Evidence mapPaperPMID 28018292Full record

ReviewFrontiers in endocrinology2016

Obesity: An Immunometabolic Perspective.

Indrani Ray, Sushil K Mahata, Rajat K De

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in endocrinology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed, 1 pooled it
8.8field-weighted citation impact, top 2% 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

49 citing papers in PubMed, 1 synthesis or guideline pooled it, 91 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. Weight Loss-Associated Remodeling of Adipose Tissue Immunometabolism.Obesity reviews : an official journal of the International Association for the Study of Obesity · 2025
    Review
  5. Review
  6. Type 2 Diabetes Mellitus Remission, Dream or Reality? A Narrative Review of Current Evidence and Integrated Care Strategies.Diabetes therapy : research, treatment and education of diabetes and related disorders · 2025
    Review
  7. Review
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Is Chemerin Associated with Gestational Diabetes Mellitus? A Case-Control Study.Diabetes, metabolic syndrome and obesity : targets and therapy · 2023
    Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. Review
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

3 authors at 2 institutions in 2 countries.

Indrani RayMachine Intelligence Unit, Indian Statistical Institute , Kolkata , India.
Sushil K MahataMetabolic Physiology & Ultrastructural Biology Laboratory, VA San Diego Healthcare System, La Jolla, CA, USA; Metabolic Physiology & Ultrastructural Biology Laboratory, University of California San Diego, La Jolla, CA, USA.
Rajat K DeMachine Intelligence Unit, Indian Statistical Institute , Kolkata , India.
Indian Statistical Institute · INUniversity of California, San Diego · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Obesity, characterized by chronic activation of inflammatory pathways, is a critical factor contributing to insulin resistance (IR) and type 2 diabetes (T2D). Free fatty acids (FFAs) are increased in obesity and are implicated as proximate causes of IR and induction of inflammatory signaling in adipose, liver, muscle, and pancreas. Cells of the innate immune system produce cytokines, and other factors that affect insulin signaling and result in the development of IR. In the lean state, adipose tissue is populated by adipose tissue macrophage of the anti-inflammatory M2 type (ATM2) and natural killer (NK) cells; this maintains the insulin-sensitive phenotype because ATM2 cells secrete IL10. In contrast, obesity induces lipolysis and release of pro-inflammatory FFAs and factors, such as chemokine (C-C motif) ligand 2 (CCL2) and tumor necrosis factor alpha (TNF-α), which recruit blood monocytes in adipose tissue, where they are converted to macrophages of the highly pro-inflammatory M1-type (ATM1). Activated ATM1 produce large amounts of pro-inflammatory mediators such as TNF-α, interleukin-1β, IL-6, leukotriene B4, nitric oxide (NO), and resistin that work in a paracrine fashion and cause IR in adipose tissue. In the liver, both pro-inflammatory Kupffer cells (M1-KCs) and recruited hepatic macrophages (Ly6C

Indexed as

ER stressinsulin resistancemacrophagesnon-alcoholic fatty liver diseasesobesityreactive oxygen speciestype 2 diabetes

Identifiers

PMID28018292
PMCPMC5149556
OpenAlexW2560283195

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.