Evidence map›Paper›PMID 33993191›Full record

ArticleInternational journal of obesity (2005)2021

In severe obesity, subcutaneous adipose tissue cell-derived cytokines are early markers of impaired glucose tolerance and are modulated by quercetin.

Vittoria D'Esposito, Maria Rosaria Ambrosio, Domenico Liguoro, Giuseppe Perruolo, Manuela Lecce, Serena Cabaro, Marianna Aprile, Ada Marino, Vincenzo Pilone, Pietro Forestieri and 5 more

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Article in International journal of obesity (2005), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

14 citing papers in PubMed, 20 citations in OpenAlex.

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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 5 institutions in 1 country.

Vittoria D'EspositoURT "Genomics of Diabetes, Institute of Experimental Endocrinology and Oncology (IEOS), National Research Council (CNR), Naples, Italy.
Maria Rosaria AmbrosioURT "Genomics of Diabetes, Institute of Experimental Endocrinology and Oncology (IEOS), National Research Council (CNR), Naples, Italy.
Domenico LiguoroURT "Genomics of Diabetes, Institute of Experimental Endocrinology and Oncology (IEOS), National Research Council (CNR), Naples, Italy.
Giuseppe PerruoloURT "Genomics of Diabetes, Institute of Experimental Endocrinology and Oncology (IEOS), National Research Council (CNR), Naples, Italy.
Manuela LecceURT "Genomics of Diabetes, Institute of Experimental Endocrinology and Oncology (IEOS), National Research Council (CNR), Naples, Italy.
Serena CabaroURT "Genomics of Diabetes, Institute of Experimental Endocrinology and Oncology (IEOS), National Research Council (CNR), Naples, Italy.
Marianna AprileInstitute of Genetics and Biophysics "Adriano Buzzati-Traverso," CNR, Naples, Italy.
Ada MarinoDepartment of Translational Medicine, "Federico II" University of Naples, Naples, Italy.
Vincenzo PiloneDepartment of Medicine, Surgery and Dentistry, University of Salerno, Salerno, Italy.
Pietro ForestieriDepartment of Medicine, Surgery and Dentistry, University of Salerno, Salerno, Italy.
Claudia MieleURT "Genomics of Diabetes, Institute of Experimental Endocrinology and Oncology (IEOS), National Research Council (CNR), Naples, Italy.
Dario BruzzeseDepartment of Public Health, "Federico II" University of Naples, Naples, Italy.
Daniela TerraccianoURT "Genomics of Diabetes, Institute of Experimental Endocrinology and Oncology (IEOS), National Research Council (CNR), Naples, Italy.
Francesco BeguinotURT "Genomics of Diabetes, Institute of Experimental Endocrinology and Oncology (IEOS), National Research Council (CNR), Naples, Italy.
Pietro FormisanoURT "Genomics of Diabetes, Institute of Experimental Endocrinology and Oncology (IEOS), National Research Council (CNR), Naples, Italy. fpietro@unina.it.ORCID http://orcid.org/0000-0001-7020-6870
Institute for Experimental Endocrinology and Oncology · ITUniversity of Salerno · ITFederico II University Hospital · ITInstitute of Genetics and Biophysics · ITUniversity of Naples Federico II · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundExcessive adiposity provides an inflammatory environment. However, in people with severe obesity, how systemic and local adipose tissue (AT)-derived cytokines contribute to worsening glucose tolerance is not clear.

methodsNinty-two severely obese (SO) individuals undergoing bariatric surgery were enrolled and subjected to detailed clinical phenotyping. Following an oral glucose tolerance test, participants were included in three groups, based on the presence of normal glucose tolerance (NGT), impaired glucose tolerance (IGT), or type 2 diabetes (T2D). Serum and subcutaneous AT (SAT) biopsies were obtained and mesenchymal stem cells (MSCs) were isolated, characterized, and differentiated in adipocytes in vitro. TNFA and PPARG mRNA levels were determined by qRT-PCR. Circulating, adipocyte- and MSC-released cytokines, chemokines, and growth factors were assessed by multiplex ELISA.

resultsSerum levels of IL-9, IL-13, and MIP-1β were increased in SO individuals with T2D, as compared with those with either IGT or NGT. At variance, SAT samples obtained from SO individuals with IGT displayed levels of TNFA which were threefold higher compared to those with NGT, but not different from those with T2D. Elevated levels of TNFα were also found in differentiated adipocytes, isolated from the SAT specimens of individuals with IGT and T2D, compared to those with NGT. Consistent with the pro-inflammatory milieu, IL-1β and IP-10 secretion was significantly higher in adipocytes from individuals with IGT and T2D. Moreover, increased levels of TNFα, both mRNA and secreted protein were detected in MSCs obtained from IGT and T2D, compared to NGT SO individuals. Exposure of T2D and IGT-derived MSCs to the anti-inflammatory flavonoid quercetin reduced TNFα levels and was paralleled by a significant decrease of the secretion of inflammatory cytokines.

conclusionIn severe obesity, enhanced SAT-derived inflammatory phenotype is an early step in the progression toward T2D and maybe, at least in part, attenuated by quercetin.

Indexed as

Obesity, MorbidSubcutaneous FatAdultBlood GlucoseCells, CulturedCytokinesFemaleGlucose IntoleranceGlucose Tolerance TestHumansMaleMiddle AgedQuercetinYoung AdultBlood GlucoseCytokinesQuercetin

Identifiers

PMID33993191
OpenAlexW3161687023

What OpenQuestion holds

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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 OpenQuestion graph.