Quantitative ultrastructural changes induced by sucrose administration in the pancreatic B cells of normal hamsters

Citation
G. Camihort et al., Quantitative ultrastructural changes induced by sucrose administration in the pancreatic B cells of normal hamsters, BIOCELL, 24(1), 2000, pp. 31-37
Citations number
35
Categorie Soggetti
Cell & Developmental Biology
Journal title
BIOCELL
ISSN journal
03279545 → ACNP
Volume
24
Issue
1
Year of publication
2000
Pages
31 - 37
Database
ISI
SICI code
0327-9545(200004)24:1<31:QUCIBS>2.0.ZU;2-N
Abstract
We have previously reported that young male Syrian hamsters receiving a suc rose-rich diet presented increased B-cell replication rate and size. The ai m of the present study was to analyze, under the same experimental conditio ns, the ultrastructural changes in B cells. For this purpose, young male Sy rian hamsters were fed with a commercial diet and 10% sucrose in their drin king water (S group) while the control group IC) received the same diet and tap water, for 5 weeks. Samples of the pancreas removed after that period were processed for the immunohistochemical identification of B cells as wel l as for measuring several ultrastructural parameters. S hamsters showed hi gher serum insulin levels, while similar serum glucose values were obtained in animals from both groups. The B cells from S group exhibited lesser num ber of dense secretory granules at expenses of an increase of the pale ones , increased number of both exocytosis profiles and fusion-granule images, a s well as enlargement of the intercellular space and mitochondrial area. Ma l ked expansions of this space, limited by junctional complexes, were obser ved between adjacent B cells. These results would indicate that sucrose adm inistration to normal hamsters not only increases the pancreatic B-cell mas s but also induces measurable subcellular changes in the individual B-cell characteristic of an enhanced secretory activity. The present model would r epresent a useful tool for testing strategies in preventing the damage or p romoting the recovery of the pancreatic B cells.