IMMUNOCYTOCHEMICAL CHANGES IN THE FETAL PANCREATIC-ISLET FOLLOWING FETAL ADMINISTRATION OF STREPTOZOTOCIN IN THE RAT

Citation
M. Yamamoto et al., IMMUNOCYTOCHEMICAL CHANGES IN THE FETAL PANCREATIC-ISLET FOLLOWING FETAL ADMINISTRATION OF STREPTOZOTOCIN IN THE RAT, The Anatomical record, 247(2), 1997, pp. 248-252
Citations number
21
Categorie Soggetti
Anatomy & Morphology
Journal title
ISSN journal
0003276X
Volume
247
Issue
2
Year of publication
1997
Pages
248 - 252
Database
ISI
SICI code
0003-276X(1997)247:2<248:ICITFP>2.0.ZU;2-3
Abstract
Background: Streptozotocin (STZ) is selectively toxic to the B cells i n the pancreatic islets. It is well known that in the adult rat, STZ c auses the death of B cells, and it eventually induces diabetes mellitu s. The present study was conducted to detect what morphological change s could be induced in the fetal B cells following a direct injection o f STZ into the fetus in utero during late pregnancy in the rat. Method s: STZ (400 mu g/g body weight) was injected into the fetus in utero a t 10:00 on day 19 of gestation. Three, 6, 24, and 48 hr after injectio n, the changes in the B cells (anti-insulin serum positive cells) were examined immunohistochemically. The total volume of the B cells was m easured, Electron microscopic observation was made as well. Results: S ix hr after STZ injection, some B cells were destroyed so that their g ranules were distorted and burst. Twenty-four hr after STZ injection, a large majority of the existing B cells were disintegrated, and a num ber of small isletlike clusters of immature cells appeared among the e xocrine acini. The total volume of anti-insulin serum positive cells w as strikingly decreased. At 48 hr after injection, however, the volume returned to a level that was comparable to that of their littermate c ontrols. Conclusions: The regeneration of the B cells may occur becaus e of the high cell proliferative activity of undifferentiated cells fo llowing the destruction of the B cells caused by an injection of STZ. (C) 1997 Wiley-Liss, Inc.