ArticleBiological trace element research2026
SIRT1 Regulates Iron Metabolism to Attenuate β-Cell Dedifferentiation by Inhibiting FoxO1 Acetylation.
Article in Biological trace element research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- Iron regulation by Sirtuins 1 & 2 and their therapeutic modulation by Sirtinol.Frontiers in pharmacology · 2026Review
- Mitochondrial bioenergetics dysfunction in T2DM: linking oxidative stress to insulin resistance.Frontiers in endocrinology · 2025Review
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Authors and funding
8 authors.
Funding
Abstract
Abnormal iron metabolism can cause β-cell dysfunction, and dedifferentiation is the core mechanism of β-cell dysfunction. However, the specific role of abnormal iron metabolism in dedifferentiation remains unclear. Forkhead Box O1 (FoxO1) is a crucial regulator of iron metabolism and dedifferentiation, and its transcriptional activity is regulated by silent information regulator 1 (SIRT1). We aimed to investigate the effects of iron metabolism on dedifferentiation under the action of SIRT1/FoxO1. In vivo, C57BL/6 mice were fed a high-fat diet (HFD). In vitro, MIN6 cells were treated with sodium palmitate (SP). Intraperitoneal glucose tolerance test and insulin tolerance test were used to detect fasting blood glucose in mice. Glucagon, ALDH1A3, Pdx1, and MaFA in the pancreatic tissue were detected by immunofluorescence. Protein levels of SIRT1, FoxO1, Ac-FoxO1, TFRC, DMT1, ferritin, Pdx1, MaFA, and ALDH1A3 in pancreatic tissue and cells were analyzed by Western blotting. Fluorescent probe was used to detect ROS and Fe
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Registered trials
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