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Immunohistochemical analysis reveals that intermittent fasting improves pancreatic islet plasticity in type 1 diabetes, indicating potential therapeutic mechanisms.
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.
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Harer et al. (2026) studied this question.
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