Evidence map›Paper›PMID 31801613›Full record

ArticleClinical epigenetics2019

Epigenetic silencing of the ANKRD26 gene correlates to the pro-inflammatory profile and increased cardio-metabolic risk factors in human obesity.

Antonella Desiderio, Michele Longo, Luca Parrillo, Michele Campitelli, Giuseppe Cacace, Sonia de Simone, Rosa Spinelli, Federica Zatterale, Serena Cabaro, Pasquale Dolce and 5 more

Open access · goldAbstract read
In one paragraph

Article in Clinical epigenetics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.0field-weighted citation impact, top 23% 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

13 citing papers in PubMed, 18 citations in OpenAlex.

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  12. Molecular basis of ageing in chronic metabolic diseases.Journal of endocrinological investigation · 2020
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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

15 authors at 3 institutions in 1 country.

Antonella DesiderioURT Genomics of Diabetes, Institute of Experimental Endocrinology and Oncology, National Research Council, Via Pansini 5, 80131, Naples, Italy.
Michele LongoURT Genomics of Diabetes, Institute of Experimental Endocrinology and Oncology, National Research Council, Via Pansini 5, 80131, Naples, Italy.
Luca ParrilloURT Genomics of Diabetes, Institute of Experimental Endocrinology and Oncology, National Research Council, Via Pansini 5, 80131, Naples, Italy.
Michele CampitelliURT Genomics of Diabetes, Institute of Experimental Endocrinology and Oncology, National Research Council, Via Pansini 5, 80131, Naples, Italy.
Giuseppe CacaceURT Genomics of Diabetes, Institute of Experimental Endocrinology and Oncology, National Research Council, Via Pansini 5, 80131, Naples, Italy.
Sonia de SimoneURT Genomics of Diabetes, Institute of Experimental Endocrinology and Oncology, National Research Council, Via Pansini 5, 80131, Naples, Italy.
Rosa SpinelliURT Genomics of Diabetes, Institute of Experimental Endocrinology and Oncology, National Research Council, Via Pansini 5, 80131, Naples, Italy.
Federica ZatteraleURT Genomics of Diabetes, Institute of Experimental Endocrinology and Oncology, National Research Council, Via Pansini 5, 80131, Naples, Italy.
Serena CabaroURT Genomics of Diabetes, Institute of Experimental Endocrinology and Oncology, National Research Council, Via Pansini 5, 80131, Naples, Italy.
Pasquale DolceDepartment of Public Health, Federico II University of Naples, Via Pansini 5, 80131, Naples, Italy.
Pietro FormisanoURT Genomics of Diabetes, Institute of Experimental Endocrinology and Oncology, National Research Council, Via Pansini 5, 80131, Naples, Italy.
Marco MiloneDepartment of Clinical Medicine and Surgery, Federico II University of Naples, Via Pansini 5, 80131, Naples, Italy.
Claudia MieleURT Genomics of Diabetes, Institute of Experimental Endocrinology and Oncology, National Research Council, Via Pansini 5, 80131, Naples, Italy. c.miele@ieos.cnr.it.
Francesco BeguinotURT Genomics of Diabetes, Institute of Experimental Endocrinology and Oncology, National Research Council, Via Pansini 5, 80131, Naples, Italy. beguino@unina.it.ORCID 0000-0002-4946-7803
Gregory A RacitiURT Genomics of Diabetes, Institute of Experimental Endocrinology and Oncology, National Research Council, Via Pansini 5, 80131, Naples, Italy.
Institute for Experimental Endocrinology and Oncology · ITFederico II University Hospital · ITUniversity of Naples Federico II · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundObesity is a major worldwide threat to human health. Increasing evidence indicates that epigenetic modifications have a major impact on the natural history of this disorder. Ankyrin Repeat Domain 26 (Ankrd26) is involved in the development of both obesity and diabetes in mice and is modulated by environmentally induced epigenetic modifications. This study aims at investigating whether impaired ANKRD26 gene expression and methylation occur in human obesity and whether they correlate to the phenotype of these subjects.

resultsWe found that downregulation of ANKRD26 mRNA and hyper-methylation of a specific region of the ANKRD26 promoter, embedding the CpG dinucleotides - 689, - 659, and - 651 bp, occur in peripheral blood leukocytes from obese compared with the lean subjects. ANKRD26 gene expression correlates inversely to the percentage of DNA methylation at these 3 CpG sites. Luciferase assays reveal a cause-effect relationship between DNA methylation at the 3 CpG sites and ANKRD26 gene expression. Finally, both ANKRD26 mRNA levels and CpG methylation correlate to body mass index and to the pro-inflammatory status and the increased cardio-metabolic risk factors of these same subjects.

conclusionDownregulation of the ANKRD26 gene and hyper-methylation at specific CpGs of its promoter are common abnormalities in obese patients. These changes correlate to the pro-inflammatory profile and the cardio-metabolic risk factors of the obese individuals, indicating that, in humans, they mark adverse health outcomes.

Indexed as

DNA MethylationDown-RegulationAdultBody Mass IndexCase-Control StudiesCholesterol, HDLCholesterol, LDLCpG IslandsDNAEpigenesis, GeneticFemaleHumansIntercellular Signaling Peptides and ProteinsMaleObesityPromoter Regions, GeneticANKRD26 protein, humanCholesterol, HDLCholesterol, LDLDNAIntercellular Signaling Peptides and ProteinsTriglyceridesANKRD26Cardio-metabolic risk factorsDNA methylationEpigenetic silencingObesity

Identifiers

PMID31801613
PMCPMC6894277
OpenAlexW2994577737

What Socratic holds

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LicenceCC BY
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Registered trials

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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 Socratic graph.