Evidence map›Paper›PMID 27179976›Full record

ReviewBiochemical pharmacology2016

Adipose extracellular matrix remodelling in obesity and insulin resistance.

De Lin, Tae-Hwa Chun, Li Kang

Open access · greenAbstract readReview
In one paragraph

Review in Biochemical pharmacology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 116 papers.

0numbers the graph read from it
0cells of the map it votes in
116citing papers in PubMed
11.2field-weighted citation impact, top 1% 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

116 citing papers in PubMed, 225 citations in OpenAlex.

  1. Article
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  14. Comprehending the Epidemiology and Aetiology of Childhood Obesity: Integrating Life Course Approaches for Prevention and Intervention.Diabetes therapy : research, treatment and education of diabetes and related disorders · 2025
    Review
  15. Article
  16. Review
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56 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

3 authors at 2 institutions in 2 countries.

De LinDivision of Cancer Research, School of Medicine, University of Dundee, Dundee, UK.
Tae-Hwa ChunDivision of Metabolism, Endocrinology & Diabetes (MEND), Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, MI, USA; Biointerfaces Institute, University of Michigan, Ann Arbor, MI, USA.
Li KangDivision of Molecular and Clinical Medicine, School of Medicine, University of Dundee, Dundee, UK. Electronic address: l.kang@dundee.ac.uk.
University of Dundee · GBBioSurfaces (United States) · US

Funding

Regional Pilot And Feasibility Study Grants ProgramP30DK020572 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Mehboob A Hussain · 2013 to 2026
$24.3M
MMP14-dependent regulation of adipose tissue remodeling and function (R01)R01DK095137 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI CHUN, TAEHWA · 2012 to 2016
$1.7M
NIDDK NIH HHS P30 DK020572NIDDK NIH HHS R01 DK095137
6 · The paper itself

Abstract

The extracellular matrix (ECM) of adipose tissues undergoes constant remodelling to allow adipocytes and their precursor cells to change cell shape and function in adaptation to nutritional cues. Abnormal accumulation of ECM components and their modifiers in adipose tissues has been recently demonstrated to cause obesity-associated insulin resistance, a hallmark of type 2 diabetes. Integrins and other ECM receptors (e.g. CD44) that are expressed in adipose tissues have been shown to regulate insulin sensitivity. It is well understood that a hypoxic response is observed in adipose tissue expansion during obesity progression and that hypoxic response accelerates fibrosis and inflammation in white adipose tissues. The expansion of adipose tissues should require angiogenesis; however, the excess deposition of ECM limits the angiogenic response of white adipose tissues in obesity. While recent studies have focused on the metabolic consequences and the mechanisms of adipose tissue expansion and remodelling, little attention has been paid to the role played by the interaction between peri-adipocyte ECM and their cognate cell surface receptors. This review will address what is currently known about the roles played by adipose ECM, their modifiers, and ECM receptors in obesity and insulin resistance. Understanding how excess ECM deposition in the adipose tissue deteriorates insulin sensitivity would provide us hints to develop a new therapeutic strategy for the treatment of insulin resistance and type 2 diabetes.

Indexed as

Adipose TissueExtracellular MatrixHumansInflammationInsulin ResistanceObesityAdipose tissueExtracellular matrixFibrosisInsulin resistanceIntegrins

Identifiers

PMID27179976
PMCPMC5061598
OpenAlexW2373449482

What OpenQuestion holds

Textmetadata
LicenceTDM
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 OpenQuestion graph.