Excess insulin binding to insulin-like growth factor receptors: proposed mechanism for acanthosis nigricans

J Invest Dermatol. 1992 Jun;98(6 Suppl):82S-85S. doi: 10.1111/1523-1747.ep12462293.

Abstract

Clinical and epidemiologic evidence has shown acanthosis nigricans to be closely related to defective tissue utilization of insulin in a number of previously recognized (e.g., obesity, lipodystrophy, and leprechaunism) as well as recently characterized (e.g., type A and type B syndromes) disorders. This article reviews the relationship of acanthosis nigricans to these insulin-resistant states. It also focuses attention on the possibility that interaction between excessive amounts of circulating insulin with insulin-like growth factor receptors on keratinocytes and dermal fibroblasts leads to the development of acanthosis nigricans.

Publication types

  • Review

MeSH terms

  • Acanthosis Nigricans / pathology*
  • Acanthosis Nigricans / physiopathology
  • Humans
  • Insulin / metabolism*
  • Insulin Resistance / physiology
  • Protein Binding
  • Receptors, Cell Surface / metabolism*
  • Receptors, Somatomedin

Substances

  • Insulin
  • Receptors, Cell Surface
  • Receptors, Somatomedin