Evidence map›Paper›PMID 39363899›Full record

ArticleFrontiers in endocrinology2024

The short-chain fatty acid receptors Gpr41/43 regulate bone mass by promoting adipogenic differentiation of mesenchymal stem cells.

Friederike Behler-Janbeck, Anke Baranowsky, Timur A Yorgan, Michelle Y Jaeckstein, Anna Worthmann, Marceline M Fuh, Karthikeyan Gunasekaran, Gisa Tiegs, Michael Amling, Thorsten Schinke and 1 more

Erratum issuedAbstract read
In one paragraph

Article in Frontiers in endocrinology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
–field-weighted citation impact
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

19 citing papers in PubMed.

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  3. Intestinal-Bone Axis Mediated byMicroorganisms · 2026
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors.

Friederike Behler-JanbeckDepartment of Biochemistry and Molecular Cell Biology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Anke BaranowskyDepartment of Trauma and Orthopaedic Surgery, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Timur A YorganDepartment of Osteology and Biomechanics, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Michelle Y JaecksteinDepartment of Biochemistry and Molecular Cell Biology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Anna WorthmannDepartment of Biochemistry and Molecular Cell Biology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Marceline M FuhDepartment of Biochemistry and Molecular Cell Biology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Karthikeyan GunasekaranDepartment of Biochemistry and Molecular Cell Biology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Gisa TiegsInstitute of Experimental Immunology and Hepatology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Michael AmlingDepartment of Osteology and Biomechanics, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Thorsten Schinke *Department of Osteology and Biomechanics, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Joerg Heeren *Department of Biochemistry and Molecular Cell Biology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Bone is a dynamic tissue that is constantly remodeled throughout adult life. Recently, it has been shown that bone turnover decreases shortly after food consumption. This process has been linked to the fermentation of non-digestible food ingredients such as inulin by gut microbes, which results in the production of the short-chain fatty acids (SCFAs) acetate, propionate and butyrate. SCFAs exert various metabolic functions, which in part can be explained by activation of G protein-coupled receptors (Gpr) 41 and 43. However, the potential relevance of a SCFA-Gpr41/43 signaling axis for bone metabolism has not been established. The aim of our study is to investigate the role of Gpr41/43 in bone metabolism and osteogenic differentiation of mesenchymal stem cells. For this purpose, we analyzed the skeletal phenotype of wild type controls (WT) and Gpr41/43 double knockout (Gpr41/43 dKO) mice fed either a chow or an inulin-enriched diet. In addition, we isolated bone marrow derived mesenchymal stem cells from WT and Gpr41/43 dKO mice and differentiated them into osteoblasts in the absence or presence of acetate. MicroCT scanning of femoral bones of Gpr41/43 dKO mice revealed a significant increase of trabecular bone volume and trabecular compared to WT controls. Treatment of WT bone marrow-derived osteoblasts with acetate resulted in decreased mineralization and substantial downregulation of bone formation markers such as

Indexed as

AdipogenesisCell DifferentiationMesenchymal Stem CellsMice, KnockoutOsteogenesisReceptors, G-Protein-CoupledAnimalsBone DensityCells, CulturedFatty Acids, VolatileMaleMiceMice, Inbred C57BLOsteoblastsFatty Acids, VolatileFfar2 protein, mouseFFAR3 protein, mouseGpcr41 protein, mouseReceptors, G-Protein-Coupledacetateadipogenesisbone formationGpr41/43G protein-coupled receptorsosteoblastsshort-chain fatty acids (SCFAs)

Identifiers

PMID39363899
PMCPMC11446854

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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.