Linked Life Data

15634339

Source:http://linkedlifedata.com/resource/pubmed/id/15634339

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2005-1-6
pubmed:abstractText
Insulin resistance is a cardinal feature of type 2 diabetes and also a consequence of trauma such as surgery. Directly after surgery and cell isolation, adipocytes were insulin resistant, but this was reversed after overnight incubation in 10% CO(2) at 37 degrees C. Tyrosine phosphorylation of the insulin receptor and insulin receptor substrate (IRS)1 was insulin sensitive, but protein kinase B (PKB) and downstream metabolic effects exhibited insulin resistance that was reversed by overnight incubation. MAP-kinases ERK1/2 and p38 were strongly phosphorylated after surgery, but was dephosphorylated during reversal of insulin resistance. Phosphorylation of MAP-kinase was not caused by collagenase treatment during cell isolation and was present also in tissue pieces that were not subjected to cell isolation procedures. The insulin resistance directly after surgery and cell isolation was different from insulin resistance of type 2 diabetes; adipocytes from patients with type 2 diabetes remained insulin resistant after overnight incubation. IRS1, PKB, and downstream metabolic effects, but not insulin-stimulated tyrosine phosphorylation of insulin receptor, exhibited insulin resistance. These findings suggest a new approach in the study of surgery-induced insulin resistance and indicate that human adipocytes should recover after surgical procedures for analysis of insulin signalling. Moreover, we pinpoint the signalling dysregulation in type 2 diabetes to be the insulin-stimulated phosphorylation of IRS1 in human adipocytes.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
1742-464X
pubmed:author
pubmed:issnType
Print
pubmed:volume
272
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
141-51
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:15634339-Adipocytes, pubmed-meshheading:15634339-Adult, pubmed-meshheading:15634339-Aged, pubmed-meshheading:15634339-Case-Control Studies, pubmed-meshheading:15634339-Diabetes Mellitus, Type 2, pubmed-meshheading:15634339-Female, pubmed-meshheading:15634339-Humans, pubmed-meshheading:15634339-Insulin Receptor Substrate Proteins, pubmed-meshheading:15634339-Insulin Resistance, pubmed-meshheading:15634339-Male, pubmed-meshheading:15634339-Middle Aged, pubmed-meshheading:15634339-Mitogen-Activated Protein Kinases, pubmed-meshheading:15634339-Phosphoproteins, pubmed-meshheading:15634339-Phosphorylation, pubmed-meshheading:15634339-Protein-Serine-Threonine Kinases, pubmed-meshheading:15634339-Proto-Oncogene Proteins, pubmed-meshheading:15634339-Proto-Oncogene Proteins c-akt
pubmed:year
2005
pubmed:articleTitle
Insulin resistance in human adipocytes occurs downstream of IRS1 after surgical cell isolation but at the level of phosphorylation of IRS1 in type 2 diabetes.
pubmed:affiliation
Department of Cell Biology and Diabetes Research Centre, University of Linköping, Sweden.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't