TY - JOUR
T1 - Thyroid hormone increases basal and insulin-stimulated glucose transport in skeletal muscle
T2 - The role of GLUT4 glucose transporter expression
AU - Weinstein, Steven P.
AU - O'Boyle, Elizabeth
AU - Haber, Richard S.
PY - 1994
Y1 - 1994
N2 - In skeletal muscle, the main site of insulin-mediated glucose disposal, the major muscle glucose transporter GLUT4 is induced by thyroid hormone. To test the hypothesis that thyroid hormone alters muscle glucose transport, we examined the effect of L-triiodothyronine (T3) on glucose transport and GLUT4 protein content in isolated rat skeletal muscles. Euthyroid rats were treated with or without T3 for 3 days, and [3H]2-deoxy-D-glucose (2-DG) uptake in soleus and extensor digitorum longus (EDL) muscles was measured under conditions in which transport was rate limiting for uptake in the absence or presence of 10 nmol/l insulin. In control animals, insulin stimulated 2-DG uptake sevenfold in soleus and fivefold in EDL. T3 treatment increased basal 2-DG uptake in soleus and EDL by 115 ± 29% and 136 ± 23%, respectively, and increased insulin-stimulated 2-DG uptake in soleus and EDL by 55 ± 9 and 42 ± 12%, respectively. Immunoblot analysis revealed that T3 treatment increased GLUT4 protein content in soleus by 43 ± 6% and in EDL by 56 ± 13%. These data demonstrate that thyroid hormone increases basal and insulin-stimulated glucose transport in skeletal muscle. The percentage increase in insulin-stimulated transport in T3-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 T3-treated muscle can be accounted for by the induction of GLUT4 protein. However, increased basal glucose transport in T3-treated muscle must reflect additional mechanisms, such as increased subcellular partitioning of GLUT4 to plasma membrane.
AB - In skeletal muscle, the main site of insulin-mediated glucose disposal, the major muscle glucose transporter GLUT4 is induced by thyroid hormone. To test the hypothesis that thyroid hormone alters muscle glucose transport, we examined the effect of L-triiodothyronine (T3) on glucose transport and GLUT4 protein content in isolated rat skeletal muscles. Euthyroid rats were treated with or without T3 for 3 days, and [3H]2-deoxy-D-glucose (2-DG) uptake in soleus and extensor digitorum longus (EDL) muscles was measured under conditions in which transport was rate limiting for uptake in the absence or presence of 10 nmol/l insulin. In control animals, insulin stimulated 2-DG uptake sevenfold in soleus and fivefold in EDL. T3 treatment increased basal 2-DG uptake in soleus and EDL by 115 ± 29% and 136 ± 23%, respectively, and increased insulin-stimulated 2-DG uptake in soleus and EDL by 55 ± 9 and 42 ± 12%, respectively. Immunoblot analysis revealed that T3 treatment increased GLUT4 protein content in soleus by 43 ± 6% and in EDL by 56 ± 13%. These data demonstrate that thyroid hormone increases basal and insulin-stimulated glucose transport in skeletal muscle. The percentage increase in insulin-stimulated transport in T3-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 T3-treated muscle can be accounted for by the induction of GLUT4 protein. However, increased basal glucose transport in T3-treated muscle must reflect additional mechanisms, such as increased subcellular partitioning of GLUT4 to plasma membrane.
UR - http://www.scopus.com/inward/record.url?scp=0028110438&partnerID=8YFLogxK
U2 - 10.2337/diab.43.10.1185
DO - 10.2337/diab.43.10.1185
M3 - Article
C2 - 7926286
AN - SCOPUS:0028110438
SN - 0012-1797
VL - 43
SP - 1185
EP - 1189
JO - Diabetes
JF - Diabetes
IS - 10
ER -