Evidence map›Paper›PMID 32063863›Full record

ReviewFrontiers in physiology2019

Chronic Adipose Tissue Inflammation Linking Obesity to Insulin Resistance and Type 2 Diabetes.

Federica Zatterale, Michele Longo, Jamal Naderi, Gregory Alexander Raciti, Antonella Desiderio, Claudia Miele, Francesco Beguinot

Registry-linked trialAbstract readReview
In one paragraph

Review in Frontiers in physiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07655739 (Temporal Changes in Fractalkine), which is not on this map. Cited by 678 papers, 6 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
678citing papers in PubMed, 6 pooled it
–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.

NCT07655739 completednot on this mapstarted 2025, after this paper: background citation

Temporal Changes in Fractalkine (CX3CL1) Levels Following Sleeve Gastrectomy and Their Association With Weight Loss: A Prospective Study

Typeobservational_patient_registrySponsorMehmet Buğra BozanRan2025 to 2026Enrolled40ConditionsObesity & Overweight
3 · Its place in the literature

Who cites it

678 citing papers in PubMed, 6 syntheses or guidelines pooled it.

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618 more citing papers are in PubMed but not listed here.

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

7 authors.

Federica ZatteraleDepartment of Translational Medicine, University of Naples Federico II, Naples, Italy.
Michele LongoDepartment of Translational Medicine, University of Naples Federico II, Naples, Italy.
Jamal NaderiURT Genomic of Diabetes, Institute of Experimental Endocrinology and Oncology, National Research Council, Naples, Italy.
Gregory Alexander RacitiDepartment of Translational Medicine, University of Naples Federico II, Naples, Italy.
Antonella DesiderioDepartment of Translational Medicine, University of Naples Federico II, Naples, Italy.
Claudia MieleDepartment of Translational Medicine, University of Naples Federico II, Naples, Italy.
Francesco BeguinotDepartment of Translational Medicine, University of Naples Federico II, Naples, Italy.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Obesity is one of the major health burdens of the 21st century as it contributes to the growing prevalence of its related comorbidities, including insulin resistance and type 2 diabetes. Growing evidence suggests a critical role for overnutrition in the development of low-grade inflammation. Specifically, chronic inflammation in adipose tissue is considered a crucial risk factor for the development of insulin resistance and type 2 diabetes in obese individuals. The triggers for adipose tissue inflammation are still poorly defined. However, obesity-induced adipose tissue expansion provides a plethora of intrinsic signals (e.g., adipocyte death, hypoxia, and mechanical stress) capable of initiating the inflammatory response. Immune dysregulation in adipose tissue of obese subjects results in a chronic low-grade inflammation characterized by increased infiltration and activation of innate and adaptive immune cells. Macrophages are the most abundant innate immune cells infiltrating and accumulating into adipose tissue of obese individuals; they constitute up to 40% of all adipose tissue cells in obesity. In obesity, adipose tissue macrophages are polarized into pro-inflammatory M1 macrophages and secrete many pro-inflammatory cytokines capable of impairing insulin signaling, therefore promoting the progression of insulin resistance. Besides macrophages, many other immune cells (e.g., dendritic cells, mast cells, neutrophils, B cells, and T cells) reside in adipose tissue during obesity, playing a key role in the development of adipose tissue inflammation and insulin resistance. The association of obesity, adipose tissue inflammation, and metabolic diseases makes inflammatory pathways an appealing target for the treatment of obesity-related metabolic complications. In this review, we summarize the molecular mechanisms responsible for the obesity-induced adipose tissue inflammation and progression toward obesity-associated comorbidities and highlight the current therapeutic strategies.

Indexed as

adaptive immunityadipose tissue inflammationdiabetesinflammatory triggersinnate immune systeminsulin resistancelow-grade inflammationobesity

Identifiers

PMID32063863
PMCPMC7000657

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Registered trials

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.