Evidence map›Paper›PMID 37598893›Full record

ArticleCellular and molecular gastroenterology and hepatology2023

SIRT1 Controls Enteroendocrine Progenitor Cell Proliferation in High-Fat Diet-Fed Mice.

Masaomi Miura, Masaki Igarashi, Ryosuke Isotani, Yoshiko Nakagawa-Nagahama, Satoshi Kuranami, Kyoko Naruse, Takashi Kadowaki, Toshimasa Yamauchi

Open access · goldAbstract read
In one paragraph

Article in Cellular and molecular gastroenterology and hepatology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
1.3field-weighted citation impact, top 20% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

4 citing papers in PubMed, 4 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Frontiers in nutrition · 2025
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 4 institutions in 2 countries.

Masaomi MiuraDepartment of Diabetes and Metabolic Diseases, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Masaki IgarashiDepartment of Diabetes and Metabolic Diseases, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan; Department of Biology, Koch Institute, Massachusetts Institute of Technology, Cambridge, Massachusetts. Electronic address: igarashima-int@h.u-tokyo.ac.jp.
Ryosuke IsotaniDepartment of Diabetes and Metabolic Diseases, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Yoshiko Nakagawa-NagahamaDepartment of Diabetes and Metabolic Diseases, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Satoshi KuranamiDepartment of Diabetes and Metabolic Diseases, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Kyoko NaruseDepartment of Diabetes and Metabolic Diseases, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Takashi KadowakiToranomon Hospital, Tokyo, Japan.
Toshimasa YamauchiDepartment of Diabetes and Metabolic Diseases, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan. Electronic address: tyamau@m.u-tokyo.ac.jp.
The University of Tokyo · JPTokyo Institute of Technology · JPToranomon Hospital · JPUniversity of Tokyo Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND &

aimsWe aimed to investigate how sirtuin 1 (SIRT1), a conserved mammalian Nicotinamide adenine dinucleotide

methodsWe used mice with specific Sirt1 disruption in the intestinal epithelium (VilKO, villin-Cre

resultsIn HFD-fed VilKO and NgnKO mice, an increase in EECs (42.3% and 37.2%), GLP-1- or GLP-2-producing L cells (93.0% and 61.4%), and GLP-1 (85.7% and 109.6%) was observed after glucose loading, explaining the improved metabolic phenotype of HFD-VilKO mice. These increases were associated with up-regulated expression of neurogenin 3 (EEPC marker) in crypts of HFD-VilKO and HFD-NgnKO mice, respectively. Conversely, Sir2d or 24-hour fasted mice showed a decrease in EECs (21.6%), L cells (41.6%), and proliferative progenitor cells. SIRT1 overexpression- or knockdown-mediated change in the progenitor cell proliferation was associated with Wnt/β-catenin activity changes. Notably, Wnt/β-catenin inhibitor completely suppressed EEC and L-cell increases in HFD-VilKO mice or organoids from HFD-VilKO and HFD-NgnKO mice.

conclusionsIntestinal SIRT1 in EECs modulates the EEPC cycle by regulating β-catenin activity and can control the number of EECs in HFD-fed mice, which is a previously unknown role.

Indexed as

Diabetes Mellitus, Type 2NeoplasmsAnimalsbeta CateninCell ProliferationDiet, High-FatGlucagon-Like Peptide 1GlucoseMammalsMiceSirtuin 1beta CateninGlucagon-Like Peptide 1GlucoseSirt1 protein, mouseSirtuin 1Cell CycleGLP-1Type 2 Diabetes

Identifiers

PMID37598893
PMCPMC10685171
OpenAlexW4385995096

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.