Sp. Weinstein et al., THYROID-HORMONE INCREASES BASAL AND INSULIN-STIMULATED GLUCOSE-TRANSPORT IN SKELETAL-MUSCLE - THE ROLE OF GLUT4 GLUCOSE-TRANSPORTER EXPRESSION, Diabetes, 43(10), 1994, pp. 1185-1189
Citations number
35
Categorie Soggetti
Endocrynology & Metabolism","Medicine, General & Internal
In skeletal muscle, the main site of insulin-mediated glucose disposal
, the major muscle glucose transporter GLUT4 is induced by thyroid hor
mone. To test the hypothesis that thyroid hormone alters muscle glucos
e transport, we examined the effect of L-triiodothyronine (T-3) on glu
cose transport and GLUT4 protein content in isolated rat skeletal musc
les. Euthyroid rats were treated with or without T-3 for 3 days, and [
H-3]2-deoxy-D-glucose (2-DG) uptake in soleus and extensor digitorum l
ongus (EDL) muscles was measured under conditions in which transport w
as rate Limiting for uptake in the absence or presence of 10 nmol/l in
sulin. In control animals, insulin stimulated 2-DG uptake sevenfold in
soleus and fivefold in EDL. T-3 treatment increased basal 2-DG uptake
in soleus and EDL by 115 +/- 29% and 136 +/- 23%, respectively, and i
ncreased insulin-stimulated 2-DG uptake in soleus and EDL by 55 +/- 9
and 42 +/- 12%, respectively. Immunoblot analysis revealed that T-3 tr
eatment increased GLUT4 protein content in soleus by 43 +/- 6% and in
EDL by 56 +/- 13%. These data demonstrate that thyroid hormone increas
es basal and insulin-stimulated glucose transport in skeletal muscle.
The percentage increase in insulin-stimulated transport in T-3-treated
muscles is similar to the increase in GLUT4 protein content, whereas
the percentage change in basal transport greatly exceeds the change in
GLUT4, Thus, increased insulin-stimulated glucose transport in T-3-tr
eated muscle can be accounted for by the induction of GLUT4 protein. H
owever, increased basal glucose transport in T-3-treated muscle must r
eflect additional mechanisms, such as increased subcellular partitioni
ng of GLUT4 to plasma membrane.