کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
1984691 | 1539986 | 2006 | 21 صفحه PDF | دانلود رایگان |

Type 2 diabetes is increasingly viewed as a disease of insulin deficiency due not only to intrinsic pancreatic β-cell dysfunction but also to reduction of β-cell mass. It is likely that, in diabetes-prone subjects, the regulated β-cell turnover that adapts cell mass to body's insulin requirements is impaired, presumably on a genetic basis. We still have a limited knowledge of how and when this derangement occurs and what might be the most effective therapeutic strategy to preserve β-cell mass. The animal models of type 2 diabetes with reduced β-cell mass described in this review can be extremely helpful (a) to have insight into the mechanisms underlying the defective growth or accelerated loss of β-cells leading to the β-cell mass reduction; (b) to investigate in prospective studies the mechanisms of compensatory adaptation and subsequent failure of a reduced β-cell mass. Furthermore, these models are of invaluable importance to test the effectiveness of potential therapeutic agents that either stimulate β-cell growth or inhibit β-cell death.
Journal: The International Journal of Biochemistry & Cell Biology - Volume 38, Issues 5–6, May–June 2006, Pages 873–893