| pubmed-article:15145709 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:15145709 | lifeskim:mentions | umls-concept:C0020663 | lld:lifeskim |
| pubmed-article:15145709 | lifeskim:mentions | umls-concept:C0001480 | lld:lifeskim |
| pubmed-article:15145709 | lifeskim:mentions | umls-concept:C1326961 | lld:lifeskim |
| pubmed-article:15145709 | lifeskim:mentions | umls-concept:C1709059 | lld:lifeskim |
| pubmed-article:15145709 | lifeskim:mentions | umls-concept:C0439799 | lld:lifeskim |
| pubmed-article:15145709 | lifeskim:mentions | umls-concept:C0332120 | lld:lifeskim |
| pubmed-article:15145709 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:15145709 | pubmed:dateCreated | 2004-5-17 | lld:pubmed |
| pubmed-article:15145709 | pubmed:abstractText | Several lines of evidence support the hypothesis that ATP-sensitive K+ channels (K+(ATP)) participate in the brain's regulation of peripheral glucose homeostasis. In testing this hypothesis we conducted a series of in vivo experiments using albino rats and bilateral intrahypothalamic injections of K+(ATP) channel blockers, glibenclamide and repaglinide. The results show that 0.2 and 2.0 nM injections of glibenclamide lowered blood glucose in a dose-dependent manner. During mild insulin-induced hypoglycemia, hypothalamic glibenclamide delayed recovery to normoglycemia. The impaired recovery was associated with a reduction in plasma norepinephrine (P<0.001), though circulating epinephrine and glucagon were not reduced. In a separate experiment, 2-deoxy-D-glucose (200 mg/kg) was intraperitoneally administered to produce neuroglucopenia. Hypothalamic injections of either glibenclamide or repaglinide significantly blunted compensatory hyperglycemic responses (P<0.01). In a feeding study, 2.0, but not 0.2 nM of hypothalamic glibenclamide, reduced chow intake over a 2-h period (P<0.01). The results support the hypothesis that hypothalamic K+(ATP) channels participate in central glucose-sensing and glucose regulation. | lld:pubmed |
| pubmed-article:15145709 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15145709 | pubmed:language | eng | lld:pubmed |
| pubmed-article:15145709 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15145709 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:15145709 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15145709 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15145709 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15145709 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15145709 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15145709 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15145709 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15145709 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15145709 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15145709 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15145709 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15145709 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:15145709 | pubmed:month | May | lld:pubmed |
| pubmed-article:15145709 | pubmed:issn | 0014-2999 | lld:pubmed |
| pubmed-article:15145709 | pubmed:author | pubmed-author:ZhouJunJ | lld:pubmed |
| pubmed-article:15145709 | pubmed:author | pubmed-author:ZhangYangY | lld:pubmed |
| pubmed-article:15145709 | pubmed:author | pubmed-author:CorllConnieC | lld:pubmed |
| pubmed-article:15145709 | pubmed:author | pubmed-author:MartinRoy JRJ | lld:pubmed |
| pubmed-article:15145709 | pubmed:author | pubmed-author:RoaneDavid... | lld:pubmed |
| pubmed-article:15145709 | pubmed:author | pubmed-author:PorterJohnnie... | lld:pubmed |
| pubmed-article:15145709 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:15145709 | pubmed:day | 10 | lld:pubmed |
| pubmed-article:15145709 | pubmed:volume | 492 | lld:pubmed |
| pubmed-article:15145709 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:15145709 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:15145709 | pubmed:pagination | 71-9 | lld:pubmed |
| pubmed-article:15145709 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
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| pubmed-article:15145709 | pubmed:meshHeading | pubmed-meshheading:15145709... | lld:pubmed |
| pubmed-article:15145709 | pubmed:meshHeading | pubmed-meshheading:15145709... | lld:pubmed |
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| pubmed-article:15145709 | pubmed:meshHeading | pubmed-meshheading:15145709... | lld:pubmed |
| pubmed-article:15145709 | pubmed:year | 2004 | lld:pubmed |
| pubmed-article:15145709 | pubmed:articleTitle | Evidence for hypothalamic K+(ATP) channels in the modulation of glucose homeostasis. | lld:pubmed |
| pubmed-article:15145709 | pubmed:affiliation | Department of Basic Pharmaceutical Sciences, University of Louisiana at Monroe, Monroe, LA 71209, USA. | lld:pubmed |
| pubmed-article:15145709 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:15145709 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:15145709 | pubmed:publicationType | Research Support, U.S. Gov't, Non-P.H.S. | lld:pubmed |
| pubmed-article:15145709 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
