Abstract
Introduction The characteristic inability to maintain glucose homeostasis in diabetes mellitus reflects an absolute or partial insulin deficiency. This lack of insulin is due to an overall reduction in the mass of properly functioning B-cells. Such a reduction occurs as a result of a combination of an increased rate of cell destruction and a decreased rate of cell repair and renewal. While considerable attention has been focused on the elucidation of the factors resulting in €3-cell loss, less information is available regarding possible common genetic control mechanisms, thus implicating alterations in islet cell repair and/or adaptive B-cell regeneration as causative factors in diabetes. There are obvious difficulties in performing studies on islet cell repair and renewal in diabetes in man. However, earlier investigations performed in models of diabetes have provided some insight into the defence and repair mechanisms activated in the islet cells following injury and onset of disease [ 11. The hypothesis that pancreatic B-cells possess defence mechanisms against cell injury gained support from observations that islets are able to survive, and even recover functional activity, after exposure to cytotoxic attack or disturbed metabolism [2, 31. The nature of the islet cell defence process is unclear but is probably due to a combination of a repair/recovery response of surviving cells and an adaptive growth response to a reduced B-cell mass. However, the magnitude and subsequent effectiveness of the islet cell defence and repair mechanisms is dependent on the extent and nature of the cytotoxic insult [4]. A short exposure of rat
Published Version
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