TY - JOUR
T1 - Excess insulin binding to insulin-like growth factor receptors
T2 - Proposed mechanism for acanthosis nigricans
AU - Cruz, Ponciano D
AU - Hud, Joseph A.
PY - 1992/6
Y1 - 1992/6
N2 - 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.
AB - 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.
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U2 - 10.1111/1523-1747.ep12462293
DO - 10.1111/1523-1747.ep12462293
M3 - Article
C2 - 1316928
AN - SCOPUS:0026520967
SN - 0022-202X
VL - 98
SP - S82-S85
JO - Journal of Investigative Dermatology
JF - Journal of Investigative Dermatology
IS - 6 SUPPL.
ER -