The effects of 5-aminoimidazole-4-carboxamide riboside on the pancreas in neonatal streptozotocin-diabetic rats

• Published in: Acta diabetologica Vol. 43; no. 3; pp. 61 - 65
• Main Authors: Ozturk, M, Bolkent, S, Kaya-Dagistanli, F, Tuncdemir, M, Yilmazer, S, Akkan, A G
• Format: Journal Article
• Language: English
• Published: Germany Springer Nature B.V 01.11.2006
• Subjects: Aminoimidazole Carboxamide - analogs & derivatives; Aminoimidazole Carboxamide - therapeutic use; Animals; Animals, Newborn; Blood Glucose - drug effects; Blood Glucose - metabolism; Body Weight; Comparative studies; Diabetes; Diabetes Mellitus, Experimental - drug therapy; Gene expression; Hypoglycemic Agents - therapeutic use; Insulin; Insulin - genetics; Insulin - metabolism; Insulin-Secreting Cells - drug effects; Insulin-Secreting Cells - pathology; Insulin-Secreting Cells - ultrastructure; Medical research; Pancreas; Pancreas - drug effects; Pancreas - pathology; Rats; Ribonucleotides - therapeutic use; RNA, Messenger - genetics; Rodents
• ISSN: 0940-5429; 1432-5233
• DOI: 10.1007/s00592-006-0214-6

In this study, we aimed to determine the alterations of beta-cell ultrastructure, insulin mRNA and protein products of the same gene on the pancreas of rats following long-term treatment of 5-aminoimidazole-4-carboxamide riboside (AICAR). A single dose of streptozotocin (STZ) 100 mg/kg was injected intraperitoneally (i.p.) to 2-day-old newborn (n2) rats. The rats were divided into three groups. The first group was the n2 STZ-diabetic rats. The second group consisted of n2 STZ-diabetic rats treated with AICAR 10 mg/kg/day for one month. The third group was non-diabetic control rats. Our findings demonstrate that AICAR treatment decreases the blood glucose level but increases the body weight in n2 STZ-diabetic rats. In the AICAR-treated group, numerous beta cells showed increased insulin gene expression. We also observed increased exocytosis in this group, in an ultrastructural manner. As a result, it is suggested that AICAR may induce insulin synthesis and betacell regeneration in n2 STZ-diabetic rats.