| pubmed-article:18511848 | rdf:type | pubmed:Citation | lld:pubmed |
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| pubmed-article:18511848 | lifeskim:mentions | umls-concept:C0033634 | lld:lifeskim |
| pubmed-article:18511848 | lifeskim:mentions | umls-concept:C0017725 | lld:lifeskim |
| pubmed-article:18511848 | lifeskim:mentions | umls-concept:C0033268 | lld:lifeskim |
| pubmed-article:18511848 | lifeskim:mentions | umls-concept:C0851285 | lld:lifeskim |
| pubmed-article:18511848 | pubmed:issue | 8 | lld:pubmed |
| pubmed-article:18511848 | pubmed:dateCreated | 2008-7-29 | lld:pubmed |
| pubmed-article:18511848 | pubmed:abstractText | A selective rise in hypothalamic lipid metabolism and the subsequent activation of SUR1/Kir6.2 ATP-sensitive K(+) (K(ATP)) channels inhibit hepatic glucose production. The mechanisms that link the ability of hypothalamic lipid metabolism to the activation of K(ATP) channels remain unknown. | lld:pubmed |
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| pubmed-article:18511848 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:18511848 | pubmed:citationSubset | AIM | lld:pubmed |
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| pubmed-article:18511848 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:18511848 | pubmed:month | Aug | lld:pubmed |
| pubmed-article:18511848 | pubmed:issn | 1939-327X | lld:pubmed |
| pubmed-article:18511848 | pubmed:author | pubmed-author:RossettiLucia... | lld:pubmed |
| pubmed-article:18511848 | pubmed:author | pubmed-author:LightPeter... | lld:pubmed |
| pubmed-article:18511848 | pubmed:author | pubmed-author:SchwartzGary... | lld:pubmed |
| pubmed-article:18511848 | pubmed:author | pubmed-author:OnoHirakuH | lld:pubmed |
| pubmed-article:18511848 | pubmed:author | pubmed-author:LiXiaosongX | lld:pubmed |
| pubmed-article:18511848 | pubmed:author | pubmed-author:LamTony K TTK | lld:pubmed |
| pubmed-article:18511848 | pubmed:author | pubmed-author:MuseEvan DED | lld:pubmed |
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| pubmed-article:18511848 | pubmed:author | pubmed-author:WangPenny Y... | lld:pubmed |
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| pubmed-article:18511848 | pubmed:author | pubmed-author:LamCarol K... | lld:pubmed |
| pubmed-article:18511848 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:18511848 | pubmed:volume | 57 | lld:pubmed |
| pubmed-article:18511848 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:18511848 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:18511848 | pubmed:pagination | 2061-5 | lld:pubmed |
| pubmed-article:18511848 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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| pubmed-article:18511848 | pubmed:year | 2008 | lld:pubmed |
| pubmed-article:18511848 | pubmed:articleTitle | Hypothalamic protein kinase C regulates glucose production. | lld:pubmed |
| pubmed-article:18511848 | pubmed:affiliation | Departments of Molecular Pharmacology, Medicine, and Neuroscience, Albert Einstein College of Medicine, Bronx, New York, USA. | lld:pubmed |
| pubmed-article:18511848 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:18511848 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| pubmed-article:18511848 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
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