pubmed-article:9401961 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:9401961 | lifeskim:mentions | umls-concept:C0007600 | lld:lifeskim |
pubmed-article:9401961 | lifeskim:mentions | umls-concept:C0034721 | lld:lifeskim |
pubmed-article:9401961 | lifeskim:mentions | umls-concept:C0034693 | lld:lifeskim |
pubmed-article:9401961 | lifeskim:mentions | umls-concept:C0299583 | lld:lifeskim |
pubmed-article:9401961 | lifeskim:mentions | umls-concept:C0030281 | lld:lifeskim |
pubmed-article:9401961 | lifeskim:mentions | umls-concept:C1955862 | lld:lifeskim |
pubmed-article:9401961 | lifeskim:mentions | umls-concept:C1515877 | lld:lifeskim |
pubmed-article:9401961 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
pubmed-article:9401961 | pubmed:dateCreated | 1998-2-3 | lld:pubmed |
pubmed-article:9401961 | pubmed:abstractText | 1. Whole-cell current-clamp recordings demonstrate that leptin (0.3-10 nm) hyperpolarizes CRI-G1 insulin-secreting cells. This effect is slow on onset and is not reversed on washout of the leptin. 2. Voltage-clamp recordings indicate that leptin activates a potassium conductance in the presence of intracellular ATP (5 mm), but has not effect in its absence. Following activation of ATP-sensitive K+ (KATP) current by diazoxide (0.2 mm), addition of leptin did not alter cell membrane potential or potassium current further. 3. The leptin-induced hyperpolarization and increased potassium conductance are completely inhibited by the application of the sulphonylureas tolbutamide (100 microM) and glibenclamide (0.5 microM). 4. Cell-attached and inside-out single-channel recordings indicate that leptin activates tolbutamide-sensitive KATP channels in CRI-G1 insulin-secreting cells. | lld:pubmed |
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pubmed-article:9401961 | pubmed:language | eng | lld:pubmed |
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pubmed-article:9401961 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:9401961 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:9401961 | pubmed:month | Nov | lld:pubmed |
pubmed-article:9401961 | pubmed:issn | 0022-3751 | lld:pubmed |
pubmed-article:9401961 | pubmed:author | pubmed-author:HarveyJJ | lld:pubmed |
pubmed-article:9401961 | pubmed:author | pubmed-author:AshfordM LML | lld:pubmed |
pubmed-article:9401961 | pubmed:author | pubmed-author:SpanswickDD | lld:pubmed |
pubmed-article:9401961 | pubmed:author | pubmed-author:HertelR FRF | lld:pubmed |
pubmed-article:9401961 | pubmed:author | pubmed-author:McKennaFF | lld:pubmed |
pubmed-article:9401961 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:9401961 | pubmed:day | 1 | lld:pubmed |
pubmed-article:9401961 | pubmed:volume | 504 ( Pt 3) | lld:pubmed |
pubmed-article:9401961 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:9401961 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:9401961 | pubmed:pagination | 527-35 | lld:pubmed |
pubmed-article:9401961 | pubmed:dateRevised | 2011-11-17 | lld:pubmed |
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pubmed-article:9401961 | pubmed:year | 1997 | lld:pubmed |
pubmed-article:9401961 | pubmed:articleTitle | Leptin activates ATP-sensitive potassium channels in the rat insulin-secreting cell line, CRI-G1. | lld:pubmed |
pubmed-article:9401961 | pubmed:affiliation | Department of Biomedical Sciences, University of Aberdeen, UK. | lld:pubmed |
pubmed-article:9401961 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:9401961 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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