Insulinomimetic effects of myricetin on lipogenesis and glucose transport in rat adipocytes but not glucose transporter translocation

Abstract

Myricetin is a naturally occurring flavonol that is commonly found in tea, berries, fruits, and medicinal plants. It mimics insulin in stimulating lipogenesis and glucose transport in rat adipocytes in vitro. It was found to stimulate lipogenesis in rat adipocytes and enhance the stimulatory effect of insulin. The EC 50 was estimated to be about 65 μM. Myricetin did not have any effect on insulin receptor autophosphorylation nor on the tyrosine kinase activity of the receptor. However, myricetin stimulated both d-glucose and D-3- O-methyl-glucose uptake in rat adipocytes. The V max of glucose transport was increased, but the K m did not change significantly. Immunoblot analysis of Glut4 in rat adipocyte plasma membrane showed that the stimulation of glucose transport was not a consequence of glucose transporter translocation. Instead, the stimulation in glucose uptake probably was due to a change in the intrinsic activity of the glucose transporter possibly caused by alterations in membrane fluidity or transporter-lipid interactions as a result of the insertion of myricetin into the membrane bilayer. Thus, myricetin may have therapeutic potential in the management of non-insulin-deendent diabetes mellitus by stimulating glucose uptake without the presence of fully functional insulin receptors.