| First Author | Ahmed Abdalhamid Osman M | Year | 2019 |
| Journal | J Cell Mol Med | Volume | 23 |
| Issue | 7 | Pages | 4653-4665 |
| PubMed ID | 31044530 | Mgi Jnum | J:295812 |
| Mgi Id | MGI:6454522 | Doi | 10.1111/jcmm.14216 |
| Citation | Ahmed Abdalhamid Osman M, et al. (2019) Deletion of pancreatic beta-cell adenosine kinase improves glucose homeostasis in young mice and ameliorates streptozotocin-induced hyperglycaemia. J Cell Mol Med 23(7):4653-4665 |
| abstractText | Severe reduction in the beta-cell number (collectively known as the beta-cell mass) contributes to the development of both type 1 and type 2 diabetes. Recent pharmacological studies have suggested that increased pancreatic beta-cell proliferation could be due to specific inhibition of adenosine kinase (ADK). However, genetic evidence for the function of pancreatic beta-cell ADK under physiological conditions or in a pathological context is still lacking. In this study, we crossed mice carrying LoxP-flanked Adk gene with Ins2-Cre mice to acquire pancreatic beta -cell ADK deficiency (Ins2-Cre(+/-) Adk(fl/fl) ) mice. Our results revealed that Ins2-Cre(+/-) Adk(fl/fl) mice showed improved glucose metabolism and beta-cell mass in younger mice, but showed normal activity in adult mice. Moreover, Ins2-Cre(+/-) Adk(fl/fl) mice were more resistant to streptozotocin (STZ) induced hyperglycaemia and pancreatic beta-cell damage in adult mice. In conclusion, we found that ADK negatively regulates beta-cell replication in young mice as well as under pathological conditions, such as STZ induced pancreatic beta-cell damage. Our study provided genetic evidence that specific inhibition of pancreatic beta-cell ADK has potential for anti-diabetic therapy. |
