Evidence map›Paper›PMID 23652017›Full record

ArticleNature communications2013

The gut microbiota suppresses insulin-mediated fat accumulation via the short-chain fatty acid receptor GPR43.

Ikuo Kimura, Kentaro Ozawa, Daisuke Inoue, Takeshi Imamura, Kumi Kimura, Takeshi Maeda, Kazuya Terasawa, Daiji Kashihara, Kanako Hirano, Taeko Tani and 5 more

Registry-linked trialOpen access · hybridAbstract read
In one paragraph

Article in Nature communications, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07373392 (Effects of LP-LDL® on Lipid Metabolism, Glycemic Control, Inflammatory Markers, and Cognitive Function in Individuals With Prediabetes and Diabetes Mellitus), which is not on this map. Cited by 779 papers, 7 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
779citing papers in PubMed, 7 pooled it
37.1field-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.

NCT07373392 nanot yet recruitingnot on this mapstarted 2026, after this paper: background citation

Effects of LP-LDL® on Lipid Metabolism, Glycemic Control, Inflammatory Markers, and Cognitive Function in Individuals With Prediabetes and Diabetes Mellitus (Type 1 and Type 2)

TypeinterventionalSponsorAalborg UniversityRan2026 to 2028Enrolled210ConditionsDiabete Type 1, Diabete Type 2, PrediabetesArmsLactobacillus plantarum ECGC 13110402, Placebo
3 · Its place in the literature

Who cites it

779 citing papers in PubMed, 7 syntheses or guidelines pooled it, 1,474 citations in OpenAlex.

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719 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

15 authors at 5 institutions in 1 country.

Ikuo KimuraDepartment of Pharmacogenomics, Kyoto University Graduate School of Pharmaceutical Sciences, Sakyo-ku, Kyoto 606-8501, Japan. ikimura@pharm.kyoto-u.ac.jp
Kentaro Ozawa
Daisuke Inoue
Takeshi Imamura
Kumi Kimura
Takeshi Maeda
Kazuya Terasawa
Daiji Kashihara
Kanako Hirano
Taeko Tani
Tomoyuki Takahashi
Satoshi Miyauchi
Go Shioi
Hiroshi Inoue
Gozoh Tsujimoto
Kyoto University · JPKanazawa University · JPGenetic Resources Center · JPNara Medical University · JPShiga University of Medical Science · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The gut microbiota affects nutrient acquisition and energy regulation of the host, and can influence the development of obesity, insulin resistance, and diabetes. During feeding, gut microbes produce short-chain fatty acids, which are important energy sources for the host. Here we show that the short-chain fatty acid receptor GPR43 links the metabolic activity of the gut microbiota with host body energy homoeostasis. We demonstrate that GPR43-deficient mice are obese on a normal diet, whereas mice overexpressing GPR43 specifically in adipose tissue remain lean even when fed a high-fat diet. Raised under germ-free conditions or after treatment with antibiotics, both types of mice have a normal phenotype. We further show that short-chain fatty acid-mediated activation of GPR43 suppresses insulin signalling in adipocytes, which inhibits fat accumulation in adipose tissue and promotes the metabolism of unincorporated lipids and glucose in other tissues. These findings establish GPR43 as a sensor for excessive dietary energy, thereby controlling body energy utilization while maintaining metabolic homoeostasis.

Indexed as

Lipid MetabolismMicrobiotaAdipose Tissue, WhiteAnimalsEnergy MetabolismFatty Acids, VolatileGastrointestinal TractGTP-Binding Protein alpha Subunits, Gi-GoGTP-Binding Protein beta SubunitsGTP-Binding Protein gamma SubunitsInsulinLiverMaleMiceMice, KnockoutModels, BiologicalFatty Acids, VolatileFfar2 protein, mouseGTP-Binding Protein alpha Subunits, Gi-GoGTP-Binding Protein beta SubunitsGTP-Binding Protein gamma SubunitsInsulinProtein Kinase CPTEN PhosphohydrolasePten protein, mouseReceptors, G-Protein-CoupledType C Phospholipases

Identifiers

PMID23652017
PMCPMC3674247
OpenAlexW2057039181

What OpenQuestion holds

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LicenceCC BY-NC-SA
Read underepoch 390

Registered trials

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.