Linked Life Data

20855892

Source:http://linkedlifedata.com/resource/pubmed/id/20855892

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
48
pubmed:dateCreated
2010-11-24
pubmed:abstractText
AMP-activated protein kinase (AMPK) ? subunits (?1 and ?2) provide scaffolds for binding ? and ? subunits and contain a carbohydrate-binding module important for regulating enzyme activity. We generated C57Bl/6 mice with germline deletion of AMPK ?2 (?2 KO) and examined AMPK expression and activity, exercise capacity, metabolic control during muscle contractions, aminoimidazole carboxamide ribonucleotide (AICAR) sensitivity, and susceptibility to obesity-induced insulin resistance. We find that ?2 KO mice are viable and breed normally. ?2 KO mice had a reduction in skeletal muscle AMPK ?1 and ?2 expression despite up-regulation of the ?1 isoform. Heart AMPK ?2 expression was also reduced but this did not affect resting AMPK ?1 or ?2 activities. AMPK ?1 and ?2 activities were not changed in liver, fat, or hypothalamus. AICAR-stimulated glucose uptake but not fatty acid oxidation was impaired in ?2 KO mice. During treadmill running ?2 KO mice had reduced maximal and endurance exercise capacity, which was associated with lower muscle and heart AMPK activity and reduced levels of muscle and liver glycogen. Reductions in exercise capacity of ?2 KO mice were not due to lower muscle mitochondrial content or defects in contraction-stimulated glucose uptake or fatty acid oxidation. When challenged with a high-fat diet ?2 KO mice gained more weight and were more susceptible to the development of hyperinsulinemia and glucose intolerance. In summary these data show that deletion of AMPK ?2 reduces AMPK activity in skeletal muscle resulting in impaired exercise capacity and the worsening of diet-induced obesity and glucose intolerance.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
1083-351X
pubmed:author
pubmed:issnType
Electronic
pubmed:day
26
pubmed:volume
285
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
37198-209
pubmed:dateRevised
2011-7-22
pubmed:meshHeading
pubmed:year
2010
pubmed:articleTitle
Whole body deletion of AMP-activated protein kinase {beta}2 reduces muscle AMPK activity and exercise capacity.
pubmed:affiliation
Department of Medicine, McMaster University, Hamilton, Ontario L8N 3Z5, Canada.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't