Evidence map›Paper›PMID 42613310›Full record

ArticleDiabetes, obesity & metabolism2026

Oral Butyrate Reduces Progression of Kidney Damage in an L-NAME-Induced Diabetic Kidney Disease Mouse Model.

Maria Novella Nicese, Angela Koudijs, Reshma Lalai, Cristina Avramut, Rico J E Derks, Elena Sánchez-López, Martin Giera, Amanda C M Pronk, Artemiy Kovynev, Sander Kooijman and 4 more

Abstract read
In one paragraph

Article in Diabetes, obesity & metabolism, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Article
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.

Maria Novella NiceseDepartment of Internal Medicine, Division of Nephrology, Leiden University Medical Center, Leiden, the Netherlands.ORCID https://orcid.org/0000-0002-1985-3826
Angela KoudijsDepartment of Internal Medicine, Division of Nephrology, Leiden University Medical Center, Leiden, the Netherlands.
Reshma LalaiDepartment of Internal Medicine, Division of Nephrology, Leiden University Medical Center, Leiden, the Netherlands.
Cristina AvramutDepartment of Cell and Chemical Biology, Leiden University Medical Center, Leiden, the Netherlands.
Rico J E DerksCenter for Proteomics and Metabolomics, Leiden University Medical Center, Leiden, the Netherlands.
Elena Sánchez-LópezCenter for Proteomics and Metabolomics, Leiden University Medical Center, Leiden, the Netherlands.
Martin GieraCenter for Proteomics and Metabolomics, Leiden University Medical Center, Leiden, the Netherlands.
Amanda C M PronkEinthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Center, Leiden, the Netherlands.
Artemiy KovynevEinthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Center, Leiden, the Netherlands.
Sander KooijmanEinthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Center, Leiden, the Netherlands.
Patrick C N RensenEinthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Center, Leiden, the Netherlands.
Roel BijkerkDepartment of Internal Medicine, Division of Nephrology, Leiden University Medical Center, Leiden, the Netherlands.
Bernard M van den BergDepartment of Internal Medicine, Division of Nephrology, Leiden University Medical Center, Leiden, the Netherlands.
Joris I RotmansDepartment of Internal Medicine, Division of Nephrology, Leiden University Medical Center, Leiden, the Netherlands.

Funding

Rembrandt Institute of Cardiovascular Science 80640
6 · The paper itself

Abstract

aimsDiabetic kidney disease (DKD) is one of the main causes of kidney failure worldwide. Interestingly, patients affected by DKD are characterised by a low abundance of gut bacteria producing short fatty acids including butyrate, which is suggested to play a role in the decline of renal function. Consequently, we aimed to test the effects of oral butyrate supplementation on kidney health in mice affected by DKD. MATERIAL AND

methodsTo this end, we treated diabetic BKS db/db mice (C57BLKS/J Lepr

resultsOral butyrate supplementation reduced mesangial expansion, glomerular enlargement and medullary fibrosis in kidney biopsies of the mice. These protective effects correlated with an increased abundance of Akkermansiaceae in the gut. In mice treated with butyrate, the abundance of Akkermansiaceae positively correlated with glomerular filtration rate (GFR) and plasma concentration of indole-3-methyl acetate and indole-3-acetaldehyde, key metabolites associated with many beneficial cardiovascular effects.

conclusionsIn conclusion, oral butyrate supplementation in mice with DKD improves kidney morphology, accompanied by an increased abundance of Akkermansiaceae in the gut. Future studies, such as transplantation of Akkermansia, should reveal whether this relationship is causal and translate into improved kidney function in DKD.

Indexed as

ButyratesDiabetic NephropathiesKidneyAdministration, OralAnimalsDisease Models, AnimalDisease ProgressionGastrointestinal MicrobiomeGlomerular Filtration RateMaleMiceMice, Inbred C57BLNG-Nitroarginine Methyl EsterButyratesNG-Nitroarginine Methyl Estercardiovascular diseasediabetic nephropathydietary interventiontype 2 diabetes

Identifiers

PMID42613310
PMCPMC13646374

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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.