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Angiotensin II-induced insulin resistance and protein tyrosine phosphatases

Mario B Marrero1, David Fulton, David Stepp

  • 1Vascular Biology Center, Medical College of Georgia, 1459 Laney Walker Boulevard, Augusta, Georgia 30912-2500, USA. mmarrero@mail.mcg.edu

Arteriosclerosis, Thrombosis, and Vascular Biology
|July 24, 2004
PubMed

Insights

Protein tyrosine phosphatases (PTPases) are crucial in cell signaling. This review explores how PTP-1B may cause insulin resistance by deactivating the insulin receptor, contributing to diabetic complications.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Endocrinology

Background:

  • Protein tyrosine phosphorylation is vital for mitogenic signaling.
  • Protein tyrosine phosphatases (PTPases) also play a critical role in cellular signaling.
  • Angiotensin II (Ang II) and insulin trigger both phosphorylation and dephosphorylation events.

Purpose of the Study:

  • To review the hypothesis that PTP-1B mediates Ang II-induced insulin resistance.
  • To elucidate the role of PTP-1B in inhibiting insulin receptor activation.
  • To explore the link between PTP-1B, insulin resistance, and diabetic complications.

Main Methods:

  • Review of existing literature on PTPases, Ang II, and insulin signaling.
  • Analysis of signaling cascades downstream of Ang II and insulin receptors.
  • Hypothetical model of PTP-1B's role in insulin resistance.

Main Results:

  • Ang II and insulin induce complex signaling pathways involving both phosphorylation and dephosphorylation.
  • PTP-1B is hypothesized to be a key mediator of Ang II-induced insulin resistance.
  • PTP-1B activation may lead to insulin receptor dephosphorylation.

Conclusions:

  • PTP-1B activation by Ang II is a potential mechanism for insulin resistance.
  • This pathway may explain maladaptive responses in diabetic vascular and renal tissues.
  • Understanding this mechanism could offer insights into type II diabetes treatment.

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