TYPE 2 DIABETES: WHAT IS THE ROLE OF INSULIN IN NF-KAPPAB, PPARϒ AND CD36 EXPRESSION?

Authors

  • Eduardo Carvalho Lira Universidade Federal de Pernambuco
  • Cristina de Oliveira Silva Universidade Federal de Pernambuco.
  • René Duarte Martins Universidade Federal de Pernambuco

DOI:

https://doi.org/10.14450/2318-9312.v26.e3.a2014.pp172-178

Keywords:

Type 2 Diabetes, advanced glycation end products, oxidative stress.

Abstract

In both type II diabetes and insulin-resistance syndromes, vascular complications result from a set of atherogenic processes, involving chronic hyperglycemia, excessive protein glycation (AGEs), nuclear factor kappa-B (NF-kappaB) activation associated with inflammatory cytokines superexpression, oxidative stress altering LDL and scavenger receptor CD36 expression. The contribution of hyperinsulinaemia in this sequence is not completely elucidated. This review adresses the modulation of NF-kappaB, PPAR gamma (PPARγ) and CD36 protein expression by insulin in rat aortic vascular smooth muscle cells (VSMCs) stimulated by AGEs.

Author Biographies

Eduardo Carvalho Lira, Universidade Federal de Pernambuco

Departamento de Fisiologia e Farmacologia

Área: Fisiologia do metabolismo intermediário

Cristina de Oliveira Silva, Universidade Federal de Pernambuco.

Departamento de Fisiologia e Farmacologia

Área: Núcleo de Nutrição/UFPE- Centro Acadêmico de Vitória, Farmacologia

René Duarte Martins, Universidade Federal de Pernambuco

Núcleo de saúde pública/UFPE - Campus de Vitória de Santo Antão

Área: Farmacologia

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Published

2014-09-17

How to Cite

Lira, E. C., Silva, C. de O., & Martins, R. D. (2014). TYPE 2 DIABETES: WHAT IS THE ROLE OF INSULIN IN NF-KAPPAB, PPARϒ AND CD36 EXPRESSION?. Infarma - Pharmaceutical Sciences, 26(3), 172–178. https://doi.org/10.14450/2318-9312.v26.e3.a2014.pp172-178

Issue

Vol. 26 No. 3 (2014)

Section

Review Article

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