Evidence map›Paper›PMID 38207130›Full record

ArticleJournal of leukocyte biology2024

Propionate functions as a feeding state-dependent regulatory metabolite to counter proinflammatory signaling linked to nutrient load and obesity.

Kim Han, Allison M Meadows, Matthew J Rodman, Anna Chiara Russo, Rahul Sharma, Komudi Singh, Shahin Hassanzadeh, Pradeep K Dagur, Rebecca D Huffstutler, Fynn N Krause and 4 more

Open access · hybridAbstract read
In one paragraph

Article in Journal of leukocyte biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
5.6field-weighted citation impact, top 4% 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

18 citing papers in PubMed, 17 citations in OpenAlex.

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  8. Restoring low-fiber diets-inducedCurrent research in food science · 2026
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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

14 authors at 3 institutions in 2 countries.

Kim HanLaboratory of Mitochondrial Biology and Metabolism, National Heart, Lung, and Blood Institute, National Institutes of Health, Room 5-3342, Bld 10-CRC, 10 Center Drive, Bethesda, MD 20817, United States.
Allison M MeadowsLaboratory of Mitochondrial Biology and Metabolism, National Heart, Lung, and Blood Institute, National Institutes of Health, Room 5-3342, Bld 10-CRC, 10 Center Drive, Bethesda, MD 20817, United States.
Matthew J RodmanLaboratory of Mitochondrial Biology and Metabolism, National Heart, Lung, and Blood Institute, National Institutes of Health, Room 5-3342, Bld 10-CRC, 10 Center Drive, Bethesda, MD 20817, United States.
Anna Chiara RussoLaboratory of Mitochondrial Biology and Metabolism, National Heart, Lung, and Blood Institute, National Institutes of Health, Room 5-3342, Bld 10-CRC, 10 Center Drive, Bethesda, MD 20817, United States.
Rahul SharmaLaboratory of Mitochondrial Biology and Metabolism, National Heart, Lung, and Blood Institute, National Institutes of Health, Room 5-3342, Bld 10-CRC, 10 Center Drive, Bethesda, MD 20817, United States.
Komudi SinghLaboratory of Mitochondrial Biology and Metabolism, National Heart, Lung, and Blood Institute, National Institutes of Health, Room 5-3342, Bld 10-CRC, 10 Center Drive, Bethesda, MD 20817, United States.ORCID 0000-0002-6413-541X
Shahin HassanzadehLaboratory of Mitochondrial Biology and Metabolism, National Heart, Lung, and Blood Institute, National Institutes of Health, Room 5-3342, Bld 10-CRC, 10 Center Drive, Bethesda, MD 20817, United States.
Pradeep K DagurFlow Cytometry Core Facility, National Heart, Lung, and Blood Institute, National Institutes of Health, 10 Center Drive, Bethesda, MD 20892, United States.
Rebecca D HuffstutlerCardiovascular Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, 10 Center Drive, Bethesda, MD 20892, United States.
Fynn N KrauseDepartment of Biochemistry, University of Cambridge, Sanger Bld, 80 Tennis Ct Rd, Cambridge CB2 1GA, United Kingdom.
Julian L GriffinDepartment of Biochemistry, University of Cambridge, Sanger Bld, 80 Tennis Ct Rd, Cambridge CB2 1GA, United Kingdom.
Yvonne BaumerSocial Determinants of Obesity and Cardiovascular Risk Laboratory, National Heart, Lung, and Blood Institute, National Institutes of Health, 10 Center Drive, Bethesda, MD 20892, United States.ORCID 0000-0001-7400-0773
Tiffany M Powell-WileySocial Determinants of Obesity and Cardiovascular Risk Laboratory, National Heart, Lung, and Blood Institute, National Institutes of Health, 10 Center Drive, Bethesda, MD 20892, United States.
Michael N SackLaboratory of Mitochondrial Biology and Metabolism, National Heart, Lung, and Blood Institute, National Institutes of Health, Room 5-3342, Bld 10-CRC, 10 Center Drive, Bethesda, MD 20817, United States.
National Institutes of Health · USUniversity of Aberdeen · GBUniversity of Cambridge · GB

Funding

Mitochondrial Biology in DiseaseZIAHL005102 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI SACK, MICHAEL · 2009 to 2025
$22.7M
Pilot Study for Geospatial Analysis of Neighborhood Environmental Stress in Relation to Biological Markers of Cardiovascular Health and Health Behaviors in WomenZIAHL006252 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI POWELL-WILEY, TIFFANY · 2020 to 2025
$5.7M
Medical Research CouncilNHLBI NIH HHS
6 · The paper itself

Abstract

Generally, fasting and refeeding confer anti- and proinflammatory effects, respectively. In humans, these caloric-load interventions function, in part, via regulation of CD4+ T cell biology. However, mechanisms orchestrating this regulation remain incomplete. We employed integrative bioinformatics of RNA sequencing and high-performance liquid chromatography-mass spectrometry data to measure serum metabolites and gene expression of peripheral blood mononuclear cells isolated from fasting and refeeding in volunteers to identify nutrient-load metabolite-driven immunoregulation. Propionate, a short chain fatty acid (SCFA), and the SCFA-sensing G protein-coupled receptor 43 (ffar2) were coordinately and inversely regulated by fasting and refeeding. Propionate and free fatty acid receptor agonists decreased interferon-γ and interleukin-17 and significantly blunted histone deacetylase activity in CD4+ T cells. Furthermore, propionate blunted nuclear factor κB activity and diminished interleukin-6 release. In parallel, propionate reduced phosphorylation of canonical T helper 1 (TH1) and TH17 regulators, STAT1 and STAT3, respectively. Conversely, knockdown of free fatty acid receptors significantly attenuated the anti-inflammatory role of propionate. Interestingly, propionate recapitulated the blunting of CD4+ TH cell activation in primary cells from obese individuals, extending the role of this metabolite to a disease associated with low-grade inflammation. Together, these data identify a nutrient-load responsive SCFA-G protein-coupled receptor linked pathway to regulate CD4+ TH cell immune responsiveness.

Indexed as

Fatty Acids, NonesterifiedPropionatesHumansLeukocytes, MononuclearObesityReceptors, G-Protein-CoupledFatty Acids, NonesterifiedPropionatesReceptors, G-Protein-CoupledCD4+ T cellsfastingFFAR2IL-6metaboliteNFκBpropionate

Identifiers

PMID38207130
PMCPMC10980352
OpenAlexW4390791906

What OpenQuestion holds

Textmetadata
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 OpenQuestion graph.