Evidence map›Paper›PMID 25720389›Full record

ArticleDiabetes2015

Cellular Stress, Excessive Apoptosis, and the Effect of Metformin in a Mouse Model of Type 2 Diabetic Embryopathy.

Yanqing Wu, Fang Wang, Mao Fu, Cheng Wang, Michael J Quon, Peixin Yang

Open access · bronzeAbstract read
In one paragraph

Article in Diabetes, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
19.5field-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

51 citing papers in PubMed, 74 citations in OpenAlex.

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  18. Human embryonic stem cells as anWorld journal of stem cells · 2020
    Review
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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

6 authors at 2 institutions in 1 country.

Yanqing WuDepartment of Obstetrics, Gynecology and Reproductive Sciences, University of Maryland School of Medicine, Baltimore, MD.
Fang WangDepartment of Obstetrics, Gynecology and Reproductive Sciences, University of Maryland School of Medicine, Baltimore, MD.
Mao FuDepartment of Medicine, University of Maryland School of Medicine, Baltimore, MD.
Cheng WangDepartment of Obstetrics and Gynecology, Olson Center for Women's Health, University of Nebraska Medical Center, Omaha, NE.
Michael J QuonDepartment of Medicine, University of Maryland School of Medicine, Baltimore, MD.
Peixin YangDepartment of Obstetrics, Gynecology and Reproductive Sciences, University of Maryland School of Medicine, Baltimore, MD Department of Biochemistry and Molecular Biology, University of Maryland School of Medicine, Baltimore, MD pyang@upi.umaryland.edu.
University of Maryland, Baltimore · USUniversity of Nebraska Medical Center · US

Funding

Apoptotic Mechanism of Maternal Diabetes-Induced Neural Tube DefectsR01DK083243 · NIDDK · UNIVERSITY OF MARYLAND BALTIMORE · PI YANG, PEIXIN · 2010 to 2019
$3.1M
Molecular Signalling Pathways and Cellular Stress in Diabetic EmbryopathyR01DK103024 · NIDDK · UNIVERSITY OF MARYLAND BALTIMORE · PI REECE, E. ALBERT, YANG, PEIXIN · 2014 to 2017
$1.7M
Autophagy and its Regulation in Diabetic EmbryopathyR01DK101972 · NIDDK · UNIVERSITY OF MARYLAND BALTIMORE · PI YANG, PEIXIN · 2014 to 2017
$1.6M
Metabolic Cellular Stress and its Regulatory Mechanism in Diabetic EmbryopathyR56DK095380 · NIDDK · UNIVERSITY OF MARYLAND BALTIMORE · PI YANG, PEIXIN · 2012 to 2012
$150k
NIDDK NIH HHS R01 DK083243NIDDK NIH HHS R01-DK-083243NIDDK NIH HHS R01 DK101972NIDDK NIH HHS R01-DK-101972NIDDK NIH HHS R01 DK103024NIDDK NIH HHS R01-DK-103024NIDDK NIH HHS R56 DK095380NIDDK NIH HHS R56-DK-095380
6 · The paper itself

Abstract

Increasing prevalence of type 2 diabetes in women of childbearing age has led to a higher incidence of diabetes-associated birth defects. We established a model of type 2 diabetic embryopathy by feeding 4-week-old female mice a high-fat diet (HFD) (60% fat). After 15 weeks on HFD, the mice showed characteristics of type 2 diabetes mellitus (DM) and were mated with lean male mice. During pregnancy, control dams fed a normal diet (10% fat) were maintained on either normal diet or HFD, serving as a control group with elevated circulating free fatty acids. DM dams produced offspring at a rate of 11.3% for neural tube defect (NTD) formation, whereas no embryos in the control groups developed NTDs. Elevated markers of oxidative stress, endoplasmic reticulum stress, caspase activation, and neuroepithelial cell apoptosis (causal events in type 1 diabetic embryopathy) were observed in embryos of DM dams. DM dams treated with 200 mg/kg metformin in drinking water ameliorated fasting hyperglycemia, glucose intolerance, and insulin resistance with consequent reduction of cellular stress, apoptosis, and NTDs in their embryos. We conclude that cellular stress and apoptosis occur and that metformin effectively reduces type 2 diabetic embryopathy in a useful rodent model.

Indexed as

ApoptosisDisease Models, AnimalPregnancy in DiabeticsStress, PhysiologicalAnimalsCaspasesDiabetes Mellitus, Type 2Diet, High-FatEndoplasmic Reticulum StressFemaleMaleMetforminMiceMice, Inbred C57BLNeural Tube DefectsOxidative StressCaspasesMetformin

Identifiers

PMID25720389
PMCPMC4477360
OpenAlexW2023895936

What OpenQuestion holds

Texttitle and abstract
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.