Evidence map›Paper›PMID 32180558›Full record

ReviewMolecular metabolism2020

Mechanisms of insulin resistance related to white, beige, and brown adipocytes.

Michael P Czech

Open access · goldAbstract readReview
In one paragraph

Review in Molecular metabolism, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 128 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
128citing papers in PubMed, 1 pooled it
17.7field-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

128 citing papers in PubMed, 1 synthesis or guideline pooled it, 241 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Cells · 2026
    Article
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  7. From Transcriptional Reprogramming to Fat Quality Improvement: DietaryAnimals : an open access journal from MDPI · 2026
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68 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

1 author at 1 institution in 1 country.

Michael P CzechProgram in Molecular Medicine, University of Massachusetts Medical School, Worcester, MA, USA. Electronic address: Michael.Czech@umassmed.edu.
University of Massachusetts Chan Medical School · US

Funding

Insulin Signaling and Metabolic Regulation in AdipocytesR37DK030898 · NIDDK · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI CZECH, MICHAEL P · 1996 to 2021
$7.2M
Adipocyte to neuron signaling in thermogenic programming of white adipose tissueR01DK116056 · NIDDK · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI CZECH, MICHAEL P · 2019 to 2023
$2.9M
Insulin Signaling and Metabolic Regulation in AdipocytesR01DK030898 · NIDDK · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI CZECH, MICHAEL P · 1986 to 2011
$2.7M
NIDDK NIH HHS R01 DK030898NIDDK NIH HHS R01 DK116056NIDDK NIH HHS R37 DK030898
6 · The paper itself

Abstract

backgroundThe diminished glucose lowering effect of insulin in obesity, called "insulin resistance," is associated with glucose intolerance, type 2 diabetes, and other serious maladies. Many publications on this topic have suggested numerous hypotheses on the molecular and cellular disruptions that contribute to the syndrome. However, significant uncertainty remains on the mechanisms of its initiation and long-term maintenance. SCOPE OF REVIEW: To simplify insulin resistance analysis, this review focuses on the unifying concept that adipose tissue is a central regulator of systemic glucose homeostasis by controlling liver and skeletal muscle metabolism. Key aspects of adipose function related to insulin resistance reviewed are: 1) the modes by which specific adipose tissues control hepatic glucose output and systemic glucose disposal, 2) recently acquired understanding of the underlying mechanisms of these modes of regulation, and 3) the steps in these pathways adversely affected by obesity that cause insulin resistance. MAJOR

conclusionsAdipocyte heterogeneity is required to mediate the multiple pathways that control systemic glucose tolerance. White adipocytes specialize in sequestering triglycerides away from the liver, muscle, and other tissues to limit toxicity. In contrast, brown/beige adipocytes are very active in directly taking up glucose in response to β adrenergic signaling and insulin and enhancing energy expenditure. Nonetheless, white, beige, and brown adipocytes all share the common feature of secreting factors and possibly exosomes that act on distant tissues to control glucose homeostasis. Obesity exerts deleterious effects on each of these adipocyte functions to cause insulin resistance.

Indexed as

Adipocytes, BeigeAdipocytes, BrownAdipocytes, WhiteAnimalsHumansInsulin ResistanceAdipokinesAdipose tissuesAdrenergic receptorsBioactive lipidsGlucose toleranceLipogenesisSignalingThermogenesisUncoupling protein

Identifiers

PMID32180558
PMCPMC6997501
OpenAlexW2999709139

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.