Evidence map›Paper›PMID 33913361›Full record

ArticleDiabetes & vascular disease research

Growth factors in the fetus and pre-adolescent offspring of hyperglycemic rats.

Lawrence Fordjour, Charles Cai, Vadim Bronshtein, Mayan Bronshtein, Jacob V Aranda, Kay D Beharry

Open access · diamondAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Diabetes & vascular disease research. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
1.0field-weighted citation impact, top 23% 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

1 citing paper in PubMed, 3 citations in OpenAlex.

  1. 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

6 authors at 1 institution in 1 country.

Lawrence FordjourDivision of Neonatal-Perinatal Medicine, Department of Pediatrics, State University of New York, Downstate Medical Center, Brooklyn, NY, USA.
Charles CaiDivision of Neonatal-Perinatal Medicine, Department of Pediatrics, State University of New York, Downstate Medical Center, Brooklyn, NY, USA.
Vadim BronshteinDivision of Neonatal-Perinatal Medicine, Department of Pediatrics, State University of New York, Downstate Medical Center, Brooklyn, NY, USA.
Mayan BronshteinDivision of Neonatal-Perinatal Medicine, Department of Pediatrics, State University of New York, Downstate Medical Center, Brooklyn, NY, USA.
Jacob V ArandaDivision of Neonatal-Perinatal Medicine, Department of Pediatrics, State University of New York, Downstate Medical Center, Brooklyn, NY, USA.
Kay D BeharryDivision of Neonatal-Perinatal Medicine, Department of Pediatrics, State University of New York, Downstate Medical Center, Brooklyn, NY, USA.ORCID 0000-0002-4129-475X
State University of New York · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMaternal hyperglycemia influences childhood metabolic syndrome, including obesity and hyperglycemia. We tested the hypothesis that the maternal hyperglycemia influences growth factors in the fetal and pre-adolescent offspring.

methodsHyperglycemia was induced in pregnant rats on embryonic day (E)16 using streptozocin followed by implantation with insulin or placebo pellets at embryonic day 18 (E18). Fetuses at E20 and pre-adolescent pups at postnatal day 14 (P14) were studied: (1) normal untreated controls (CTL) at E20; (2) hyperglycemic placebo-treated (HPT) at E20; (3) hyperglycemic insulin-treated (HIT) at E20; (4) CTL at P14; and (5) HIT at P14. Fetal and pre-adolescent growth factors were determined.

resultsBiomarkers of hypoxia were elevated in the HPT group at E20. This group did not survive to term. Maternal insulin improved fetal survival despite lower fetal body weight at E20, however, at normal birth (postnatal day 0 (P0)) and at P14, body weights and blood glucose were higher than CTL. These high levels correlated with aberrant growth factors. Maternal hyperglycemia influenced glucose-6-phosphate dehydrogenase, glucagon, insulin, interleukin-10, and leptin genes.

conclusionsThe impact of maternal hyperglycemia on pre-adolescent glucose and body weight was not a consequence of maternal overnutrition. This suggests an independent link which may affect offspring metabolic health in later life.

Indexed as

Prenatal Exposure Delayed EffectsAge FactorsAnimalsBiomarkersBlood GlucoseDiabetes, GestationalDisease Models, AnimalFemaleFetusGene Expression RegulationGestational AgeHypoglycemic AgentsInsulinIntercellular Signaling Peptides and ProteinsPregnancyRatsBiomarkersBlood GlucoseHypoglycemic AgentsInsulinIntercellular Signaling Peptides and ProteinsFetusglucosegrowth factorsinsulinmaternal hyperglycemia

Identifiers

PMID33913361
PMCPMC8482349
OpenAlexW3157602994

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Registered trials

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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.