Evidence map›Paper›PMID 30483218›Full record

ReviewFrontiers in endocrinology2018

Maternal Diabetes and Fetal Programming Toward Neurological Diseases: Beyond Neural Tube Defects.

Berenice Márquez-Valadez, Rocío Valle-Bautista, Guadalupe García-López, Néstor Fabián Díaz, Anayansi Molina-Hernández

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in endocrinology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 1 pooled it
2.4field-weighted citation impact, top 10% 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

22 citing papers in PubMed, 1 synthesis or guideline pooled it, 45 citations in OpenAlex.

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  15. Nutrient sensitive proteinLife science alliance · 2022
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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

5 authors at 2 institutions in 1 country.

Berenice Márquez-ValadezDepartment of Physiology and Cell Development, Instituto Nacional de Perinatología Isidro Espinosa de los Reyes, Mexico City, Mexico.
Rocío Valle-BautistaDepartment of Physiology and Cell Development, Instituto Nacional de Perinatología Isidro Espinosa de los Reyes, Mexico City, Mexico.
Guadalupe García-LópezDepartment of Physiology and Cell Development, Instituto Nacional de Perinatología Isidro Espinosa de los Reyes, Mexico City, Mexico.
Néstor Fabián DíazDepartment of Physiology and Cell Development, Instituto Nacional de Perinatología Isidro Espinosa de los Reyes, Mexico City, Mexico.
Anayansi Molina-HernándezDepartment of Physiology and Cell Development, Instituto Nacional de Perinatología Isidro Espinosa de los Reyes, Mexico City, Mexico.
Instituto Nacional de Perinatología · MXInstituto Politécnico Nacional · MX

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The purpose of this review was to search for experimental or clinical evidence on the effect of hyperglycemia in fetal programming to neurological diseases, excluding evident neural tube defects. The lack of timely diagnosis and the inadequate control of diabetes during pregnancy have been related with postnatal obesity, low intellectual and verbal coefficients, language and motor deficits, attention deficit with hyperactivity, problems in psychosocial development, and an increased predisposition to autism and schizophrenia. It has been proposed that several childhood or adulthood diseases have their origin during fetal development through a phenomenon called fetal programming. However, not all the relationships between the outcomes mentioned above and diabetes during gestation are clear, well-studied, or have been related to fetal programming. To understand this relationship, it is imperative to understand how developmental processes take place in health, in order to understand how the functional cytoarchitecture of the central nervous system takes place; to identify changes prompted by hyperglycemia, and to correlate them with the above postnatal impaired functions. Although changes in the establishment of patterns during central nervous system fetal development are related to a wide variety of neurological pathologies, the mechanism by which several maternal conditions promote fetal alterations that contribute to impaired neural development with postnatal consequences are not clear. Animal models have been extremely useful in studying the effect of maternal pathologies on embryo and fetal development, since obtaining central nervous system tissue in humans with normal appearance during fetal development is an important limitation. This review explores the state of the art on this topic, to help establish the way forward in the study of fetal programming under hyperglycemia and its impact on neurological and psychiatric disorders.

Indexed as

diabetesfetal programmingneurological disorderspregnancypsychiatric disease

Identifiers

PMID30483218
PMCPMC6243582
OpenAlexW2901790312

What OpenQuestion holds

Textmetadata
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.