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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
6 Suppl
|
pubmed:dateCreated |
1992-6-25
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pubmed:abstractText |
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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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
|
pubmed:month |
Jun
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pubmed:issn |
0022-202X
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pubmed:author | |
pubmed:issnType |
Print
|
pubmed:volume |
98
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pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
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pubmed:pagination |
82S-85S
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pubmed:dateRevised |
2011-11-17
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pubmed:meshHeading |
pubmed-meshheading:1316928-Acanthosis Nigricans,
pubmed-meshheading:1316928-Humans,
pubmed-meshheading:1316928-Insulin,
pubmed-meshheading:1316928-Insulin Resistance,
pubmed-meshheading:1316928-Protein Binding,
pubmed-meshheading:1316928-Receptors, Cell Surface,
pubmed-meshheading:1316928-Receptors, Somatomedin
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pubmed:year |
1992
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pubmed:articleTitle |
Excess insulin binding to insulin-like growth factor receptors: proposed mechanism for acanthosis nigricans.
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pubmed:affiliation |
Department of Dermatology, University of Texas Southwestern Medical Center, Dallas 75235.
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pubmed:publicationType |
Journal Article,
Review
|