ISSN:
1058-8388
Keywords:
Islet cell populations
;
Islet cell proliferation
;
Islet cell morphogenesis
;
Islet development
;
Pancreatic islets
;
Life and Medical Sciences
;
Cell & Developmental Biology
Source:
Wiley InterScience Backfile Collection 1832-2000
Topics:
Medicine
Notes:
Rats from 18 days fetal to 28 days neonatal ages were studied for the total population sizes and cell proliferation activities of insulin secreting B cells, glucagon secreting A cells, somatostain secreting D cells, and pancreatic polypeptide secreting PP cells. Cell population sizes were assessed by morphometric quantitation of immunohistochemically stained cells by a linear scanning method and cell proliferation activities were estimated by [3H]-thymidine labeling indices of these cell populations. There was a continuous increase in population sizes for all 4 islet cell types, with the fastest increase occurring in the last 4 days of gestation. The accelerated growth of these islet cell populations during late gestation was accomplished by a high cell proliferative activity at 20-22 days of gestation and a large influx of undifferentiated epithelial cells differentiating into the specific islet cell populations during this period. There was a reduction of population growth and cell proliferation for all islet cell types during the first 3-4 days of life. Growth activities continued for all islet cell populations after the 4th postnatal day, with a renewed acceleration in growth activities for B and A cells at this time. After the 10th neonatal day, the cell proliferation and total population growth continued at slow rates for all 4 islet cell types. The contribution from undifferentiated epithelial cells into the specific islet cell populations was negligible for B and A cells but continued at a low rate for PP and D cells during the first 10 days after birth. For B and A cell populations, there was a possibility that some cell loss occurred during the first 10 days of neonatal life. These dynamic changes of the growth characteristics provide a basis for understanding the abnormal growth of the endocrine pancreas. © 1994 Wiley-Liss, Inc.
Additional Material:
6 Ill.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1002/aja.1002000208
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