Linked Life Data

12376590

Source:http://linkedlifedata.com/resource/pubmed/id/12376590

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
10
pubmed:dateCreated
2002-10-11
pubmed:abstractText
In recent decades, there has been an increasing interest in the role of endogenous glucocorticoids such as cortisol in the pathogenesis of metabolic syndrome. Studies in humans have suggested a positive association between obesity, hypertension, and insulin resistance, with alleles at the glucocorticoid receptor (GR) gene. For instance, the BclI polymorphism within the intron upstream of GR exon 2 has been associated with cardiovascular risk factors such as visceral obesity, hypertension, insulin resistance, and elevated cortisol concentrations. However, the location of the BclI polymorphism is not known, and the variant has so far not been compared with the wild-type receptor for its ability to be activated by glucocorticoids. Although several other mutations in the GR gene have been postulated as being relevant to the progression to type 2 diabetes and cardiovascular diseases, conflicting results makes it difficult to determine exactly what effect these GR variations have on metabolic syndrome incidence and progression. Further studies focusing on the most compelling GR mutations might offer a better understanding of metabolic syndrome pathogenesis and progression, aiding in the development of more effective treatments for this condition.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
1071-7323
pubmed:author
pubmed:issnType
Print
pubmed:volume
10
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1078-86
pubmed:dateRevised
2005-11-16
pubmed:meshHeading
pubmed:year
2002
pubmed:articleTitle
The glucocorticoid receptor gene and its association to metabolic syndrome.
pubmed:affiliation
Department of Clinical Chemistry, Sahlgrenska University Hospital, Göteborg, Sweden. rolandrosmond@hotmail.com
pubmed:publicationType
Journal Article, Review