Abstract
In vivo and in vitro data obtained in rodents indicate that (β-cells can trigger efficient repair mechanisms following nonlethal injury. Recent observations suggest that human pancreatic islets are more resistant than rodent islets to damage by alkylating agents, free oxygen radicals, nitric oxide and cytokines. This increased resistance to injury is associated with higher expression of heat shock protein 70, catalase and superoxide dismutase. These findings emphasise the potential relevance of (β-cell repair and/or defence mechanisms in the development of human IDDM.
Key words
Beta-Cell Repair - NO - HSP - Superoxide Dismutase - Catalase - IDDM
