Source:http://linkedlifedata.com/resource/pubmed/id/15877289
Switch to
| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
5
|
| pubmed:dateCreated |
2005-5-6
|
| pubmed:abstractText |
Obesity is associated with impaired insulin-stimulated glucose disposal in the skeletal muscle, but whether this is an intrinsic or acquired factor is unknown. In many patients with type 2 diabetes mellitus (T2D) and their nondiabetic relatives, who have a genetic predisposition for diabetes, insulin resistance is maintained in cultured muscle cells. To study the association of obesity with defects in insulin action, we investigated insulin stimulation of both insulin receptor (IR) autophosphorylation and subsequent glucose transport in primary skeletal muscle cell cultures obtained from both nonobese and obese nondiabetic subjects. In these 2 groups, there was no difference in the ability of insulin to induce autophosphorylation of the IR, phosphorylation of the downstream serine kinase Akt/PKB, or stimulation of glucose transport. Moreover, there were no major differences in cultured muscle cell content of either the IR, the IR antagonist PC-1, or GLUT 1 and GLUT 4. These data therefore indicate that the insulin resistance associated with obesity is not maintained in cultured muscle cells and suggest that this insulin resistance is an acquired feature of obesity.
|
| pubmed:grant | |
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/AKT1 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Glucose,
http://linkedlifedata.com/resource/pubmed/chemical/Insulin,
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
|
| pubmed:status |
MEDLINE
|
| pubmed:month |
May
|
| pubmed:issn |
0026-0495
|
| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:volume |
54
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
598-603
|
| pubmed:dateRevised |
2011-11-17
|
| pubmed:meshHeading |
pubmed-meshheading:15877289-Adult,
pubmed-meshheading:15877289-Biological Transport,
pubmed-meshheading:15877289-Case-Control Studies,
pubmed-meshheading:15877289-Cell Differentiation,
pubmed-meshheading:15877289-Cells, Cultured,
pubmed-meshheading:15877289-Glucose,
pubmed-meshheading:15877289-Humans,
pubmed-meshheading:15877289-Insulin,
pubmed-meshheading:15877289-Insulin Resistance,
pubmed-meshheading:15877289-Middle Aged,
pubmed-meshheading:15877289-Muscle, Skeletal,
pubmed-meshheading:15877289-Obesity,
pubmed-meshheading:15877289-Phosphorylation,
pubmed-meshheading:15877289-Protein-Serine-Threonine Kinases,
pubmed-meshheading:15877289-Proto-Oncogene Proteins,
pubmed-meshheading:15877289-Proto-Oncogene Proteins c-akt,
pubmed-meshheading:15877289-Receptor, Insulin,
pubmed-meshheading:15877289-Signal Transduction
|
| pubmed:year |
2005
|
| pubmed:articleTitle |
Analysis of insulin-stimulated insulin receptor activation and glucose transport in cultured skeletal muscle cells from obese subjects.
|
| pubmed:affiliation |
Division of Diabetes and Endocrine Research, Department of Medicine, Mount Zion Medical Center, University of California-San Francisco, Box 1616, San Francisco, CA 94143, USA.
|
| pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, N.I.H., Extramural
|