Evidence map›Paper›PMID 34519830›Full record

ArticleThe Journal of clinical endocrinology and metabolism2022

Insulin Increases Adipose Adiponectin in Pregnancy by Inhibiting Ubiquitination and Degradation: Impact of Obesity.

Irving L M H Aye, Fredrick J Rosario, Anita Kramer, Oddrun Kristiansen, Trond M Michelsen, Theresa L Powell, Thomas Jansson

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical endocrinology and metabolism, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

12 citing papers in PubMed, 18 citations in OpenAlex.

  1. Review
  2. Regulation of placental development and function by ubiquitination.Molecular medicine (Cambridge, Mass.) · 2025
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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

7 authors at 3 institutions in 3 countries.

Irving L M H AyeDepartment of Obstetrics & Gynaecology, and Centre for Trophoblast Research, University of Cambridge, Cambridge, UK.ORCID 0000-0003-3400-5005
Fredrick J RosarioDepartment of Obstetrics and Gynecology, University of Colorado Anschutz Medical Campus, Aurora, Colorado, USA.
Anita KramerDepartment of Obstetrics and Gynecology, University of Colorado Anschutz Medical Campus, Aurora, Colorado, USA.
Oddrun KristiansenDepartment of Obstetrics, Division of Obstetrics and Gynecology, Oslo University Hospital, Oslo, Norway.
Trond M MichelsenDepartment of Obstetrics, Division of Obstetrics and Gynecology, Oslo University Hospital, Oslo, Norway.
Theresa L PowellDepartment of Obstetrics and Gynecology, University of Colorado Anschutz Medical Campus, Aurora, Colorado, USA.
Thomas JanssonDepartment of Obstetrics and Gynecology, University of Colorado Anschutz Medical Campus, Aurora, Colorado, USA.
University of Colorado Anschutz Medical Campus · USOslo University Hospital · NOUniversity of Cambridge · GB

Funding

University of Colorado Anschutz Medical Campus DRCP30DK116073 · NIDDK · UNIVERSITY OF COLORADO DENVER · PI LORI SUSSEL · 2020 to 2026
$10.8M
ZEBRAFISH TRANSGENIC CORE - ROCKY MOUNTAIN NEUROLOGICAL DISORDERS CORE CENTERP30NS048154 · NINDS · UNIVERSITY OF COLORADO DENVER · PI RIBERA, ANGELES BADELL · 2004 to 2020
$10.1M
Placental adiponectin signaling and fetal programming in maternal obesityR01HD065007 · NICHD · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI JANSSON, THOMAS, POWELL, THERESA L · 2011 to 2022
$3.8M
NICHD NIH HHS R01 HD065007NIDDK NIH HHS P30 DK116073NIH HHS HD065007NINDS NIH HHS P30 NS048154
6 · The paper itself

Abstract

contextCirculating adiponectin levels are decreased in pregnant women with obesity or gestational diabetes, and this is believed to contribute to the insulin resistance and increased risk of fetal overgrowth associated with these conditions. However, the molecular mechanisms regulating adiponectin secretion from maternal adipose tissues in pregnancy are poorly understood.

objectiveWe tested the hypothesis that obesity in pregnancy is associated with adipose tissue insulin resistance and increased adiponectin ubiquitination and degradation, caused by inflammation and endoplasmic reticulum (ER) stress.

methodsVisceral adipose tissues were collected from lean and obese pregnant humans and mice. Total and ubiquitinated adiponectin, and markers of inflammation, ER stress, and insulin resistance were examined in adipose tissues. The role of insulin, inflammation, and ER stress in mediating adiponectin ubiquitination and degradation was examined using 3T3L-1 adipocytes.

resultsObesity in pregnancy is associated with adipose tissue inflammation, ER stress, insulin resistance, increased adiponectin ubiquitination, and decreased total abundance of adiponectin. Adiponectin ubiquitination was increased in visceral fat of obese pregnant women as compared to lean pregnant women. We further observed that insulin prevents, whereas ER stress and inflammation promote, adiponectin ubiquitination and degradation in differentiated 3T3-L1 adipocytes.

conclusionWe have identified adiponectin ubiquitination as a key mechanism by which obesity diminishes adiponectin secretion in pregnancy. This information will help us better understand the mechanisms controlling maternal insulin resistance and fetal growth in pregnancy and may provide a foundation for the development of strategies aimed at improving adiponectin production in pregnant women with obesity or gestational diabetes.

Indexed as

3T3-L1 CellsAdipocytesAdiponectinAdultAnimalsCohort StudiesDiabetes, GestationalDisease Models, AnimalFemaleHumansInfant, NewbornInsulinInsulin ResistanceIntra-Abdominal FatMaleMiceAdiponectinADIPOQ protein, humanAdipoq protein, mouseInsulinadipose tissuehumaninsulin resistance

Identifiers

PMID34519830
PMCPMC8684469
OpenAlexW3201415881

What OpenQuestion holds

Textmetadata
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.