REGULATION OF GLUCOSE-TRANSPORT IN CLONE-9 CELLS BY THYROID-HORMONE
REGULATION OF GLUCOSE-TRANSPORT IN CLONE-9 CELLS BY THYROID-HORMONE
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DOI：
10.1016/0167-4889(91)90090-k
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发表时间：
1991-09-24
期刊：
影响因子：
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通讯作者：
LOEB, JN
中科院分区：
文献类型：
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作者：
KURUVILLA, AK;PEREZ, C;LOEB, JN
Triiodothyronine (T3) is found to stimulate cytochalasin B-inhibitable glucose transport in Clone 9 cells, a 'non-transformed' rat liver cell line. After an initial lag period of more than 3 h, glucose transport rate is significantly increased at 6 h and reaches more than 3-times the control rate at 24 h. The enhancement of glucose transport by T3 is due to an increase in transport V(max) and occurs in the absence of a change in either the K(m) for glucose transport (approximately 3 mM) or the K(i) for inhibition of transport by cytochalasin B ((1-2) . 10(-7) M). Consistent with the observed K(i) for cytochalasin B, Northern blot analysis of RNA from control and T3-treated cells employing cDNA probes encoding GTs of the human erythrocyte / rat brain / HepG2 cell transporter (GLUT-1), rat muscle / fat cell transporter (GLUT-4), and rat liver transporter (GLUT-2) types indicates expression of only the GLUT-1 mRNA isoform in these cells. The abundance of GLUT-1 mRNA increases approx. 1.9-fold after 24 h of T3 treatment and is accompanied by an approx. 1.3-fold increase in the abundance of GLUT-1 in whole-cell extracts as demonstrated by Western blot analysis employing a polyclonal antibody directed against the 13 amino acid C-terminal peptide of GLUT-1. The more than 3-fold stimulation of glucose transport at 24 h substantially exceeds the fractional increment in transporter abundance suggesting that, in addition to increasing total GLUT-1 abundance, exposure to T3 may result in a translocation of transporters to the plasma membrane or an activation of pre-existing membrane transporter sites.
