| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
Departamento de Clínica Médica, Faculdade de Ciências Médicas, Universidade Estadual de Campinas, Campinas, São Paulo 13081-970, Brazil
Address all correspondence and requests for reprints to: Mario J. A. Saad, M.D., Departamento de Clínica Médica, Faculdade de Ciências Médicas, Universidade Estadual de Campinas, Cidade Universitária Zeferino Vaz, Campinas, São Paulo 13081-970, Brazil. E-mail: msaad{at}fcm.unicamp.br.
Insulin and angiotensin II (AngII) may act through overlapping intracellular pathways to promote cardiac myocyte growth. In this report insulin and AngII signaling, through the phosphatidylinositol 3-kinase (PI 3-kinase) and MAPK pathways, were compared in cardiac tissues of control and obese Zucker rats. AngII induced Janus kinase 2 tyrosine phosphorylation and coimmunoprecipitation with insulin receptor substrate 1 (IRS-1) and IRS-2 as well as an increase in tyrosine phosphorylation of IRS and its association with growth factor receptor-binding protein 2. Simultaneous treatment with both hormones led to marked increases in the associations of IRS-1 and -2 with growth factor receptor-binding protein 2 and in the dual phosphorylation of ERK1/2 compared with the administration of AngII or insulin alone. In contrast, an acute inhibition of both basal and insulin-stimulated PI 3-kinase activity was induced by both hormones. Insulin stimulated the phosphorylation of MAPK equally in lean and obese rats. Conversely, insulin-induced phosphorylation of Akt in heart was decreased in obese rats. Pretreatment with losartan did not change insulin-induced activation of ERK1/2 and attenuated the reduction of Akt phosphorylation in the heart of obese rats. Thus, the imbalance between PI 3-kinase-Akt and MAPK signaling pathways in the heart may play a role in the development of cardiovascular abnormalities observed in insulin-resistant states, such as in obese Zucker rats.
This article has been cited by other articles:
 |
|
 |
|
  I. Tabbi-Anneni, J. Buchanan, R. C. Cooksey, and E. D. Abel Captopril Normalizes Insulin Signaling and Insulin-Regulated Substrate Metabolism in Obese (ob/ob) Mouse Hearts Endocrinology, August 1, 2008; 149(8): 4043 - 4050. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. F. Giani, M. M. Gironacci, M. C. Munoz, C. Pena, D. Turyn, and F. P. Dominici Angiotensin-(1 7) stimulates the phosphorylation of JAK2, IRS-1 and Akt in rat heart in vivo: role of the AT1 and Mas receptors Am J Physiol Heart Circ Physiol, August 1, 2007; 293(2): H1154 - H1163. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A.-M. Samuelsson, E. Bollano, R. Mobini, B.-M. Larsson, E. Omerovic, M. Fu, F. Waagstein, and A. Holmang Hyperinsulinemia: effect on cardiac mass/function, angiotensin II receptor expression, and insulin signaling pathways Am J Physiol Heart Circ Physiol, August 1, 2006; 291(2): H787 - H796. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Z. He, D. M. Opland, K. J. Way, K. Ueki, N. Bodyak, P. M. Kang, S. Izumo, R. N. Kulkarni, B. Wang, R. Liao, et al. Regulation of Vascular Endothelial Growth Factor Expression and Vascularization in the Myocardium by Insulin Receptor and PI3K/Akt Pathways in Insulin Resistance and Ischemia Arterioscler Thromb Vasc Biol, April 1, 2006; 26(4): 787 - 793. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
V. C. Calegari, M. Alves, P. K. Picardi, R. Y. Inoue, K. G. Franchini, M. J. A. Saad, and L. A. Velloso Suppressor of Cytokine Signaling-3 Provides a Novel Interface in the Cross-Talk between Angiotensin II and Insulin Signaling Systems Endocrinology, February 1, 2005; 146(2): 579 - 588. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Endocrinology | Endocrine Reviews | J. Clin. End. & Metab. |
| Molecular Endocrinology | Recent Prog. Horm. Res. | All Endocrine Journals |
