Evidence map›Paper›PMID 27506731›Full record

ReviewMetabolism: clinical and experimental2016

Endoplasmic reticulum stress in obesity and obesity-related disorders: An expanded view.

Michael J Pagliassotti, Paul Y Kim, Andrea L Estrada, Claire M Stewart, Christopher L Gentile

Abstract readReview
In one paragraph

Review in Metabolism: clinical and experimental, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed
9.7field-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

67 citing papers in PubMed, 134 citations in OpenAlex.

  1. Review
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  3. Analysis ofInternational journal of molecular sciences · 2026
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  16. HFrontiers in chemistry · 2023
    Review
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7 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

5 authors at 2 institutions in 1 country.

Michael J PagliassottiDepartment of Food Science and Human Nutrition, Colorado State University. Electronic address: michael.pagliassotti@colostate.edu.
Paul Y KimDepartment of Biological Sciences, Grambling State University.
Andrea L EstradaDepartment of Food Science and Human Nutrition, Colorado State University.
Claire M StewartDepartment of Food Science and Human Nutrition, Colorado State University.
Christopher L GentileDepartment of Food Science and Human Nutrition, Colorado State University.
Colorado State University · USGrambling State University · US

Funding

STABILITY' (symptomatic review during biologic therapy) Review in Inflammatory Bowel DiseaseP20GM103424 · NIGMS · LOUISIANA STATE UNIV A&M COL BATON ROUGE · PI Konstantin G Kousoulas · 2012 to 2026
$57.4M
PILOT STUDY--SUBSTRATE METABOLISM IN EXTREMELY LOW BIRTH WEIGHT INFANTSP30DK048520 · NIDDK · UNIVERSITY OF COLORADO DENVER · PI Wendy M Kohrt · 1995 to 2026
$32.6M
Obesity and Hepatic SteatosisR01DK072017 · NIDDK · COLORADO STATE UNIVERSITY-FORT COLLINS · PI PAGLIASSOTTI, MICHAEL J · 2005 to 2014
$2.2M
Obesity and Hepatic SteatosisR56DK072017 · NIDDK · COLORADO STATE UNIVERSITY · PI PAGLIASSOTTI, MICHAEL J · 2010 to 2010
$249k
NIDDK NIH HHS R01 DK072017NIDDK NIH HHS R56 DK072017NIGMS NIH HHS P20 GM103424
6 · The paper itself

Abstract

The endoplasmic reticulum (ER) is most notable for its central roles in calcium ion storage, lipid biosynthesis, and protein sorting and processing. By virtue of its extensive membrane contact sites that connect the ER to most other organelles and to the plasma membrane, the ER can also regulate diverse cellular processes including inflammatory and insulin signaling, nutrient metabolism, and cell proliferation and death via a signaling pathway called the unfolded protein response (UPR). Chronic UPR activation has been observed in liver and/or adipose tissue of dietary and genetic murine models of obesity, and in human obesity and non-alcoholic fatty liver disease (NAFLD). Activation of the UPR in obesity and obesity-related disorders likely has two origins. One linked to classic ER stress involving the ER lumen and one linked to alterations to the ER membrane environment. This review discusses both of these origins and also considers the role of post-translational protein modifications, such as acetylation and palmitoylation, and ER-mitochondrial interactions to obesity-mediated impairments in the ER and activation of the UPR.

Indexed as

Endoplasmic Reticulum StressAnimalsHumansNon-alcoholic Fatty Liver DiseaseObesityUnfolded Protein ResponseLiverNon-alcoholic fatty liver diseaseUnfolded protein response

Identifiers

PMID27506731
PMCPMC4980576
OpenAlexW2379931407

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.