Different molecular mechanisms are involved in the multihormonal control of glucose transport in FRTL5 rat thyroid cells

J Endocrinol Invest. 1994 May;17(5):323-7. doi: 10.1007/BF03348991.


We investigated the molecular mechanisms by which TSH, insulin and IGF-1 modulate the glucose transport system in FRTL5 cells. We found that TSH, insulin and IGF-1 increased the glucose transporter Glut-1 specific mRNA levels 6, 8 and 5 fold over control, respectively. The effect on Glut-1 mRNA was evident after 2 hours, followed by an increased Glut-1 protein expression in whole cells, as judged by western blot analysis, after 5 hours of stimulation with all the hormones studied. In contrast, plasma membrane Glut-1 increased (300-400% over control) after 2 hours of stimulation with TSH (10 mU/ml), dibutyryl-cAMP (1mM), IGF-1 (10 ng/ml) and insulin (10 nM). These data indicate that the glucose transport system is under multihormonal control in FRTL5 cells. Two different mechanisms are involved in TSH, IGF-1 and insulin stimulation of the glucose transport: a) neosynthesis of Glut-1 by activation of gene expression; b) recruitment of carriers from the intracellular pool to the plasma membrane.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cell Line
  • Glucose / metabolism*
  • Glucose Transporter Type 1
  • Insulin / pharmacology*
  • Insulin-Like Growth Factor I / pharmacology*
  • Monosaccharide Transport Proteins / biosynthesis
  • Monosaccharide Transport Proteins / genetics
  • RNA, Messenger / analysis
  • Rats
  • Thyroid Gland / metabolism*
  • Thyrotropin / pharmacology*


  • Glucose Transporter Type 1
  • Insulin
  • Monosaccharide Transport Proteins
  • RNA, Messenger
  • Slc2a1 protein, rat
  • Insulin-Like Growth Factor I
  • Thyrotropin
  • Glucose