| HOME | HELP | CONTACT US | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
Articles |
The aim of this study was to investigate the alpha cell population during the development of type 1 diabetes following multiple low-dose streptozotocin administration in mice. For this purpose C57BL/Ks male mice were injected with streptozotocin (40 mg/kg body weight for 5 days). Development of hyperglycemia was monitored over 28 days and a morphometric analysis of islet endocrine cells was performed. A reduction of islet cell area was observed after two injections of streptozotocin. The subsequent decrease of the area throughout the study period averaged 35%. Insulin-positive beta cells gradually disappeared from the identified islets. Hyperglycemia was present from day 7 onwards and in parallel with hyperglycemia, insulitis developed. An analysis of the alpha cell number per islet area revealed a 2- to 3-fold increase in this cell population, with the highest value on day 21. Confocal microscopy analysis of the ICA 512 protein tyrosine phosphatase revealed strong expression in the alpha cells at day 21, suggesting high secretory activity in the diabetic state. It is concluded that multiple low-dose streptozotocin treatment of C57BL/Ks male mice causes the disappearance of a fraction of the islets of Langerhans. In the remaining islet tissue an expansion of alpha cells occurs, reflecting a loss of intraislet beta cells as well as a regeneration of alpha cells.
This article has been cited by other articles:
|
|
 |
|
  R. D. Wideman, S. D. Covey, G. C. Webb, D. J. Drucker, and T. J. Kieffer A Switch From Prohormone Convertase (PC)-2 to PC1/3 Expression in Transplanted {alpha}-Cells Is Accompanied by Differential Processing of Proglucagon and Improved Glucose Homeostasis in Mice Diabetes, November 1, 2007; 56(11): 2744 - 2752. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. F. Luco, M. A. Maestro, N. del Pozo, W. M. Philbrick, P. P. de la Ossa, and J. Ferrer A Conditional Model Reveals That Induction of Hepatocyte Nuclear Factor-1{alpha} in Hnf1{alpha}-Null Mutant {beta}-Cells Can Activate Silenced Genes Postnatally, Whereas Overexpression Is Deleterious. Diabetes, August 1, 2006; 55(8): 2202 - 2211. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 E Kim, S Sohn, M Lee, J Jung, R D Kineman, and S Park Differential responses of the growth hormone axis in two rat models of streptozotocin-induced insulinopenic diabetes J. Endocrinol., February 1, 2006; 188(2): 263 - 270. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. Shiota, J. V. Rocheleau, M. Shiota, D. W. Piston, and M. A. Magnuson Impaired glucagon secretory responses in mice lacking the type 1 sulfonylurea receptor Am J Physiol Endocrinol Metab, October 1, 2005; 289(4): E570 - E577. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 E Ludvigsen, M Stridsberg, E T Janson, and S Sandler Expression of somatostatin receptor subtypes 1-5 in pancreatic islets of normoglycaemic and diabetic NOD mice Eur. J. Endocrinol., September 1, 2005; 153(3): 445 - 454. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. M. Kennedy and D. W. Zochodne Experimental Diabetic Neuropathy With Spontaneous Recovery: Is There Irreparable Damage? Diabetes, March 1, 2005; 54(3): 830 - 837. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K. H. Yoon, S. H. Ko, J. H. Cho, J. M. Lee, Y. B. Ahn, K. H. Song, S. J. Yoo, M. I. Kang, B. Y. Cha, K. W. Lee, et al. Selective {beta}-Cell Loss and {alpha}-Cell Expansion in Patients with Type 2 Diabetes Mellitus in Korea J. Clin. Endocrinol. Metab., May 1, 2003; 88(5): 2300 - 2308. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | CONTACT US | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
