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

化学 安普克 根皮苷 生物化学 碳水化合物代谢 脂肪酸合酶 胞浆 糖酵解 脂肪组织 过剩1 胰岛素抵抗 过剩2 新陈代谢 AMP活化蛋白激酶 蛋白激酶B 脂肪细胞
作者
Kian Chung Ong,Hoon Eng Khoo
出处
期刊:Biochemical Pharmacology [Elsevier BV]
卷期号:51 (4): 423-429 被引量:75
标识
DOI:10.1016/0006-2952(95)02195-7
摘要

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 EC50 was estimated to be about 65 microM. 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-methylglucose uptake in rat adipocytes. The Vmax of glucose transport was increased, but the Km 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-dependent diabetes mellitus by stimulating glucose uptake without the presence of fully functional insulin receptor.
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