Linked Life Data

3681036

Source:http://linkedlifedata.com/resource/pubmed/id/3681036

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1988-1-6
pubmed:abstractText
Rats maintained on a diet deficient in copper for up to 8-10 weeks exhibit marked necrosis and depletion of acinar cells in the pancreas. When these animals are subsequently fed a copper-supplemented diet, foci of hepatocyte differentiation emerge by about 12 weeks. The present study deals with pancreatic changes during copper depletion and determines the extent of regenerative capacity of the pancreas during the early phases of copper supplementation. During the period of copper depletion, the pancreas gradually decreased in size, and by eight weeks of deficiency weighed approx. 30% as much as the control pancreas. Light-microscopic examination showed focal necrosis of acinar cells at 4 weeks, loss of lobular architecture by six weeks and loss of 85-90% of acinar tissue by eight weeks. Regeneration of the pancreas was initiated by feeding copper-supplemented diet at the end of eight weeks of copper deficiency. The wet weight of the pancreas increased gradually, and by 17 days it weighed 50% more than on the first day of regeneration. Mitotic activity was observed mainly in the acinar cells, beginning at 24 h and reaching a maximum of 19 +/- 1/1000 acinar cells at 72 h, and decreasing steadily thereafter. [3H]Thymidine autoradiography showed a labeling index of 51 +/- 1.7/1000 acinar cell nuclei at 24 h, reaching a peak value of 261 +/- 5.5/1000 acinar cells at 96 h. By 17 days, pancreatic regeneration was only partially complete; however, the proliferative activity was still persistent, albeit at a slower pace. Morphometric analysis of the pancreas on the 17th day of regeneration showed that acinar tissue occupied only 37% of the volume, as compared to 84% in the normal pancreas. These studies clearly demonstrate that acinar tissue of the pancreas following copper deficiency is capable of regeneration, but that the recovery of the pancreas is only partial. Additional studies are necessary to establish the role of this early acinar cell regeneration in pancreatic hepatocyte differentiation.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0169-4197
pubmed:author
pubmed:issnType
Print
pubmed:volume
2
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
71-85
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1987
pubmed:articleTitle
Pancreatic acinar cell regeneration following copper deficiency-induced pancreatic necrosis.
pubmed:affiliation
Department of Pathology, Northwestern University Medical School, Chicago, IL 60611.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.