Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2002-1-17
pubmed:abstractText
Exercise training improves skeletal muscle insulin sensitivity in the obese Zucker rat. The purpose of this study was to investigate whether the improvement in insulin action in response to exercise training is associated with enhanced insulin receptor signaling. Obese Zucker rats were trained for 7 wk and studied by using the hindlimb-perfusion technique 24 h, 96 h, or 7 days after their last exercise training bout. Insulin-stimulated glucose uptake (traced with 2-deoxyglucose) was significantly reduced in untrained obese Zucker rats compared with lean controls (2.2 +/- 0.17 vs. 5.4 +/- 0.46 micromol x g(-1) x h(-1)). Glucose uptake was normalized 24 h after the last exercise bout (4.9 +/- 0.41 micromol x g(-1) x h(-1)) and remained significantly elevated above the untrained obese Zucker rats for 7 days. However, exercise training did not increase insulin receptor or insulin receptor substrate-1 (IRS-1) tyrosine phosphorylation, phosphatidylinositol 3-kinase (PI3-kinase) activity associated with IRS-1 or tyrosine phosphorylated immunoprecipitates, or Akt serine phosphorylation. These results are consistent with the hypothesis that, in obese Zucker rats, adaptations occur during training that lead to improved insulin-stimulated muscle glucose uptake without affecting insulin receptor signaling through the PI3-kinase pathway.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/Akt1 protein, rat, http://linkedlifedata.com/resource/pubmed/chemical/Deoxyglucose, http://linkedlifedata.com/resource/pubmed/chemical/Glucose Transporter Type 4, http://linkedlifedata.com/resource/pubmed/chemical/Insulin Receptor Substrate Proteins, http://linkedlifedata.com/resource/pubmed/chemical/Irs1 protein, rat, http://linkedlifedata.com/resource/pubmed/chemical/Monosaccharide Transport Proteins, http://linkedlifedata.com/resource/pubmed/chemical/Muscle Proteins, http://linkedlifedata.com/resource/pubmed/chemical/Phosphatidylinositol 3-Kinases, http://linkedlifedata.com/resource/pubmed/chemical/Phosphoproteins, http://linkedlifedata.com/resource/pubmed/chemical/Protein-Serine-Threonine Kinases, http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins, http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins c-akt, http://linkedlifedata.com/resource/pubmed/chemical/Receptor, Insulin, http://linkedlifedata.com/resource/pubmed/chemical/Slc2a4 protein, rat
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
8750-7587
pubmed:author
pubmed:issnType
Print
pubmed:volume
92
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
736-44
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed-meshheading:11796688-Animals, pubmed-meshheading:11796688-Deoxyglucose, pubmed-meshheading:11796688-Glucose Transporter Type 4, pubmed-meshheading:11796688-Insulin Receptor Substrate Proteins, pubmed-meshheading:11796688-Insulin Resistance, pubmed-meshheading:11796688-Monosaccharide Transport Proteins, pubmed-meshheading:11796688-Muscle, Skeletal, pubmed-meshheading:11796688-Muscle Proteins, pubmed-meshheading:11796688-Obesity, pubmed-meshheading:11796688-Phosphatidylinositol 3-Kinases, pubmed-meshheading:11796688-Phosphoproteins, pubmed-meshheading:11796688-Physical Conditioning, Animal, pubmed-meshheading:11796688-Protein-Serine-Threonine Kinases, pubmed-meshheading:11796688-Proto-Oncogene Proteins, pubmed-meshheading:11796688-Proto-Oncogene Proteins c-akt, pubmed-meshheading:11796688-Rats, pubmed-meshheading:11796688-Rats, Zucker, pubmed-meshheading:11796688-Receptor, Insulin, pubmed-meshheading:11796688-Signal Transduction
pubmed:year
2002
pubmed:articleTitle
Exercise training improves muscle insulin resistance but not insulin receptor signaling in obese Zucker rats.
pubmed:affiliation
Department of Physiology, University of Texas Health Sciences Center, San Antonio, Texas 78712, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't