Evidence mapPaperPMID 34552271Full record

ArticleNature metabolism2021

Diet-induced alteration of intestinal stem cell function underlies obesity and prediabetes in mice.

Alexandra Aliluev, Sophie Tritschler, Michael Sterr, Lena Oppenländer, Julia Hinterdobler, Tobias Greisle, Martin Irmler, Johannes Beckers, Na Sun, Axel Walch and 8 more

Open access · hybridAbstract read
In one paragraph

Article in Nature metabolism, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.

0numbers the graph read from it
0cells of the map it votes in
68citing papers in PubMed
14.4field-weighted citation impact, top 1% 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

68 citing papers in PubMed, 128 citations in OpenAlex.

  1. Review
  2. Article
  3. Regional organization of nutrient absorption across the small intestine.Nature reviews. Gastroenterology & hepatology · 2026
    Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. The Use of Organoid Cultures in Advancing Nutrition Research.Advances in nutrition (Bethesda, Md.) · 2025
    Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Review
  20. Article

8 more citing papers are in PubMed but not listed here.

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

18 authors at 2 institutions in 1 country.

Alexandra Aliluev *Institute of Diabetes and Regeneration Research, Helmholtz Diabetes Center, Helmholtz Center Munich, Neuherberg, Germany.
Sophie Tritschler *Institute of Diabetes and Regeneration Research, Helmholtz Diabetes Center, Helmholtz Center Munich, Neuherberg, Germany.ORCID http://orcid.org/0000-0003-0977-9957
Michael SterrInstitute of Diabetes and Regeneration Research, Helmholtz Diabetes Center, Helmholtz Center Munich, Neuherberg, Germany.
Lena OppenländerInstitute of Diabetes and Regeneration Research, Helmholtz Diabetes Center, Helmholtz Center Munich, Neuherberg, Germany.
Julia HinterdoblerInstitute of Diabetes and Regeneration Research, Helmholtz Diabetes Center, Helmholtz Center Munich, Neuherberg, Germany.ORCID http://orcid.org/0000-0003-4708-4814
Tobias GreisleInstitute of Diabetes and Regeneration Research, Helmholtz Diabetes Center, Helmholtz Center Munich, Neuherberg, Germany.
Martin IrmlerInstitute of Experimental Genetics, Helmholtz Center Munich, Neuherberg, Germany.ORCID http://orcid.org/0000-0003-3169-479X
Johannes BeckersGerman Center for Diabetes Research (DZD), Neuherberg, Germany.ORCID http://orcid.org/0000-0001-7874-3822
Na SunResearch Unit of Analytical Pathology, Helmholtz Center Munich, Neuherberg, Germany.
Axel WalchResearch Unit of Analytical Pathology, Helmholtz Center Munich, Neuherberg, Germany.
Kerstin StemmerInstitute of Diabetes and Obesity, Helmholtz Diabetes Center, Helmholtz Center Munich, Neuherberg, Germany.
Alida KindtInstitute of Computational Biology, Helmholtz Center Munich, Neuherberg, Germany.ORCID http://orcid.org/0000-0001-6551-6030
Jan KrumsiekInstitute of Computational Biology, Helmholtz Center Munich, Neuherberg, Germany.
Matthias H TschöpGerman Center for Diabetes Research (DZD), Neuherberg, Germany.ORCID http://orcid.org/0000-0002-4744-371X
Malte D LueckenInstitute of Computational Biology, Helmholtz Center Munich, Neuherberg, Germany.ORCID http://orcid.org/0000-0001-7464-7921
Fabian J TheisInstitute of Computational Biology, Helmholtz Center Munich, Neuherberg, Germany. fabian.theis@helmholtz-muenchen.de.ORCID http://orcid.org/0000-0002-2419-1943
Heiko LickertInstitute of Diabetes and Regeneration Research, Helmholtz Diabetes Center, Helmholtz Center Munich, Neuherberg, Germany. heiko.lickert@helmholtz-muenchen.de.ORCID http://orcid.org/0000-0002-4597-8825
Anika BöttcherInstitute of Diabetes and Regeneration Research, Helmholtz Diabetes Center, Helmholtz Center Munich, Neuherberg, Germany. anika.boettcher@helmholtz-muenchen.de.ORCID http://orcid.org/0000-0001-5473-3136
Helmholtz Zentrum München · DEJustus-Liebig-Universität Gießen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Excess nutrient uptake and altered hormone secretion in the gut contribute to a systemic energy imbalance, which causes obesity and an increased risk of type 2 diabetes and colorectal cancer. This functional maladaptation is thought to emerge at the level of the intestinal stem cells (ISCs). However, it is not clear how an obesogenic diet affects ISC identity and fate. Here we show that an obesogenic diet induces ISC and progenitor hyperproliferation, enhances ISC differentiation and cell turnover and changes the regional identities of ISCs and enterocytes in mice. Single-cell resolution of the enteroendocrine lineage reveals an increase in progenitors and peptidergic enteroendocrine cell types and a decrease in serotonergic enteroendocrine cell types. Mechanistically, we link increased fatty acid synthesis, Ppar signaling and the Insr-Igf1r-Akt pathway to mucosal changes. This study describes molecular mechanisms of diet-induced intestinal maladaptation that promote obesity and therefore underlie the pathogenesis of the metabolic syndrome and associated complications.

Indexed as

Diet, High-FatAnimalsCell LineageCell ProliferationFatty AcidsIntestinesMiceObesityPeroxisome Proliferator-Activated ReceptorsPrediabetic StateSignal TransductionStem CellsFatty AcidsPeroxisome Proliferator-Activated Receptors

Identifiers

PMID34552271
PMCPMC8458097
OpenAlexW3199769720

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

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 Socratic graph.