help button home button Endocrine Society Endocrinology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
This Article
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow Request Copyright Permission
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Patel, Y. C.
Right arrow Articles by Orci, L.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Patel, Y. C.
Right arrow Articles by Orci, L.

Endocrinology, Vol 103, 917-923, Copyright © 1978 by Endocrine Society

ARTICLES

Changes in somatostatin concentration in pancreas and other tissues of streptozotocin diabetic rats

YC Patel, DP Cameron, A Bankier, F Malaisse-Lagae, M Ravazzola, P Studer and L Orci

Changes in immunoreactive somatostatin were examined in islets, whole pancreas, stomach, and hypothalamus of streptozotocin-diabetic rats. There was no change in islet somatostatin content at 2 days after the administration of streptozotocin, but thereafter, somatostatin progressively increased in the diabetic animals by 45% at 2 weeks, 230% at 6 weeks, and 500% by 6 months. By contrast, islet glucagon rose acutely and maintained a constant 2-fold elevation irrespective of the duration of the diabetes. Morphometric analysis of the somatostatin- and glucagon-producing cells in the islets revealed an apparent augmentation of both cell types. The concentration of somatostatin per total pancreas was also increased in the diabetic animals, suggesting that the islet increase was part of a true increase in pancreatic somatostatin. Pancreatic glucagon was unchanged despite the islet increase. The increase in pancreatic somatostatin was paralleled by an elevation in gastric somatostatin concentration, implying a common mechanism in response to streptozotocin for the somatostatin cells in these two sites. There was no change in hypothalamic somatostatin concentration. Islet somatostatin was also increased in alloxan- diabetic rats. suggesting that streptozotocin does not stimulate the D cells directly.


This article has been cited by other articles:


Home page
 EndocrinologyHome page
Y.-C. Lu, C. Sternini, E. Rozengurt, and E. Zhukova
Release of Transgenic Human Insulin from Gastric G Cells: A Novel Approach for the Amelioration of Diabetes
Endocrinology, June 1, 2005; 146(6): 2610 - 2619.
[Abstract] [Full Text] [PDF]

Home page
 DiabetesHome page
S. Julien, J. Laine, and J. Morisset
Regulation of Rat Pancreatic CCKB Receptor and Somatostatin Expression by Insulin
Diabetes, June 1, 2004; 53(6): 1526 - 1534.
[Abstract] [Full Text] [PDF]

Home page
 ScienceHome page
Y. Patel, M Amherdt, and L Orci
Quantitative electron microscopic autoradiography of insulin, glucagon, and somatostatin binding sites on islets
Science, September 17, 1982; 217(4565): 1155 - 1156.
[Abstract] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Endocrinology Endocrine Reviews J. Clin. End. & Metab.
Molecular Endocrinology Recent Prog. Horm. Res. All Endocrine Journals
Copyright © 1978 by The Endocrine Society