Switch to
| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
2
|
| pubmed:dateCreated |
1992-7-7
|
| pubmed:abstractText |
The acute effects of 2-deoxy-D-glucose (2-DG)-induced glucoprivic feeding on the anorectic drug recognition site and Na+K(+)-ATPase in the brain were examined in adult rats and in lean and genetically obese mice. The marked hyperglycemia and the induction of feeding caused by the administration of 2-DG to satiated rats and lean mice were associated with significant increases in Na+K(+)-ATPase activity, and in [3H]ouabain binding and [3H]mazindol binding to the anorectic drug recognition site in hypothalamic membranes. Basal and 2-DG-stimulated levels of blood glucose were significantly correlated to the levels of hypothalamic [3H]ouabain (r = + .91, p less than 0.01) and [3H]mazindol (r = + .87, p less than 0.01) binding. A significant correlation (r = .74, p less than 0.05) was also observed between [3H]mazindol binding and [3H]ouabain binding supporting the hypothesis that these hypothalamic binding sites are functionally coupled in their response to circulating glucose. Following the intracerebroventricular (ICV) administration of the diabetogenic drug alloxan, 2-DG did not stimulate feeding or increase [3H]mazindol and [3H]ouabain binding sites in the hypothalamic paraventricular area. Since 2-DG still caused hyperglycemia in alloxan-treated rats, alloxan-induced inactivation of glucoreceptor mechanisms led to an uncoupling of the anorectic drug recognition site from a hypothalamic glucostat. In genetically obese mice (ob/ob), 2-DG also could not induce feeding or increase hypothalamic [3H]ouabain or [3H]mazindol binding, despite a significant hyperglycemic response. In contrast, 2-DG did increase feeding and the binding of [3H]ouabain and [3H]mazindol to the hypothalamus of lean littermates.(ABSTRACT TRUNCATED AT 250 WORDS)
|
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Alloxan,
http://linkedlifedata.com/resource/pubmed/chemical/Blood Glucose,
http://linkedlifedata.com/resource/pubmed/chemical/Deoxyglucose,
http://linkedlifedata.com/resource/pubmed/chemical/Glucose,
http://linkedlifedata.com/resource/pubmed/chemical/Mazindol,
http://linkedlifedata.com/resource/pubmed/chemical/Ouabain,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Cell Surface,
http://linkedlifedata.com/resource/pubmed/chemical/Sodium-Potassium-Exchanging ATPase,
http://linkedlifedata.com/resource/pubmed/chemical/glucose receptor
|
| pubmed:status |
MEDLINE
|
| pubmed:month |
Feb
|
| pubmed:issn |
0361-9230
|
| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:volume |
28
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
201-7
|
| pubmed:dateRevised |
2007-11-15
|
| pubmed:meshHeading |
pubmed-meshheading:1317740-Alloxan,
pubmed-meshheading:1317740-Animals,
pubmed-meshheading:1317740-Blood Glucose,
pubmed-meshheading:1317740-Cerebral Ventricles,
pubmed-meshheading:1317740-Deoxyglucose,
pubmed-meshheading:1317740-Feeding Behavior,
pubmed-meshheading:1317740-Glucose,
pubmed-meshheading:1317740-Hypothalamus,
pubmed-meshheading:1317740-Injections, Intraventricular,
pubmed-meshheading:1317740-Male,
pubmed-meshheading:1317740-Mazindol,
pubmed-meshheading:1317740-Mice,
pubmed-meshheading:1317740-Mice, Obese,
pubmed-meshheading:1317740-Obesity,
pubmed-meshheading:1317740-Organ Specificity,
pubmed-meshheading:1317740-Ouabain,
pubmed-meshheading:1317740-Rats,
pubmed-meshheading:1317740-Rats, Inbred Strains,
pubmed-meshheading:1317740-Receptors, Cell Surface,
pubmed-meshheading:1317740-Sodium-Potassium-Exchanging ATPase
|
| pubmed:year |
1992
|
| pubmed:articleTitle |
Regulation of the anorectic drug recognition site during glucoprivic feeding.
|
| pubmed:affiliation |
Clinical Neuroscience Branch, National Institute of Mental Health, NIH, Bethesda, MD 20985.
|
| pubmed:publicationType |
Journal Article,
Comparative Study
|