Evidence map›Paper›PMID 35440795›Full record

ArticleCommunications biology2022

Targeting colonic macrophages improves glycemic control in high-fat diet-induced obesity.

Theresa V Rohm, Lena Keller, Angela J T Bosch, Shefaa AlAsfoor, Zora Baumann, Amandine Thomas, Sophia J Wiedemann, Laura Steiger, Elise Dalmas, Josua Wehner and 14 more

Open access · goldAbstract read
In one paragraph

Article in Communications biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
3.2field-weighted citation impact, top 7% 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

17 citing papers in PubMed, 27 citations in OpenAlex.

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  12. Macrophages in intestinal homeostasis and inflammatory bowel disease.Nature reviews. Gastroenterology & hepatology · 2023
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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

24 authors at 5 institutions in 3 countries.

Theresa V RohmClinic of Endocrinology, Diabetes and Metabolism, University Hospital Basel, Basel, Switzerland.
Lena KellerClinic of Endocrinology, Diabetes and Metabolism, University Hospital Basel, Basel, Switzerland.ORCID 0000-0002-3181-263X
Angela J T BoschClinic of Endocrinology, Diabetes and Metabolism, University Hospital Basel, Basel, Switzerland.
Shefaa AlAsfoorClinic of Endocrinology, Diabetes and Metabolism, University Hospital Basel, Basel, Switzerland.ORCID 0000-0002-2179-3682
Zora BaumannClinic of Endocrinology, Diabetes and Metabolism, University Hospital Basel, Basel, Switzerland.ORCID 0000-0002-0796-5011
Amandine ThomasBiozentrum, University of Basel, Basel, Switzerland.
Sophia J WiedemannClinic of Endocrinology, Diabetes and Metabolism, University Hospital Basel, Basel, Switzerland.
Laura SteigerClinic of Endocrinology, Diabetes and Metabolism, University Hospital Basel, Basel, Switzerland.
Elise DalmasClinic of Endocrinology, Diabetes and Metabolism, University Hospital Basel, Basel, Switzerland.
Josua WehnerClinic of Endocrinology, Diabetes and Metabolism, University Hospital Basel, Basel, Switzerland.
Leila RachidClinic of Endocrinology, Diabetes and Metabolism, University Hospital Basel, Basel, Switzerland.
Catherine MooserDepartment of Visceral Surgery und Medicine, Bern University Hospital, University of Bern, Bern, Switzerland.
Bahtiyar YilmazDepartment of Visceral Surgery und Medicine, Bern University Hospital, University of Bern, Bern, Switzerland.ORCID 0000-0003-1888-9226
Nerea Fernandez TrigoDepartment of Visceral Surgery und Medicine, Bern University Hospital, University of Bern, Bern, Switzerland.
Annaise J JauchDepartment of Biomedicine (DBM), University of Basel, University Hospital Basel, Basel, Switzerland.
Stephan WueestDivision of Pediatric Endocrinology and Diabetology, and Children's Research Center, University Children's Hospital, University of Zurich, Zurich, Switzerland.ORCID 0000-0002-0176-8906
Daniel KonradDivision of Pediatric Endocrinology and Diabetology, and Children's Research Center, University Children's Hospital, University of Zurich, Zurich, Switzerland.ORCID 0000-0001-9067-4356
Sandrine HenriCentre d'Immunologie de Marseille-Luminy, Aix Marseille Université, INSERM, CNRS, Marseille, France.ORCID 0000-0002-8980-9193
Jan H NiessDepartment of Biomedicine (DBM), University of Basel, University Hospital Basel, Basel, Switzerland.
Petr HruzDepartment of Biomedicine (DBM), University of Basel, University Hospital Basel, Basel, Switzerland.
Stephanie C Ganal-VonarburgDepartment of Visceral Surgery und Medicine, Bern University Hospital, University of Bern, Bern, Switzerland.
Julien RouxDepartment of Biomedicine (DBM), University of Basel, University Hospital Basel, Basel, Switzerland.ORCID 0000-0002-4192-5099
Daniel T MeierClinic of Endocrinology, Diabetes and Metabolism, University Hospital Basel, Basel, Switzerland.ORCID 0000-0003-3348-4657
Claudia Cavelti-WederClinic of Endocrinology, Diabetes and Metabolism, University Hospital Basel, Basel, Switzerland. claudia.cavelti-weder@usb.ch.ORCID 0000-0002-0650-6091
University of Basel · CHUniversity of Bern · CHUniversity of Zurich · CHCentre National de la Recherche Scientifique · FRSIB Swiss Institute of Bioinformatics · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The obesity epidemic continues to worsen worldwide. However, the mechanisms initiating glucose dysregulation in obesity remain poorly understood. We assessed the role that colonic macrophage subpopulations play in glucose homeostasis in mice fed a high-fat diet (HFD). Concurrent with glucose intolerance, pro-inflammatory/monocyte-derived colonic macrophages increased in mice fed a HFD. A link between macrophage numbers and glycemia was established by pharmacological dose-dependent ablation of macrophages. In particular, colon-specific macrophage depletion by intrarectal clodronate liposomes improved glucose tolerance, insulin sensitivity, and insulin secretion capacity. Colonic macrophage activation upon HFD was characterized by an interferon response and a change in mitochondrial metabolism, which converged in mTOR as a common regulator. Colon-specific mTOR inhibition reduced pro-inflammatory macrophages and ameliorated insulin secretion capacity, similar to colon-specific macrophage depletion, but did not affect insulin sensitivity. Thus, pharmacological targeting of colonic macrophages could become a potential therapy in obesity to improve glycemic control.

Indexed as

Diet, High-FatInsulin ResistanceAnimalsBlood GlucoseColonGlycemic ControlMacrophagesMiceObesityTOR Serine-Threonine KinasesBlood GlucoseTOR Serine-Threonine Kinases

Identifiers

PMID35440795
PMCPMC9018739
OpenAlexW4224283385

What OpenQuestion holds

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LicenceCC BY
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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.