Evidence map›Paper›PMID 38902253›Full record

ArticleNutrition & diabetes2024

Dietary resistant starch enhances immune health of the kidney in diabetes via promoting microbially-derived metabolites and dampening neutrophil recruitment.

Matthew Snelson, Devy Deliyanti, Sih Min Tan, Anna M Drake, Cassandra de Pasquale, Vinod Kumar, Trent M Woodruff, Jennifer L Wilkinson-Berka, Melinda T Coughlan

Abstract read
In one paragraph

Article in Nutrition & diabetes, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

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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

3 citing papers in PubMed.

  1. Trial
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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

9 authors.

Matthew SnelsonDepartment of Diabetes, School of Translational Medicine, Alfred Medical Research and Education Precinct, Monash University, Melbourne, VIC, Australia. matthew.snelson@monash.edu.ORCID 0000-0003-4829-9550
Devy DeliyantiDepartment of Anatomy and Physiology, School of Biomedical Sciences, University of Melbourne, Parkville, VIC, Australia.
Sih Min TanDepartment of Diabetes, School of Translational Medicine, Alfred Medical Research and Education Precinct, Monash University, Melbourne, VIC, Australia.
Anna M DrakeDepartment of Diabetes, School of Translational Medicine, Alfred Medical Research and Education Precinct, Monash University, Melbourne, VIC, Australia.
Cassandra de PasqualeDepartment of Diabetes, School of Translational Medicine, Alfred Medical Research and Education Precinct, Monash University, Melbourne, VIC, Australia.
Vinod KumarSchool of Biomedical Sciences, Faculty of Medicine, The University of Queensland, Brisbane, QLD, Australia.
Trent M WoodruffSchool of Biomedical Sciences, Faculty of Medicine, The University of Queensland, Brisbane, QLD, Australia.
Jennifer L Wilkinson-BerkaDepartment of Anatomy and Physiology, School of Biomedical Sciences, University of Melbourne, Parkville, VIC, Australia.
Melinda T CoughlanDepartment of Diabetes, School of Translational Medicine, Alfred Medical Research and Education Precinct, Monash University, Melbourne, VIC, Australia.

Funding

Department of Health | National Health and Medical Research Council (NHMRC) APP1043753Department of Health | National Health and Medical Research Council (NHMRC) APP586645
6 · The paper itself

Abstract

backgroundDietary-resistant starch is emerging as a potential therapeutic tool to limit the negative effects of diabetes on the kidneys. However, its metabolic and immunomodulatory effects have not yet been fully elucidated.

methodsSix-week-old db/db mice were fed a diet containing 12.5% resistant starch or a control diet matched for equivalent regular starch for 10 weeks. db/m mice receiving the control diet were utilised as non-diabetic controls. Freshly collected kidneys were digested for flow cytometry analysis of immune cell populations. Kidney injury was determined by measuring albuminuria, histology, and immunohistochemistry. Portal vein plasma was collected for targeted analysis of microbially-derived metabolites. Intestinal histology and tight junction protein expression were assessed.

resultsResistant starch limited the development of albuminuria in db/db mice. Diabetic db/db mice displayed a decline in portal vein plasma levels of acetate, propionate, and butyrate, which was increased with resistant starch supplementation. Diabetic db/db mice receiving resistant starch had a microbially-derived metabolite profile similar to that of non-diabetic db/m mice. The intestinal permeability markers lipopolysaccharide and lipopolysaccharide binding protein were increased in db/db mice consuming the control diet, which was not seen in db/db mice receiving resistant starch supplementation. Diabetes was associated with an increase in the kidney neutrophil population, neutrophil activation, number of C5aR1+ neutrophils, and urinary complement C5a excretion, all of which were reduced with resistant starch. These pro-inflammatory changes appear independent of fibrotic changes in the kidney.

conclusionsResistant starch supplementation in diabetes promotes beneficial circulating microbially-derived metabolites and improves intestinal permeability, accompanied by a modulation in the inflammatory profile of the kidney including neutrophil infiltration, complement activation, and albuminuria. These findings indicate that resistant starch can regulate immune and inflammatory responses in the kidney and support the therapeutic potential of resistant starch supplementation in diabetes on kidney health.

Indexed as

AlbuminuriaDiabetic NephropathiesKidneyNeutrophil InfiltrationAnimalsDiabetes Mellitus, ExperimentalGastrointestinal MicrobiomeMaleMiceMice, Inbred C57BLResistant StarchStarchResistant StarchStarch

Identifiers

PMID38902253
PMCPMC11190267

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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.