GLUT4 at the glucose transportation channel, suggesting the possibility of a competition between kaempferitrin and glucose during the transport. Taken together, our data demonstrates that kaempferitrin inhibits GLUT4 mediated glucose uptake at least by two different mechanisms, one by interfering with the insulin signaling pathway and the other by a possible competition with glucose during the transport. © 2009 Elsevier Inc. All rights reserved.</p>


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Cite this Research Publication

C. N. Vishnu Prasad, S. Mohan, S., Banerji, A., and Gopalakrishnapillai, A., “Kaempferitrin inhibits GLUT4 translocation and glucose uptake in 3T3-L1 adipocytes”, Biochemical and Biophysical Research Communications, vol. 380, pp. 39-43, 2009.