Evidence map›Paper›PMID 32785109›Full record

ReviewInternational journal of molecular sciences2020

Metabolic and Molecular Mechanisms of Macrophage Polarisation and Adipose Tissue Insulin Resistance.

Lucie Orliaguet, Tina Ejlalmanesh, Fawaz Alzaid

Abstract readReview
In one paragraph

Review in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed, 1 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.

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

30 citing papers in PubMed, 1 synthesis or guideline pooled it.

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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

3 authors.

Lucie OrliaguetCordeliers Research Centre, INSERM, IMMEDIAB Laboratory, Sorbonne Université, Université de Paris, F-75006 Paris, France.ORCID 0000-0002-3209-457X
Tina EjlalmaneshCordeliers Research Centre, INSERM, IMMEDIAB Laboratory, Sorbonne Université, Université de Paris, F-75006 Paris, France.
Fawaz AlzaidCordeliers Research Centre, INSERM, IMMEDIAB Laboratory, Sorbonne Université, Université de Paris, F-75006 Paris, France.ORCID 0000-0003-3056-3640

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inflammation plays a key role in the development and progression of type-2 diabetes (T2D), a disease characterised by peripheral insulin resistance and systemic glucolipotoxicity. Visceral adipose tissue (AT) is the main source of inflammation early in the disease course. Macrophages are innate immune cells that populate all peripheral tissues, including AT. Dysregulated AT macrophage (ATM) responses to microenvironmental changes are at the root of aberrant inflammation and development of insulin resistance, locally and systemically. The inflammatory activation of macrophages is regulated at multiple levels: cell surface receptor stimulation, intracellular signalling, transcriptional and metabolic levels. This review will cover the main mechanisms involved in AT inflammation and insulin resistance in T2D. First, we will describe the physiological and pathological changes in AT that lead to inflammation and insulin resistance. We will next focus on the transcriptional and metabolic mechanisms described that lead to the activation of ATMs. We will discuss more novel metabolic mechanisms that influence macrophage polarisation in other disease or tissue contexts that may be relevant to future work in insulin resistance and T2D.

Indexed as

Macrophage ActivationAdipose TissueAnimalsCell PolarityCytokinesDiabetes Mellitus, Type 2HumansInflammationInsulinInsulin ResistanceMacrophagesObesityReceptors, Cell SurfaceSignal TransductionCytokinesInsulinReceptors, Cell Surfaceadipose tissueimmunometabolisminflammationinsulin resistancemacrophagesT2Dtype-2 diabetes

Identifiers

PMID32785109
PMCPMC7460862

What OpenQuestion holds

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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 OpenQuestion graph.