Recovery of Function and Mass of Endogenous β-Cells in Streptozotocin-Induced Diabetic Rats Treated with Islet Transplantation

• Published in: Biochemical and biophysical research communications Vol. 287; no. 1; pp. 104 - 109
• Main Authors: Hamamoto, Yoshiyuki, Tsuura, Yoshiyuki, Fujimoto, Shimpei, Nagata, Masao, Takeda, Tomomi, Mukai, Eri, Fujita, Jun, Yamada, Yuichirou, Seino, Yutaka
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 14-09-2001
• Subjects: Animals; arginine; Cell Transplantation; Diabetes Mellitus, Experimental - pathology; Diabetes Mellitus, Experimental - surgery; Disease Models, Animal; endogenous islet; Evaluation Studies as Topic; glucose; insulin; Insulin - metabolism; Insulin Secretion; islet transplantation; Islets of Langerhans - physiology; Islets of Langerhans Transplantation; KCl; Male; Rats; Rats, Wistar; streptozotocin; streptozotocin (STZ); α-ketoisocaproate (KIC); β-cell function; β-cell mass; β-cell mass; arginine; KCl; endogenous islet; streptozotocin (STZ); islet transplantation; β-cell function; insulin secretion; α-ketoisocaproate (KIC)
• ISSN: 0006-291X; 1090-2104
• DOI: 10.1006/bbrc.2001.5563

Islet transplantation corrects chronic hyperglycemia by augmentation of insulin supply from the graft tissue, but the role of endogenous β-cells after transplantation is not clear. In the present study, we examined endogenous β-cell function after glucose homeostasis had been reestablished by islet graft in streptozotocin (STZ)-induced diabetic rats. Fed plasma glucose levels in diabetic rats transplanted with a large number of islets (2500 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 exhibited a pattern of plasma glucose response almost identical to control. The insulin and DNA contents, islet area, and the distribution of β-cells that were markedly deteriorated in islets of STZ rats were significantly restored in transplanted rats. The insulin release in response to glucose or α-ketoisocaproate was less in STZ rats, while in islets of transplanted rats the secretion recovered to levels similar to controls. On the other 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 β-cells show a recovery of function that cannot be accounted for by the increase in mass alone.