Recovery of function and mass of endogenous beta-cells in streptozotocin-induced diabetic rats treated with islet transplantation

Citation
Y. Hamamoto et al., Recovery of function and mass of endogenous beta-cells in streptozotocin-induced diabetic rats treated with islet transplantation, BIOC BIOP R, 287(1), 2001, pp. 104-109
Citations number
24
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Biochemistry & Biophysics
Journal title
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
ISSN journal
0006-291X → ACNP
Volume
287
Issue
1
Year of publication
2001
Pages
104 - 109
Database
ISI
SICI code
0006-291X(20010914)287:1<104:ROFAMO>2.0.ZU;2-2
Abstract
Islet transplantation corrects chronic hyperglycemia by augmentation of ins ulin supply from the graft tissue, but the role of endogenous beta -cells a fter transplantation is not clear. In the present study, we examined endoge nous beta -cell function after glucose homeostasis had been reestablished b y islet graft in streptozotocin (STZ)-induced diabetic rats. Fed plasma glu cose levels in diabetic rats transplanted with a large number of islets (25 00 islets) into the left kidney capsule soon became lower (139.8 +/- 8.2 mg /dl) and close to the level in controls (129.7 +/- 11.3 mg/dl), and IPGTT e xhibited a pattern of plasma glucose response almost identical to control. The insulin and DNA contents, islet area, and the distribution of beta -cel ls that were markedly deteriorated in islets of STZ rats were significantly restored in transplanted rats. The insulin release in response to glucose or alpha -ketoisocaproate was less in STZ rats, while in islets of transpla nted rats the secretion recovered to levels similar to controls. On the oth er hand, arginine-induced insulin release was conversely hyperresponsive in STZ rats, but in transplanted rats, the response was decreased similar to controls. Thus, as the plasma glucose level normalizes, residual beta -cell s show a recovery of function that cannot be accounted for by the increase in mass alone. (C) 2001 Academic Press.