Evidence map›Paper›PMID 30739252›Full record

ArticleCellular and molecular neurobiology2019

Severe Uncontrolled Maternal Hyperglycemia Induces Microsomia and Neurodevelopment Delay Accompanied by Apoptosis, Cellular Survival, and Neuroinflammatory Deregulation in Rat Offspring Hippocampus.

Francele Valente Piazza, Ethiane Segabinazi, André Luís Ferreira de Meireles, Filipe Mega, Christiano de Figueiredo Spindler, Otávio Américo Augustin, Gabriela Dos Santos Salvalaggio, Matilde Achaval, Maria Sol Kruse, Héctor Coirini and 1 more

Open access · greenAbstract read
In one paragraph

Article in Cellular and molecular neurobiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 2 pooled it
6.2field-weighted citation impact, top 4% 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

29 citing papers in PubMed, 2 syntheses or guidelines pooled it, 40 citations in OpenAlex.

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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

11 authors at 3 institutions in 2 countries.

Francele Valente PiazzaPrograma de Pós-Graduação em Neurociências, Instituto de Ciências Básicas da Saúde, Universidade Federal do Rio Grande do Sul, Sarmento Leite 500, Porto Alegre, RS, CEP 90050-170, Brazil. francele_valente@hotmail.com.
Ethiane SegabinaziPrograma de Pós-Graduação em Neurociências, Instituto de Ciências Básicas da Saúde, Universidade Federal do Rio Grande do Sul, Sarmento Leite 500, Porto Alegre, RS, CEP 90050-170, Brazil.
André Luís Ferreira de MeirelesPrograma de Pós-Graduação em Neurociências, Instituto de Ciências Básicas da Saúde, Universidade Federal do Rio Grande do Sul, Sarmento Leite 500, Porto Alegre, RS, CEP 90050-170, Brazil.
Filipe MegaPrograma de Pós-Graduação em Neurociências, Instituto de Ciências Básicas da Saúde, Universidade Federal do Rio Grande do Sul, Sarmento Leite 500, Porto Alegre, RS, CEP 90050-170, Brazil.
Christiano de Figueiredo SpindlerPrograma de Pós-Graduação em Neurociências, Instituto de Ciências Básicas da Saúde, Universidade Federal do Rio Grande do Sul, Sarmento Leite 500, Porto Alegre, RS, CEP 90050-170, Brazil.
Otávio Américo AugustinLaboratório de Histofisiologia Comparada, Departamento de Ciências Morfológicas, Instituto de Ciências Básicas da Saúde, Universidade Federal do Rio Grande do Sul, Sarmento Leite 500, sala 142, Porto Alegre, RS, CEP 90050-170, Brazil.
Gabriela Dos Santos SalvalaggioLaboratório de Histofisiologia Comparada, Departamento de Ciências Morfológicas, Instituto de Ciências Básicas da Saúde, Universidade Federal do Rio Grande do Sul, Sarmento Leite 500, sala 142, Porto Alegre, RS, CEP 90050-170, Brazil.
Matilde AchavalPrograma de Pós-Graduação em Neurociências, Instituto de Ciências Básicas da Saúde, Universidade Federal do Rio Grande do Sul, Sarmento Leite 500, Porto Alegre, RS, CEP 90050-170, Brazil.
Maria Sol KruseLaboratorio de Neurobiología, Instituto de Biología y Medicina Experimental, Vuelta de Obligado 2490, C1428ADN, Buenos Aires, Argentina.
Héctor CoiriniLaboratorio de Neurobiología, Instituto de Biología y Medicina Experimental, Vuelta de Obligado 2490, C1428ADN, Buenos Aires, Argentina.
Simone MarcuzzoPrograma de Pós-Graduação em Neurociências, Instituto de Ciências Básicas da Saúde, Universidade Federal do Rio Grande do Sul, Sarmento Leite 500, Porto Alegre, RS, CEP 90050-170, Brazil.
Universidade Federal do Rio Grande do Sul · BRExperimental Medicine and Biology Institute · ARUniversity of Buenos Aires · AR

Funding

Fundação de Amparo à Pesquisa do Estado do Rio Grande do Sul 002097-2552/13-6?1
6 · The paper itself

Abstract

Maternal diabetes constitutes an unfavorable intrauterine environment for offspring development. Although it is known that diabetes can cause brain alterations and increased risk for neurologic disorders, the relationship between neuroimmune activation, brain changes, and neurodevelopment deficits in the offspring remains unclear. In order to elucidate the short- and long-term biological basis of the developmental outcomes caused by the severe uncontrolled maternal hyperglycemia, we studied apoptosis, neurogenesis, and neuroinflammation pathways in the hippocampus of neonates and young rats born to diabetic dams. Diabetes was induced on gestational day 5 by an injection of streptozotocin. Evaluations of milestones, body growth, and inhibitory avoidance were performed to monitor the offspring development and behavior. Hippocampal modifications were studied through cellular survival by BrdU in the dentate gyrus, expression of apoptosis-regulatory proteins (procaspase 3, caspase 3, and Bcl-2), BDNF, and neuroinflammatory modulation by interleukins, MHC-I, MHC-II, Iba-1, and GFAP proteins. Severe maternal diabetes caused microsomia and neurodevelopmental delay in pups and decrease of Bcl-2, procaspase 3, and caspase 3 in the hippocampus. Moreover, in a later stage of development, it was found an increase of TNF-α and a decrease of procaspase 3, caspase 3, MHC-I, IL-1β, and BDNF in the hippocampus, as well as impairment in cellular survival in the dentate gyrus. This study showed significant short- and long-term commitments on the development, apoptosis, cell survival, and neuroinflammation in the offspring hippocampus induced by severe uncontrolled maternal hyperglycemia. The data reinforce the need for treatment of maternal hyperglycemic states during pregnancy and breast-feeding.

Indexed as

ApoptosisAdrenal GlandsAnimalsAnimals, NewbornAvoidance LearningBody WeightBrain-Derived Neurotrophic FactorCell SurvivalCytokinesFemaleGlucose Tolerance TestHippocampusHyperglycemiaInflammationLiverOrgan SizeBrain-Derived Neurotrophic FactorCytokinesStreptozocinAstrocytesBcl-2BrdUCaspase 3Gestational diabetesMicroglia

Identifiers

PMID30739252
PMCPMC11469913
OpenAlexW2911921180

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.