| pubmed-article:1317740 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:1317740 | lifeskim:mentions | umls-concept:C0013227 | lld:lifeskim |
| pubmed-article:1317740 | lifeskim:mentions | umls-concept:C0205145 | lld:lifeskim |
| pubmed-article:1317740 | lifeskim:mentions | umls-concept:C0524637 | lld:lifeskim |
| pubmed-article:1317740 | lifeskim:mentions | umls-concept:C0204695 | lld:lifeskim |
| pubmed-article:1317740 | lifeskim:mentions | umls-concept:C0851285 | lld:lifeskim |
| pubmed-article:1317740 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:1317740 | pubmed:dateCreated | 1992-7-7 | lld:pubmed |
| pubmed-article:1317740 | 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) | lld:pubmed |
| pubmed-article:1317740 | pubmed:language | eng | lld:pubmed |
| pubmed-article:1317740 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1317740 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:1317740 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1317740 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1317740 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1317740 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1317740 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1317740 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1317740 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1317740 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1317740 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1317740 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:1317740 | pubmed:month | Feb | lld:pubmed |
| pubmed-article:1317740 | pubmed:issn | 0361-9230 | lld:pubmed |
| pubmed-article:1317740 | pubmed:author | pubmed-author:PaulS MSM | lld:pubmed |
| pubmed-article:1317740 | pubmed:author | pubmed-author:AngelII | lld:pubmed |
| pubmed-article:1317740 | pubmed:author | pubmed-author:HaugerR LRL | lld:pubmed |
| pubmed-article:1317740 | pubmed:author | pubmed-author:GiblinB ABA | lld:pubmed |
| pubmed-article:1317740 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:1317740 | pubmed:volume | 28 | lld:pubmed |
| pubmed-article:1317740 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:1317740 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:1317740 | pubmed:pagination | 201-7 | lld:pubmed |
| pubmed-article:1317740 | pubmed:dateRevised | 2007-11-15 | lld:pubmed |
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| pubmed-article:1317740 | pubmed:meshHeading | pubmed-meshheading:1317740-... | lld:pubmed |
| pubmed-article:1317740 | pubmed:year | 1992 | lld:pubmed |
| pubmed-article:1317740 | pubmed:articleTitle | Regulation of the anorectic drug recognition site during glucoprivic feeding. | lld:pubmed |
| pubmed-article:1317740 | pubmed:affiliation | Clinical Neuroscience Branch, National Institute of Mental Health, NIH, Bethesda, MD 20985. | lld:pubmed |
| pubmed-article:1317740 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:1317740 | pubmed:publicationType | Comparative Study | lld:pubmed |
