Linked Life Data

10444024

Source:http://linkedlifedata.com/resource/pubmed/id/10444024

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1999-8-19
pubmed:abstractText
Protein tyrosine phosphatases (PTPs) are required for the dephosphorylation of the insulin receptor (IR) and its initial cellular substrates, and it has recently been reported that PTP-1B may play a role in the pathogenesis of insulin resistance in obesity and type 2 diabetes mellitus (DM). We therefore determined the amount and activity of PTP-1B in abdominal adipose tissue obtained from lean nondiabetic subjects (lean control (LC)), obese nondiabetic subjects (obese control (OC)), and subjects with both type 2 DM (DM2) and obesity (obese diabetic (OD)). PTP-1B protein levels were 3-fold higher in OC than in LC (1444 +/- 195 U vs 500 +/- 146 U (mean +/- SEM), P < .015), while OD exhibited a 5.5-fold increase (2728 +/- 286 U, P < .01). PTP activity was assayed by measuring the dephosphorylating activity toward a phosphorus 32-labeled synthetic dodecapeptide. In contrast to the increased PTP-1B protein levels, PTP-1B activity per unit of PTP-1B protein was markedly reduced, by 71% and 88% in OC and OD, respectively. Non-PTP-1B tyrosine phosphatase activity was comparable in all three groups. Similar results were obtained when PTP-1B activity was measured against intact human IR. A significant correlation was found between body mass index (BMI) and PTP-1B level (r = 0.672, P < .02), whereas BMI and PTP-1B activity per unit of PTP-1B showed a strong inverse correlation (r = -0.801, P < .002). These data suggest that the insulin resistance of obesity and DM2 is characterized by the increased expression of a catalytically impaired PTP-1B in adipose tissue and that impaired PTP-1B activity may be pathogenic for insulin resistance in these conditions.
pubmed:grant
pubmed:commentsCorrections
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0022-2143
pubmed:author
pubmed:issnType
Print
pubmed:volume
134
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
115-23
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed-meshheading:10444024-Adipose Tissue, pubmed-meshheading:10444024-Adult, pubmed-meshheading:10444024-Aged, pubmed-meshheading:10444024-Animals, pubmed-meshheading:10444024-Blotting, Western, pubmed-meshheading:10444024-Cell Line, pubmed-meshheading:10444024-Diabetes Mellitus, Type 2, pubmed-meshheading:10444024-Enzyme Activation, pubmed-meshheading:10444024-Female, pubmed-meshheading:10444024-Fibroblasts, pubmed-meshheading:10444024-Humans, pubmed-meshheading:10444024-Hydrolysis, pubmed-meshheading:10444024-Male, pubmed-meshheading:10444024-Middle Aged, pubmed-meshheading:10444024-Nerve Tissue Proteins, pubmed-meshheading:10444024-Obesity, pubmed-meshheading:10444024-Phosphorus Radioisotopes, pubmed-meshheading:10444024-Phosphorylation, pubmed-meshheading:10444024-Precipitin Tests, pubmed-meshheading:10444024-Protein Tyrosine Phosphatases, pubmed-meshheading:10444024-Rats, pubmed-meshheading:10444024-Receptor-Like Protein Tyrosine Phosphatases, Class 5
pubmed:year
1999
pubmed:articleTitle
Marked impairment of protein tyrosine phosphatase 1B activity in adipose tissue of obese subjects with and without type 2 diabetes mellitus.
pubmed:affiliation
Department of Medicine, University of Tennessee College of Medicine, Memphis, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't