| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Submitted on May 9, 2003
Accepted on September 24, 2003
1 Departamento de Clínica Médica, Faculdade de Ciências Médicas, Universidade Estadual de Campinas, 13081-970, Campinas, SP, Brazil.
* To whom correspondence should be addressed. E-mail: msaad{at}fcm.unicamp.br.
The PI(3)K-independent pathway to induce glucose transport may involve the tyrosine phosphorylation of the proto-oncogene c-Cbl. In the present study, we examined whether acute exposure to insulin stimulates the tyrosine phosphorylation of Cbl and its association with CAP in muscle and adipose tissue of rats in vivo. We report, herein, that insulin induces Cbl tyrosine phosphorylation and association with CAP in adipose tissue, but not in muscle. We also examined the expression and tyrosyl-phosphorylation state of Cbl and CAP/Cbl association in adipose tissue of rats submitted to prolonged fasting, and in monosodium glutamate (MSG)-insulin resistant rats. An increase in Cbl phosphorylation is observed in the fat of MSG rats, parallel with an increase in association of CAP-Cbl, as well as an augment in CAP and Cbl protein expression in the adipose tissue of these animals. These events are accompanied by a decrease in insulin-stimulated IR/IRS-1 tyrosine phosphorylation and by an increase in the IRS-2/PI (3)K/Akt/Foxo1 pathway. In adipocytes of fasted rats there is a decrease in CAP and Cbl protein expression, in insulin-induced Cbl phosphorylation and in the association with CAP. In parallel, there is also a decrease in the IR/IRSs/Akt/Foxo1 pathway. Thus, insulin is able to induce Cbl tyrosine phosphorylation and its association with CAP in the adipose tissue of normal rats. In addition, our data provide evidence that the CAP-Cbl pathway may have a role in the modulation of adiposity in fasting and in MSG-treated rats.
This article has been cited by other articles:
 |
|
 |
|
  D. M.L. Tsukumo, M. A. Carvalho-Filho, J. B.C. Carvalheira, P. O. Prada, S. M. Hirabara, A. A. Schenka, E. P. Araujo, J. Vassallo, R. Curi, L. A. Velloso, et al. Loss-of-Function Mutation in Toll-Like Receptor 4 Prevents Diet-Induced Obesity and Insulin Resistance Diabetes, August 1, 2007; 56(8): 1986 - 1998. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 F. S. L. Thong, C. B. Dugani, and A. Klip Turning Signals On and Off: GLUT4 Traffic in the Insulin-Signaling Highway Physiology, August 1, 2005; 20(4): 271 - 284. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 E. P. Araujo, C. T. De Souza, A. L. Gasparetti, M. Ueno, A. C. Boschero, M. J. A. Saad, and L. A. Velloso Short-Term in Vivo Inhibition of Insulin Receptor Substrate-1 Expression Leads to Insulin Resistance, Hyperinsulinemia, and Increased Adiposity Endocrinology, March 1, 2005; 146(3): 1428 - 1437. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. T. Brozinick Jr., E. D. Hawkins, A. B. Strawbridge, and J. S. Elmendorf Disruption of Cortical Actin in Skeletal Muscle Demonstrates an Essential Role of the Cytoskeleton in Glucose Transporter 4 Translocation in Insulin-sensitive Tissues J. Biol. Chem., September 24, 2004; 279(39): 40699 - 40706. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. Mitra, X. Zheng, and M. P. Czech RNAi-based Analysis of CAP, Cbl, and CrkII Function in the Regulation of GLUT4 by Insulin J. Biol. Chem., September 3, 2004; 279(36): 37431 - 37435. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 L. JeBailey, A. Rudich, X. Huang, C. D. Ciano-Oliveira, A. Kapus, and A. Klip Skeletal Muscle Cells and Adipocytes Differ in Their Reliance on TC10 and Rac for Insulin-Induced Actin Remodeling Mol. Endocrinol., February 1, 2004; 18(2): 359 - 372. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| Endocrinology | Endocrine Reviews | J. Clin. End. & Metab. |
| Molecular Endocrinology | Recent Prog. Horm. Res. | All Endocrine Journals |
