Regulating Insulin Signaling and Beta-Cell Function Through IRS Proteins

Can J Physiol Pharmacol. 2006 Jul;84(7):725-37. doi: 10.1139/y06-008.

Abstract

Diabetes mellitus is a complex disorder that arises from various causes, including dysregulated glucose sensing and impaired insulin secretion (maturity onset diabetes of youth, MODY), autoimmune-mediated beta-cell destruction (type 1), or insufficient compensation for peripheral insulin resistance (type 2). Type 2 diabetes is the most prevalent form that usually occurs at middle age; it afflicts more than 30 million people over the age of 65, but is appearing with greater frequency in children and adolescents. Dysregulated insulin signaling exacerbated by chronic hyperglycemia promotes a cohort of systemic disorders--including dyslipidemia, hypertension, cardiovascular disease, and female infertility. Understanding the molecular basis of insulin resistance can prevent these disorders and their inevitable progression to type 2 diabetes.

Publication types

  • Review

MeSH terms

  • Diabetes Mellitus / physiopathology
  • Humans
  • Hyperglycemia / physiopathology
  • Insulin / physiology*
  • Insulin Receptor Substrate Proteins
  • Insulin Resistance / physiology
  • Insulin-Secreting Cells / physiology*
  • Intracellular Signaling Peptides and Proteins / physiology*
  • Models, Biological
  • Phosphoproteins / physiology*
  • Signal Transduction / physiology*

Substances

  • IRS1 protein, human
  • IRS2 protein, human
  • Insulin
  • Insulin Receptor Substrate Proteins
  • Intracellular Signaling Peptides and Proteins
  • Phosphoproteins