Research
Hormonal
Intermittent fasting preserves pancreatic beta-cell mass and improves glucose tolerance in obesity-induced diabetes by stimulating the autophagy-lysosome pathway.
Intermittent fasting may help preserve insulin-producing cells in obesity, but only if your cells can properly recycle waste (autophagy). If you have underlying cellular defects, fasting might stress your pancreas instead of helping it.
ModerateSupportsMEDIUM confidence
Our data show that despite continued high-fat intake, intermittent fasting restores autophagic flux in islets and improves glucose tolerance by enhancing glucose-stimulated insulin secretion, beta cell survival, and nuclear expression of NEUROG3, a marker of pancreatic regeneration.
Why this rating
The study is conducted in mouse models (diet-induced obesity), not humans.
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 stimulates beta-cell regeneration markers (NEUROG3) in obesity-induced diabetes, but this effect is dependent on an intact 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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