請用此 Handle URI 來引用此文件: http://hdl.handle.net/11455/61701
標題: AGE-Induced Interference of Glucose Uptake and Transport as a Possible Cause of Insulin Resistance in Adipocytes
作者: Wu, Chi-Hao
Huang, Hsiao-Wen
Huang, Shang-Ming
Lin, Jer-An
Yeh, Chi-Tai
Yen, Gow-Chin
關鍵字: adipocytes
advanced glycation end products
insulin resistance
inflammation
oxidative stress
receptor for AGEs
glycation end-products
skeletal-muscle cells
reactive oxygen
signaling pathways
adipose-tissue
receptor
protein
methylglyoxal
inhibition
obesity
摘要: The purpose of this study was to investigate the distinct roles of advanced glycation end products (AGEs) on insulin-mediated glucose disposal in 3T3-L1 adipocytes and C2C12 skeletal muscle cells. AGE-modified proteins, namely, GO-AGEs, were prepared by incubating bovine serum albumin (BSA) with glyoxal (GO) for 7 days. Glucose utilization rates and the expression of insulin signaling-associated proteins, including Akt, insulin receptor substrate-1, and glucose transporter 4, were determined. GO-AGEs caused insulin resistance (IR) by suppressing insulin-stimulated glucose uptake both in 3T3-L1 adipocytes and C2C12 muscle cells. Interestingly, an unexpected finding was that insulin-stimulated glucose transport in adipocytes was affected by GO-AGEs in a biphasic manner, with an initial steep increase (168%) during the first 8 h of incubation followed by a significantly impaired uptake after extended culture times (24-48 h,p <0.05). Treatment with GO-AGEs for 24 h markedly accelerated lipid droplet formation compared to the BSA control; however, it was blocked by incubation with an anti-RAGE antibody. Our study suggests that GO-AGEs induce an early dramatic elevation of glucose transport in adipocytes that may be related to the activation of insulin signaling; however, subsequent IR may result from increased oxidative stress and proinflammatory TNF-alpha production.
URI: http://hdl.handle.net/11455/61701
ISSN: 0021-8561
顯示於類別:食品暨應用生物科技學系

文件中的檔案:
沒有與此文件相關的檔案。


在 DSpace 系統中的文件,除了特別指名其著作權條款之外,均受到著作權保護,並且保留所有的權利。