PARENT SESSION

2D - Mechanisms of toxic action
Poster Hall
8:30 AM - Monday, 28 April 2003
Chair: Dietrich, D.¹, ¹
Co-chair: Haux, C.², ²

(MOP/91) CdCl2-Induced glucose uptake might be mainly caused by the activation of pentose phosphate pathway in 3T3-L1 adipocytes.

Moon, Chang-Kiu¹, Lee, Hwa-Bok¹, Chae, Sang-Ho¹, Kim, Min-Hwa ¹, Lee, Yoon-Hee¹, Chung, Ah-Young¹, Kim, Kwan-Soo¹, Cho, Yang-Young¹, Kim, Mi-Hee¹, ¹ Seoul National University, Seoul, KOREA, KOREA

ABSTRACT- The present study was undertaken to elucidate the mechanism of CdCl2-induced glucose transport in 3T3-L1 adipocytes.The exposure of adipocytes to 10 and 25uM CdCl2 caused the increase in 2.1 and 2.6 times uptake of 2-DOG respectively.To confirm,whether CdCl2-induced glucose transport was mediated by insulin signaling pathway,we investigated glucose uptake under CdCl2 exposure using wortmannin,a PI3K inhibitor,and PD98059,a MAPK-inhibitor.But any significant effect was not observed on the glucose transport.The followed trials were to investigate the effects of CdCl2 on some other factors inluencing glucose uptake.Calcium depletion by using nifedifine,a Ca channel blocker,resulted in decrese of the 2-DOG uptake to the basal level.We also measured ROS formation and GSH level under CdCl2 exposure to understand the correlation betwen glucose uptake and ROS generation.Incresed 2-DOG uptake caused by CdCl2 and ROS production were significantly inhibited by the treatment of N-acetylcystein(NAC).2-DOG uptake was also inhibited by BSO,a potent r-GCS inhibitor.In addition, celluar GSH levels were modulated by the treatment of NAC and BSO ,but GSH/GSSG ratio remained unchanged at up to 25 uM CdCl2.The results suggest that CdCl2 stimilated glucose uptake is mainly caused by the activation of pentose phosphate pathway,which is an important antioxidant defense mechanism in the adipocytes.

Key words: Glucose uptake, CdCl2, Pentose phosphate pathway