Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4 Pt 1
pubmed:dateCreated
1991-11-18
pubmed:abstractText
Adrenalectomy prevents development of obesity in genetically obese (ob/ob) mice. Replacement studies have shown that these mice exhibit hypersensitivity to corticosterone. This study was conducted to determine if this increased sensitivity was associated with alterations in corticoid receptor number or binding affinity. Cytosolic glucocorticoid receptor numbers were lower by 26% in liver, 23% in brain, and 26% in brown adipose tissue of 8-wk-old male ob/ob mice when compared with lean mice. Cytosolic glucocorticoid receptor numbers were similar in liver and brain of 4-wk-old lean and ob/ob mice is likely secondary to elevated plasma corticosterone concentrations in these older mice. Adrenalectomy increased cytosolic glucocorticoid receptor numbers in liver and brain of 8-wk-old ob/ob mice to values comparable to those in lean mice. Injection of dexamethasone (0.5 or 5 micrograms/g body wt) equally lowered cytosolic glucocorticoid receptor numbers in liver and brain of adrenalectomized ob/ob and lean mice. Brain mineralocorticoid receptor numbers and response to dexamethasone were similar in ob/ob and lean mice. These results suggest that the site responsible for increased sensitivity of ob/ob mice to corticosterone is postreceptor binding.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0002-9513
pubmed:author
pubmed:issnType
Print
pubmed:volume
261
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
E495-9
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1991
pubmed:articleTitle
Glucocorticoid and mineralocorticoid receptor-binding characteristics in obese (ob/ob) mice.
pubmed:affiliation
Department of Food Science and Human Nutrition, Michigan State University, East Lansing 48824-1224.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't