Evidence map›Paper›PMID 34203166›Full record

ArticleInternational journal of molecular sciences2021

Disruption of O-Linked N-Acetylglucosamine Signaling in Placenta Induces Insulin Sensitivity in Female Offspring.

Mackenzie Moore, Nandini Avula, Seokwon Jo, Megan Beetch, Emilyn U Alejandro

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2021. 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
6.3field-weighted citation impact, top 3% 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, 23 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Article
  6. Review
  7. The role of O-GlcNAcylation in development.Development (Cambridge, England) · 2023
    Article
  8. Article
  9. Review
  10. Early Life Nutrition and the Development of Offspring Metabolic Health.International journal of molecular sciences · 2022
    Article
  11. Cells · 2022
    Review
  12. Article
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 1 institution in 1 country.

Mackenzie MooreDepartment of Integrative Biology and Physiology, University of Minnesota Medical School, University of Minnesota, Minneapolis, MN 55455, USA.ORCID 0000-0002-7987-4274
Nandini AvulaDepartment of Integrative Biology and Physiology, University of Minnesota Medical School, University of Minnesota, Minneapolis, MN 55455, USA.
Seokwon JoDepartment of Integrative Biology and Physiology, University of Minnesota Medical School, University of Minnesota, Minneapolis, MN 55455, USA.
Megan BeetchDepartment of Integrative Biology and Physiology, University of Minnesota Medical School, University of Minnesota, Minneapolis, MN 55455, USA.
Emilyn U AlejandroDepartment of Integrative Biology and Physiology, University of Minnesota Medical School, University of Minnesota, Minneapolis, MN 55455, USA.ORCID 0000-0002-7941-8439
University of Minnesota Medical Center · US

Funding

TRAINING GRANT IN DIABETES, ENDOCRINOLOGY, &METABOLISMT32DK007203 · NIDDK · UNIVERSITY OF MINNESOTA TWIN CITIES · PI LISA Senye CHOW, Douglas G Mashek · 1986 to 2026
$4.3M
The role of O-linked N-Acetylglucosamine Homeostasis in Pancreatic Beta-cell Development and FunctionR01DK115720 · NIDDK · UNIVERSITY OF MINNESOTA · PI ALEJANDRO, EMILYN · 2018 to 2022
$1.9M
Training the Next Generation of Surgeon-Scientists in PancreatologyT32DK108733 · NIDDK · UNIVERSITY OF MINNESOTA · PI Srinath Chinnakotla, MASATO YAMAMOTO · 2017 to 2026
$1.4M
O-linked-N-acetylglucosamine Post-translational Modification in Pancreatic Beta-cells Regulating ER Stress and Mitochondrial FunctionR21DK112144 · NIDDK · UNIVERSITY OF MINNESOTA · PI ALEJANDRO, EMILYN · 2017 to 2019
$576k
Innate Immune Complement System and Developmental Programming of Functional β Cell MassR21HD100840 · NICHD · UNIVERSITY OF MINNESOTA · PI ALEJANDRO, EMILYN, REGAL, JEAN F. · 2020 to 2021
$425k
Eunice Kennedy Shriver National Institute of Child Health and Human Development R21HD100840NIDDK NIH HHS R01DK115720NIDDK NIH HHS R21DK112144NIDDK NIH HHS T32 DK007203NIDDK NIH HHS T32DK108733Regenerative Medicine Minnesota 00085565
6 · The paper itself

Abstract

Placental dysfunction can lead to fetal growth restriction which is associated with perinatal morbidity and mortality. Fetal growth restriction increases the risk of obesity and diabetes later in life. Placental O-GlcNAc transferase (OGT) has been identified as a marker and a mediator of placental insufficiency in the setting of prenatal stress, however, its role in the fetal programming of metabolism and glucose homeostasis remains unknown. We aim to determine the long-term metabolic outcomes of offspring with a reduction in placental OGT. Mice with a partial reduction and a full knockout of placenta-specific OGT were generated utilizing the Cre-Lox system. Glucose homeostasis and metabolic parameters were assessed on a normal chow and a high-fat diet in both male and female adult offspring. A reduction in placental OGT did not demonstrate differences in the metabolic parameters or glucose homeostasis compared to the controls on a standard chow. The high-fat diet provided a metabolic challenge that revealed a decrease in body weight gain (

Indexed as

AcetylglucosamineAnimalsBody WeightFemaleInsulinInsulin ResistanceMaleMiceN-AcetylglucosaminyltransferasesPlacentaPregnancyAcetylglucosamineInsulinN-Acetylglucosaminyltransferasesbeta-cellsfetal programmingglucose homeostasisisletmetabolismO-GlcNAcylationOGTO-linked N-acetylglucosamine (GlcNAc) transferasepancreasplacenta

Identifiers

PMID34203166
PMCPMC8267851
OpenAlexW3174714839

What OpenQuestion holds

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LicenceCC BY
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.