Linked Life Data

6987319

Source:http://linkedlifedata.com/resource/pubmed/id/6987319

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
1980-5-30
pubmed:abstractText
The etiology of diabetes in some conditions of iron overload is not known. We studied growth, glucose tolerance, and pancreatic islet cell morphology and cytochemistry in rats administered parenteral FeNTA. These rats developed glucosuria, slowing of growth with eventual weight loss, polyuria, polydipsia, and death. They had normal fasting plasma glucose levels but decreased glucose tolerance and insulin response to glucose. Although no Prussian blue staining of iron was observed in pancreatic islets by light microscopy, at the ultrastructural level insulin-secreting beta-cells showed ferrin iron deposits localized to the plasmalemma and the cytoplasmic surface of secretory granule membranes. Prussian blue staining was also observed in parenchymal cells of the liver, heart, and kidney, in order of decreasing intensity. Animals treated with an equivalent dose of NTA, saline, or iron-dextran in saline had normal growth and response to glucose and did not exhibit pancreatic iron deposits at the light or ultrastructural level. These results support the hypothesis that iron affects pancreatic islet cell function and may be an etiologic agent of diabetes mellitus in hemochromatosis.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0022-2143
pubmed:author
pubmed:issnType
Print
pubmed:volume
95
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
525-35
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1980
pubmed:articleTitle
Iron nitrilotriacetate--induced experimental diabetes in rats.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.