Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
9
pubmed:dateCreated
2009-10-20
pubmed:abstractText
The most prevalent phenotypes of polycystic ovary syndrome (PCOS) are characterized by insulin resistance and androgen excess. The adipose tissue (AT) expandability hypothesis explains the development of insulin resistance in obesity and in cases of AT deficit. In line with this hypothesis, we propose that hyperinsulinemic androgen excess in PCOS is often underpinned by exhaustion of the capacity to expand subcutaneous AT in a metabolically safe way. Such exhaustion might occur when a positive energy imbalance meets a normal fat-storage capacity and/or when a normal energy balance faces a low fat storage capacity. This concept thus explains how PCOS phenotypes might result from obesity, prenatal growth restraint or a genetic lipodystrophy, or, experimentally, from prenatal androgen excess.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
1879-3061
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
20
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
418-23
pubmed:meshHeading
pubmed:year
2009
pubmed:articleTitle
Adipose tissue expandability and the early origins of PCOS.
pubmed:affiliation
Department of Woman & Child, University of Leuven, Belgium. Francis.deZegher@uzleuven.be
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't