Insulin Action on Membrane Components: The Glucose Transporter and the Type II Insulinlike Growth Factor Receptor

1985 ◽  
pp. 433-449
Author(s):  
Yoshitomo Oka ◽  
Michael P. Czech
Keyword(s):  
Growth Factor ◽  
Insulin Action ◽  
Glucose Transporter ◽  
Growth Factor Receptor ◽  
Type Ii ◽  
Insulinlike Growth Factor ◽  
Membrane Components

Polar surface distribution of type II insulin-like growth factor receptor in rat hepatocytes

1990 ◽  
Vol 74 (1) ◽  
pp. 69-74 ◽  
Author(s):  
Silvia E. Jaeggi-Groisman ◽  
Susanne Keller ◽  
Brigitte Zimmerii ◽  
Peter J. Meier ◽  
E.Rudolf Froesch
Keyword(s):  
Growth Factor ◽  
Growth Factor Receptor ◽  
Rat Hepatocytes ◽  
Insulin Like Growth Factor ◽  
Type Ii ◽  
Surface Distribution ◽  
Polar Surface

Evidence for the phosphorylation of the type II insulin-like growth factor receptor in cultured cells

1985 ◽  
Vol 130 (2) ◽  
pp. 793-799 ◽  
Author(s):  
J.F. Haskell ◽  
S.P. Nissley ◽  
M.M. Rechler ◽  
N. Sasaki ◽  
L. Greenstein ◽  
...  
Keyword(s):  
Growth Factor ◽  
Cultured Cells ◽  
Growth Factor Receptor ◽  
Insulin Like Growth Factor ◽  
Type Ii

Insulin signal transduction in human skeletal muscle: identifying the defects in Type II diabetes

2005 ◽  
Vol 33 (2) ◽  
pp. 354-357 ◽  
Author(s):  
M. Björnholm ◽  
J.R. Zierath
Keyword(s):  
Skeletal Muscle ◽  
Type Ii Diabetes ◽  
Insulin Action ◽  
Glucose Transporter ◽  
Whole Body ◽  
Diabetic Patients ◽  
Type Ii ◽  
Peripheral Tissues ◽  
Glucose Homoeostasis ◽  
Insulin Receptor Signalling

Type II diabetes is characterized by defects in insulin action on peripheral tissues, such as skeletal muscle, adipose tissue and liver and pancreatic β-cell defects. Since the skeletal muscle accounts for approx. 75% of whole body insulin-stimulated glucose uptake, defects in this tissue play a major role in the impaired glucose homoeostasis in Type II diabetic patients. Thus identifying defective steps in this process may reveal attractive targets for drug development to combat insulin resistance and Type II diabetes. This review will describe the effects of insulin on glucose transport and other metabolic events in skeletal muscle that are mediated by intracellular signalling cascades. Evidence for impaired activation of the insulin receptor signalling cascade and defective glucose transporter 4 translocation in the skeletal muscle from Type II diabetic patients will be presented. Through the identification of the intracellular defects in insulin action that control glucose homoeostasis, a better understanding of the disease pathogenesis can be gained and strategies for intervention may be developed.

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