There are major barriers for widespread use of islet also-transplantation that can help people with type 1 diabetes. The shortage of islets from donors is a huge obstacle. The other obstacle is that this is still considered an experimental procedure and until the procedure is considered successful enough to be labeled therapeutic by the FDA instead of experimental, the costs of these transplants come from limited research funds.
The accepted view has been that the β-cell dysfunction of established diabetes progresses inexorably (79,82,83), whereas insulin resistance can be modified at least to some extent. However, it is now clear that the β-cell defect, not solely hepatic insulin resistance, may be reversible by weight loss at least early in the course of type 2 diabetes (21,84). The low insulin sensitivity of muscle tissue does not change materially either during the onset of diabetes or during subsequent reversal. Overall, the information on the inhibitory effects of excess fat on β-cell function and apoptosis permits a new understanding of the etiology and time course of type 2 diabetes.
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