Pancreatic cell growth and beta-cell differentiation: dynamics of
pancreatic cell growth and beta-cell differentiation during diabetes
reversion in streptozotocin-treated newborn rat.
Ferrand, Nathalie, Any Astesano, Hoang-Huan Phan, Christophe Lelong,
and Gabriel Rosselin.
Unit[umlaut]a de Recherches sur les Peptides Neurodigestifs et le
Diab[angstrom]ate, Institut National de la Sant[umlaut]a et de la
Recherche M[umlaut]adicale U.55, Centre de recherches Paris-Saint
-Antoine, 75571 paris cedex 12, France
APStracts 2:0179C, 1995.
Cellular processes underlying ontogenesis and regression of
streptozotocin (STZ)-induced diabetes in newborn rat were
investigated at the most severe stage of diabetes at day 3 (d3) and
after recovery of normoglycemia at d8, by immunocytochemistry and
quantitative analysis. A previously unknown endocrine cell type
subpopulation (PEPS) was identified. It was characterized by granule
polymorphism, co-expression of insulin and glucagon immunoreactivity
and a proliferative capacity transiently higher than in B-cells. In
STZ-treated rats at d3, B-cell mass decreased 14-fold whereas PEPS
-cells were unaffected. The islet mass was restored to 55.7% by day 8
with a concomitant appearance of numerous small islets contiguous to
small ducts. B-cell mass increased by 6.9-fold as compared to 1.8
-fold in control rats although proliferative capacities remained
similar. Proliferation dropped considerably by d8, preventing
complete B-cell mass recovery in STZ-treated rats. STZ-induced
neonatal diabetes thus stimulates neogenesis of islets close to ducts
and proliferation of PEPS-cells. Those partially differentiated islet
cells appear to be on the differentiation pathway of stem-cells to
fully differentiated B-cells.
Received 30 January 1994; accepted in final form 25 April 1995.
APS Manuscript Number C698-4.
Article publication pending Am. J. Physiol. (Cell Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 2 May 1995.