Effect of IGF-I on phosphatidylinositol 3-kinase in soleus muscle of lean and insulin-resistant obese mice

被引:14
作者
Jullien, D [1 ]
Heydrick, SJ [1 ]
Gautier, N [1 ]
VanObberghen, E [1 ]
LeMarchandBrustel, Y [1 ]
机构
[1] FAC MED NICE, INSERM, U145, F-06107 NICE 02, FRANCE
关键词
D O I
10.2337/diabetes.45.7.869
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Insulin and IGF-I induced a similar stimulation of glucose transport in isolated soleus muscle. These actions require phosphatidylinositol (PI) 3-kinase activation since the PI 3-kinase inhibitor, wortmannin, blocked the stimulation by both peptides. We compared IGF-I with insulin in the ability to activate PI 3-kinase in the isolated soleus muscle from lean and gold thioglucose-induced obese insulin-resistant mice. In muscles from lean mice, IGF-I and insulin were able to activate PI 3-kinase with a similar time course, the effects being maximal within 3-5 min of stimulation. However, the IGF-I concentrations required to obtain similar effects on PI 3-kinase were about 10 times higher than the corresponding insulin doses. To determine through which receptor IGF-I was activating PI 3-kinase, the ability of IGF-I to activate both its own receptor and insulin receptor was simultaneously measured. Whatever the dose used (100 or 500 nmol/l), IGF-I activated to a nearly similar extent both the tyrosine kinase activity of its own receptor and that of the insulin receptor, suggesting that IGF-I was not only activating its receptor but was also able to stimulate the insulin receptor kinase. In muscles of obese insulin-resistant mice, although the defect of PI 3-kinase activation in response to IGF-I was relatively less pronounced (45%) than in response to insulin (70%) when compared with lean mice, PI 3-kinase stimulation was still markedly altered in response to IGF-I.
引用
收藏
页码:869 / 875
页数:7
相关论文
共 37 条
[1]   PHOSPHORYLATION OF INSULIN-LIKE GROWTH FACTOR-I RECEPTOR BY INSULIN-RECEPTOR TYROSINE KINASE IN INTACT CULTURED SKELETAL-MUSCLE CELLS [J].
BEGUINOT, F ;
SMITH, RJ ;
KAHN, CR ;
MARON, R ;
MOSES, AC ;
WHITE, MF .
BIOCHEMISTRY, 1988, 27 (09) :3222-3228
[2]   A TIGHTLY ASSOCIATED SERINE THREONINE PROTEIN-KINASE REGULATES PHOSPHOINOSITIDE 3-KINASE ACTIVITY [J].
CARPENTER, CL ;
AUGER, KR ;
DUCKWORTH, BC ;
HOU, WM ;
SCHAFFHAUSEN, B ;
CANTLEY, LC .
MOLECULAR AND CELLULAR BIOLOGY, 1993, 13 (03) :1657-1665
[3]   PHOSPHATIDYLINOSITOL 3-KINASE ACTIVATION IS REQUIRED FOR INSULIN STIMULATION OF PP70 S6 KINASE, DNA-SYNTHESIS, AND GLUCOSE-TRANSPORTER TRANSLOCATION [J].
CHEATHAM, B ;
VLAHOS, CJ ;
CHEATHAM, L ;
WANG, L ;
BLENIS, J ;
KAHN, CR .
MOLECULAR AND CELLULAR BIOLOGY, 1994, 14 (07) :4902-4911
[4]   INSULIN ACTION AND THE INSULIN SIGNALING NETWORK [J].
CHEATHAM, B ;
KAHN, CR .
ENDOCRINE REVIEWS, 1995, 16 (02) :117-142
[5]   PI-3-KINASE IS A DUAL-SPECIFICITY ENZYME - AUTOREGULATION BY AN INTRINSIC PROTEIN-SERINE KINASE-ACTIVITY [J].
DHAND, R ;
HILES, I ;
PANAYOTOU, G ;
ROCHE, S ;
FRY, MJ ;
GOUT, I ;
TOTTY, NF ;
TRUONG, O ;
VICENDO, P ;
YONEZAWA, K ;
KASUGA, M ;
COURTNEIDGE, SA ;
WATERFIELD, MD .
EMBO JOURNAL, 1994, 13 (03) :522-533
[6]   IGF-I STIMULATED GLUCOSE-TRANSPORT IN HUMAN SKELETAL-MUSCLE AND IGF-I RESISTANCE IN OBESITY AND NIDDM [J].
DOHM, GL ;
ELTON, CW ;
RAJU, MS ;
MOONEY, ND ;
DIMARCHI, R ;
PORIES, WJ ;
FLICKINGER, EG ;
ATKINSON, SM ;
CARO, JF .
DIABETES, 1990, 39 (09) :1028-1032
[8]   RECOMBINANT HUMAN INSULIN-LIKE GROWTH-FACTOR-I - A THERAPEUTIC CHALLENGE FOR DIABETES-MELLITUS [J].
FROESCH, ER ;
HUSSAIN, M .
DIABETOLOGIA, 1994, 37 :S179-S185
[9]  
GIORGETTI S, 1993, J BIOL CHEM, V268, P7358
[10]   INSULIN-RECEPTOR PHOSPHORYLATION, INSULIN-RECEPTOR SUBSTRATE-1 PHOSPHORYLATION, AND PHOSPHATIDYLINOSITOL 3-KINASE ACTIVITY ARE DECREASED IN INTACT SKELETAL-MUSCLE STRIPS FROM OBESE SUBJECTS [J].
GOODYEAR, LJ ;
GIORGINO, F ;
SHERMAN, LA ;
CAREY, J ;
SMITH, RJ ;
DOHM, GL .
JOURNAL OF CLINICAL INVESTIGATION, 1995, 95 (05) :2195-2204