Evidence map›Paper›PMID 27739225›Full record

ReviewJournal of internal medicine2016

Epigenomic and transcriptional control of insulin resistance.

E D Rosen

Open access · greenAbstract readReview
In one paragraph

Review in Journal of internal medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
1.4field-weighted citation impact, top 18% 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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 37 citations in OpenAlex.

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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

1 author at 1 institution in 1 country.

E D RosenDivision of Endocrinology and Metabolism, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA, USA. erosen@bidmc.harvard.edu.
Beth Israel Deaconess Medical Center · US

Funding

Role of IRF3 in Energy and Glucose HomeostasisR01DK102170 · NIDDK · BETH ISRAEL DEACONESS MEDICAL CENTER · PI ROSEN, EVAN D · 2015 to 2024
$5.1M
Transcriptional Mechanisms of Human Insulin ResistanceR01DK102173 · NIDDK · BETH ISRAEL DEACONESS MEDICAL CENTER · PI ROSEN, EVAN D · 2015 to 2022
$4.4M
REGULATION OF NUTRIENT HOMEOSTASIS BY IRF4R01DK085171 · NIDDK · BETH ISRAEL DEACONESS MEDICAL CENTER · PI ROSEN, EVAN D · 2010 to 2018
$3.7M
Epigenomics of Human Insulin ResistanceR01DK087092 · NIDDK · BETH ISRAEL DEACONESS MEDICAL CENTER · PI ROSEN, EVAN D · 2009 to 2013
$3.3M
NIDDK NIH HHS R01 DK085171NIDDK NIH HHS R01 DK087092NIDDK NIH HHS R01 DK102170NIDDK NIH HHS R01 DK102173
6 · The paper itself

Abstract

Insulin resistance is one of the defining features of type 2 diabetes and the metabolic syndrome and accompanies many other clinical conditions, ranging from obesity to lipodystrophy to glucocorticoid excess. Extraordinary efforts have gone into defining the mechanisms that underlie insulin resistance, with most attention focused on altered signalling as well as mitochondrial and endoplasmic reticulum stress. Here, nuclear mechanisms of insulin resistance, including transcriptional and epigenomic effects, will be discussed. Three levels of control involving transcription factors, transcriptional cofactors, and chromatin-modifying enzymes will be considered. Well-studied examples of the first include PPAR-γ in adipose tissue and the glucocorticoid receptor and FoxO1 in a variety of insulin-sensitive tissues. These proteins work in concert with cofactors such as PGC-1α and CRTC2, and chromatin-modifying enzymes including DNA methyltransferases and histone acetyltransferases, to regulate key genes that promote insulin-stimulated glucose uptake, gluconeogenesis or other pathways that affect systemic insulin action. Furthermore, genetic variation associated with increased risk of type 2 diabetes is often related to altered transcription factor binding, either by affecting the transcription factor itself, or more commonly by changing the binding affinity of a noncoding regulatory region. Finally, several avenues for therapeutic exploitation in the battle against metabolic disease will be discussed, including small-molecule inhibitors and activators of these factors and their related pathways.

Indexed as

EpigenomicsTranscription, GeneticAdipose TissueAnimalsChromatin Assembly and DisassemblyDiabetes Mellitus, Type 2HumansInsulin ResistanceTranscriptional Elongation FactorsTranscription FactorsTranscriptional Elongation FactorsTranscription Factorsadipocytechromatin-modifying enzymeinsulin resistancetranscriptional cofactortranscription factortype 2 diabetes

Identifiers

PMID27739225
PMCPMC5119639
OpenAlexW2531648358

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.