Linked Life Data

2195130

Source:http://linkedlifedata.com/resource/pubmed/id/2195130

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
1990-8-13
pubmed:abstractText
To clarify a mechanism of insulin resistance associated with myotonic dystrophy, we studied the insulin receptor by using three different types of cells--circulating erythrocytes, cultured skin fibroblasts, and Epstein-Barr virus(EBV)-transformed lymphocytes. In myotonic dystrophy, insulin binding to erythrocytes and fibroblasts was significantly decreased as a result of a reduction of the binding affinity. Insulin binding to EBV-transformed lymphocytes was normal. When the receptors were purified from fibroblasts with wheat germ agglutinin, we could not find a decrease in the binding affinity seen in the intact cells. No difference was observed in the magnitude of basal and insulin-stimulated autophosphorylation of insulin receptors from EBV-transformed lymphocytes between the control and myotonic dystrophy. Southern blot analysis of the insulin receptor gene revealed no restriction fragment length polymorphism associated with myotonic dystrophy. These findings suggest that there is no primary defect of the insulin receptor per se in terms of insulin binding and autophosphorylation in myotonic dystrophy. The reduction of the insulin binding to erythrocytes and fibroblasts may be caused by the plasma membrane abnormality that affects the binding affinity of the receptor.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0022-2143
pubmed:author
pubmed:issnType
Print
pubmed:volume
115
pubmed:owner
NLM
pubmed:authorsComplete
N
pubmed:pagination
688-95
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed:year
1990
pubmed:articleTitle
Binding activity and autophosphorylation of the insulin receptor from patients with myotonic dystrophy.
pubmed:affiliation
Kyoto University School of Medicine, Department of Medicine, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't