cells increased significantly after fasting and tended to remain high after refeeding, thereby indicating increased pancreatic islet plasticity after fasting. In STEM images, the insulin granule core-to-halo ratio increased significantly after fasting. The fasting but not the refeeding group showed impaired glucose tolerance. The more crystallized mature β-cell granules indicate increased insulin secretory capacity, and the reduced proinsulin-to-insulin ratio suggests reduced endoplasmic reticulum stress in ß-cells after fasting. We propose that this observed plasticity may provide a basis for novel concepts of in vivo β-cell regeneration. However, further studies to investigate molecular mechanisms of fasting/refeeding in murine type 1 diabetes to evaluate its therapeutic potential are needed.
Harer et al. (Mon,) studied this question.