Evidence map›Paper›PMID 41361331›Full record

ArticleBMC medicine2025

Adipose tissue-derived microRNAs as epigenetic modulators of type 2 diabetes.

Ratika Sehgal, Neele Haacke, Alice Maguolo, Fiorella A Solari, Markus Jähnert, Pascal Gottmann, Emma Nilsson, Allan Vaag, Pamela Fischer-Posovszky, Anja Werberger and 8 more

Abstract read
In one paragraph

Article in BMC medicine, 2025. 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

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

3 citing papers in PubMed.

  1. Biochemistry and biophysics reports · 2026
    Article
  2. 1α,25(OH)Nutrients · 2026
    Review
  3. 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

18 authors.

Ratika Sehgal *Department of Experimental Diabetology, German Institute of Human Nutrition Potsdam- Rehbruecke, Nuthetal, Germany.
Neele Haacke *Department of Experimental Diabetology, German Institute of Human Nutrition Potsdam- Rehbruecke, Nuthetal, Germany.
Alice MaguoloEpigenetics and Diabetes Unit, Department of Clinical Sciences, Lund University Diabetes Centre, Scania University Hospital, Lund University, Malmö, Sweden.
Fiorella A SolariLeibniz Institut Für Analytische Wissenschaften-ISAS-E.V., Dortmund, Germany.
Markus JähnertDepartment of Experimental Diabetology, German Institute of Human Nutrition Potsdam- Rehbruecke, Nuthetal, Germany.
Pascal GottmannDepartment of Experimental Diabetology, German Institute of Human Nutrition Potsdam- Rehbruecke, Nuthetal, Germany.
Emma NilssonEpigenetics and Diabetes Unit, Department of Clinical Sciences, Lund University Diabetes Centre, Scania University Hospital, Lund University, Malmö, Sweden.
Allan VaagDepartment of Clinical Sciences in Malmö, Lund University Diabetes Centre, Scania University Hospital, Malmö, Sweden.
Pamela Fischer-PosovszkyDepartment of Pediatrics and Adolescent Medicine, Ulm University Medical Center, Ulm, Germany.
Anja WerbergerDepartment of Pediatrics and Adolescent Medicine, Ulm University Medical Center, Ulm, Germany.
Andreas L BirkenfeldGerman Center for Diabetes Research (DZD), Munich-Neuherberg, Germany.
Andreas FritscheGerman Center for Diabetes Research (DZD), Munich-Neuherberg, Germany.
Hans-Ulrich HäringGerman Center for Diabetes Research (DZD), Munich-Neuherberg, Germany.
Albert SickmannLeibniz Institut Für Analytische Wissenschaften-ISAS-E.V., Dortmund, Germany.
Heike VogelDepartment of Experimental Diabetology, German Institute of Human Nutrition Potsdam- Rehbruecke, Nuthetal, Germany.
Charlotte LingEpigenetics and Diabetes Unit, Department of Clinical Sciences, Lund University Diabetes Centre, Scania University Hospital, Lund University, Malmö, Sweden.
Meriem OuniDepartment of Experimental Diabetology, German Institute of Human Nutrition Potsdam- Rehbruecke, Nuthetal, Germany.
Annette SchürmannDepartment of Experimental Diabetology, German Institute of Human Nutrition Potsdam- Rehbruecke, Nuthetal, Germany. schuermann@dife.de.

Funding

Bundesministerium für Bildung und Forschung BMBF: DZD grant 82DZD03D03HORIZON EUROPE Framework Programme OBELISK grant agreement 101080465Stiftelsen för Strategisk Forskning Dnr IRC15-0067swedish research council region Skane Dnr 2009-1039
6 · The paper itself

Abstract

backgroundWhite adipose tissue (WAT) dysfunction including an aberrant expression of miRNAs is strongly associated with the risk of developing type 2 diabetes (T2D), with limited evidence linking early changes in the WAT-derived miRNAs and T2D. The present study aims to identify early miRNome changes prognostic for T2D in mice and humans.

methodsGonadal (g) WAT of diabetes-resistant and diabetes-prone mice were subjected to multi-omics analyses (transcriptome, miRNome, methylome, proteome). Metabolic phenotypes linked with T2D were correlated with adipose tissue miRNA expression and DNA methylation from 14 monozygotic twin pairs discordant for T2D. Plasma miRNA levels from females at high risk of developing T2D (TÜF study) were included.

resultsAdipose tissue of the diabetes-susceptible mice was less insulin sensitive with ~ 200 differentially expressed mature miRNAs compared to diabetes-resistant mice. Integrative analysis of miRNome-transcriptome-proteome identified 227 proteins involved in amino acid metabolism, inflammation, signalling pathways, and insulin resistance. More than 20 differentially expressed miRNAs are located in the imprinted region Dlk1-Gtl2 and Mest (miR-335) potentially regulated by DNA methylation. Imprinted miRNAs also exhibited similar alterations in adipose tissue from monozygotic twin pairs discordant for T2D, with miR-335 expression altered only in females. Moreover, plasma levels of miR-335-5p were negatively correlated with fasting blood glucose in females at high risk of developing T2D.

conclusionsEarly alterations of WAT-derived miRNAs such as miR-335-5p could contribute to systemic metabolic changes associated with the risk of developing T2D.

Indexed as

Adipose TissueAdipose Tissue, WhiteDiabetes Mellitus, Type 2Epigenesis, GeneticMicroRNAsAnimalsDNA MethylationFemaleHumansMaleMiceMice, Inbred C57BLMiddle AgedMicroRNAsAdipose tissueDiscordant monozygotic twinsEpigeneticsImprintingMicroRNA (miRNA)MultiomicsNew Zealand Obese (NZO) miceType 2 diabetes (T2D)

Identifiers

PMID41361331
PMCPMC12690927

What Socratic holds

Textmetadata
LicenceCC BY
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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 Socratic graph.