Research
Hormonal
Intermittent fasting stimulates beta-cell regeneration markers (NEUROG3) in obesity-induced diabetes, but this effect is dependent on an intact autophagy-lysosome pathway.
Fasting may trigger regeneration signals in the pancreas during obesity, but this process is blocked if your cells cannot perform autophagy.
ModerateConditionalMEDIUM confidence
Interestingly, we observed that IF did induce an increase in NEUROG3 nuclear localization only in HF diet fed mice... IF may provoke pancreatic beta cell regeneration in a manner that requires an intact autophagy-lysosome pathway.
Why this rating
Mouse model data.
Source
Intermittent fasting preserves beta-cell mass in obesity-induced diabetes via the autophagy-lysosome pathway
Haiyan Liu et al. · Autophagy · 2017
DOI 10.1080/15548627.2017.1368596
mechanism_onlyCited 189×
Read the paper DOI resolved against Crossref · corpus check 2026-06-10
More from this paper
- Intermittent fasting preserves pancreatic beta-cell mass and improves glucose tolerance in obesity-induced diabetes by stimulating the autophagy-lysosome pathway.Moderate
- Intermittent fasting worsens glucose tolerance and induces beta-cell death in mice with lysosomal dysfunction (LAMP2 deficiency) or impaired autophagosome formation (BECN1 deficiency).Moderate
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