Linked Life Data

11202213

Source:http://linkedlifedata.com/resource/pubmed/id/11202213

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
2001-1-30
pubmed:abstractText
The failure of insulin to stimulate muscle glucose uptake and suppress hepatic glucose production represents two of the fundamental pathophysiologic lesions in type 2 diabetes mellitus (DM). Defining insulin action at the molecular level, therefore, provides the critical background against which to elucidate the mechanisms of insulin resistance that underlie type 2 DM, obesity and many other disorders. Over the past two decades substantial progress has been made in identifying many of the molecular mechanisms involved in insulin signaling. Much of this progress has been due to the use of homologous recombinant gene targeting. The present review examines the various insights that have been provided by studies of knockout mice strains. Taken together, the results present the possibility of a unifying hypothesis for type 2 DM, in which insulin resistance in the beta-cell synergizes with insulin resistance in the periphery to produce the two classic defects of this disease: relative hypoinsulinemia and peripheral insulin resistance.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0334-018X
pubmed:author
pubmed:issnType
Print
pubmed:volume
13 Suppl 6
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1377-84
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed:year
2000
pubmed:articleTitle
Knockout mice challenge our concepts of glucose homeostasis and the pathogenesis of diabetes mellitus.
pubmed:affiliation
Joslin Diabetes Center and Department of Medicine, Harvard Medical School, Boston, Massachusetts, USA. c.ronald.kahn@joslin.harvard.edu
pubmed:publicationType
Journal Article, Review