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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
3
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pubmed:dateCreated |
2011-3-1
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pubmed:abstractText |
AMP-activated protein kinase (AMPK) signaling acts as a sensor of nutrients and hormones in the hypothalamus, thereby regulating whole-body energy homeostasis. Deletion of Ampk?2 in pro-opiomelanocortin (POMC) neurons causes obesity and defective neuronal glucose sensing. LKB1, the Peutz-Jeghers syndrome gene product, and Ca(2+)-calmodulin-dependent protein kinase kinase ? (CaMKK?) are key upstream activators of AMPK. This study aimed to determine their role in POMC neurons upon energy and glucose homeostasis regulation.
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pubmed:grant |
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
AIM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Mar
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pubmed:issn |
1939-327X
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pubmed:author |
pubmed-author:Al-QassabHindH,
pubmed-author:AshfordMichael LML,
pubmed-author:AshworthAlanA,
pubmed-author:BatterhamRachel LRL,
pubmed-author:BegumGhazalaG,
pubmed-author:BurcelinRemyR,
pubmed-author:CaniPatrice DPD,
pubmed-author:CarlingDavidD,
pubmed-author:ClaretMarcM,
pubmed-author:ColomAndréA,
pubmed-author:EmmanuelJulian JJJ,
pubmed-author:GieseK PeterKP,
pubmed-author:HeslegraveAmandaA,
pubmed-author:KnaufClaudeC,
pubmed-author:MizunoKeikoK,
pubmed-author:MucketPhillipP,
pubmed-author:PetersMarcoM,
pubmed-author:PiipariKaisaK,
pubmed-author:SmithMark AMA,
pubmed-author:ValetPhilippeP,
pubmed-author:WhiteAnneA,
pubmed-author:WithersDominic JDJ,
pubmed-author:WoodsAngelaA
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pubmed:issnType |
Electronic
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pubmed:volume |
60
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
735-45
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pubmed:meshHeading |
pubmed-meshheading:21266325-Analysis of Variance,
pubmed-meshheading:21266325-Animals,
pubmed-meshheading:21266325-Area Under Curve,
pubmed-meshheading:21266325-Body Weight,
pubmed-meshheading:21266325-Cell Count,
pubmed-meshheading:21266325-Eating,
pubmed-meshheading:21266325-Electrophysiology,
pubmed-meshheading:21266325-Energy Metabolism,
pubmed-meshheading:21266325-Female,
pubmed-meshheading:21266325-Glucose,
pubmed-meshheading:21266325-Glucose Clamp Technique,
pubmed-meshheading:21266325-Homeostasis,
pubmed-meshheading:21266325-Hypothalamus,
pubmed-meshheading:21266325-Immunohistochemistry,
pubmed-meshheading:21266325-Insulin Resistance,
pubmed-meshheading:21266325-Male,
pubmed-meshheading:21266325-Mice,
pubmed-meshheading:21266325-Mice, Transgenic,
pubmed-meshheading:21266325-Neurons,
pubmed-meshheading:21266325-Pro-Opiomelanocortin,
pubmed-meshheading:21266325-Protein-Serine-Threonine Kinases,
pubmed-meshheading:21266325-Reverse Transcriptase Polymerase Chain Reaction,
pubmed-meshheading:21266325-Signal Transduction,
pubmed-meshheading:21266325-Statistics, Nonparametric
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pubmed:year |
2011
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pubmed:articleTitle |
Deletion of Lkb1 in pro-opiomelanocortin neurons impairs peripheral glucose homeostasis in mice.
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pubmed:affiliation |
Laboratory of Diabetes and Obesity, Endocrinology and Nutrition Unit, Institut d'Investigacions Biomèdiques August Pi i Sunyer, Hospital Clinic de Barcelona, Barcelona, Spain.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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