Excess insulin binding to insulin-like growth factor receptors: proposed mechanism for acanthosis nigricans.
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.
Cruz
P D
PD
Department of Dermatology, University of Texas Southwestern Medical Center, Dallas 75235.
Hud
J A
JA
D000052:Acanthosis Nigricans / Q000473:pathology* / Q000503:physiopathology; D006801:Humans; D007328:Insulin / Q000378:metabolism*; D007333:Insulin Resistance / Q000502:physiology; D011485:Protein Binding; D011956:Receptors, Cell Surface / Q000378:metabolism*; D017451:Receptors, Somatomedin
D007328:Insulin; D011956:Receptors, Cell Surface; D017451:Receptors, Somatomedin