Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1981-10-25
pubmed:abstractText
Hyperglycemia, hypoinsulinemia and ketonemia often develop abruptly in previously normal young "BB" rats. The syndrome mimics human juvenile diabetes closely and is, thus, appropriate for assessing pancreatic transplantation. Transplantation of islet cells from closely histocompatible Wistar Furth (WF) donor resulted in permanent normoglycemia when immunosuppression with ALS was given. However, when islet cells from nondiabetic "BB" donors were transplanted to nonimmunosuppressed diabetic "BB" recipients, only transient normoglycemia followed. Transplantation of WF islets cells also failed in diabetic "BB" rats which were tolerant of WF antigens, again suggesting destruction of transplanted islet cells by the original disease process-possibly autoimmunity. Evidence for autoimmunity was strengthened by the finding that newly diabetic "BB" rats could be rendered normoglycemic by immunosuppression. Since genetic susceptibility to spontaneous autoimmune diabetes is unique to some members of the "BB" stock, an attempt was made to alter their vulnerability by modifying their cellular immune system. Accordingly, 50 million bone marrow cells from WF donors were inoculated into half the newborn members of "BB" litters, leaving the littermates as unmodified controls. Most bone marrow recipients were protected, only four of 37 (10.8%) ever becoming diabetic, while the incidence of diabetes in noninoculated littermates was 22 of 39 (56.4%). The ultimate goal in human diabetes, which also seems very likely to be an autoimmune disease, may not be replacement of destroyed islet cells but identification of potentially susceptible children and prevention of islet destruction by immunologic manipulation.
pubmed:grant
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/6791599-219345, http://linkedlifedata.com/resource/pubmed/commentcorrection/6791599-223249, http://linkedlifedata.com/resource/pubmed/commentcorrection/6791599-350681, http://linkedlifedata.com/resource/pubmed/commentcorrection/6791599-362209, http://linkedlifedata.com/resource/pubmed/commentcorrection/6791599-388619, http://linkedlifedata.com/resource/pubmed/commentcorrection/6791599-4139522, http://linkedlifedata.com/resource/pubmed/commentcorrection/6791599-4266674, http://linkedlifedata.com/resource/pubmed/commentcorrection/6791599-522085, http://linkedlifedata.com/resource/pubmed/commentcorrection/6791599-5630193, http://linkedlifedata.com/resource/pubmed/commentcorrection/6791599-6997182, http://linkedlifedata.com/resource/pubmed/commentcorrection/6791599-7006384, http://linkedlifedata.com/resource/pubmed/commentcorrection/6791599-7006386, http://linkedlifedata.com/resource/pubmed/commentcorrection/6791599-7193616, http://linkedlifedata.com/resource/pubmed/commentcorrection/6791599-763312, http://linkedlifedata.com/resource/pubmed/commentcorrection/6791599-814643
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0003-4932
pubmed:author
pubmed:issnType
Print
pubmed:volume
194
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
328-38
pubmed:dateRevised
2009-11-18
pubmed:meshHeading
pubmed:year
1981
pubmed:articleTitle
Prevention of diabetes in rats by bone marrow transplantation.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't