Evidence map›Paper›PMID 28751453›Full record

ReviewThe Journal of endocrinology2017

Maternal modifiers of the infant gut microbiota: metabolic consequences.

Christopher M Mulligan, Jacob E Friedman

Open access · bronzeAbstract readReview
In one paragraph

Review in The Journal of endocrinology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed, 3 pooled it
10.6field-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, 3 syntheses or guidelines pooled it, 101 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. The role of gut micorbiome in obesity and diabetes.World journal of pediatrics : WJP · 2019
    Pooled it
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  16. Ecoevolutionary processes structure milk microbiomes across the mammalian tree of life.Proceedings of the National Academy of Sciences of the United States of America · 2023
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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

2 authors at 1 institution in 1 country.

Christopher M MulliganSection of NeonatologyDepartment of Pediatrics, University of Colorado Anschutz Medical Campus, Aurora, Colorado, USA.
Jacob E FriedmanSection of NeonatologyDepartment of Pediatrics, University of Colorado Anschutz Medical Campus, Aurora, Colorado, USA jed.friedman@ucdenver.edu.
University of Colorado Anschutz Medical Campus · US

Funding

PILOT STUDY--SUBSTRATE METABOLISM IN EXTREMELY LOW BIRTH WEIGHT INFANTSP30DK048520 · NIDDK · UNIVERSITY OF COLORADO DENVER · PI Edward L Melanson · 1995 to 2026
$32.6M
MECHANISMS FOR FETAL HEPATIC PROGRAMMING IN THE NON-HUMAN PRIMATE (NHP)R01DK078590 · NIDDK · UNIVERSITY OF COLORADO DENVER · PI FRIEDMAN, JACOB E · 2007 to 2010
$1.5M
NIDDK NIH HHS P30 DK048520NIDDK NIH HHS R01 DK078590
6 · The paper itself

Abstract

Transmission of metabolic diseases from mother to child is multifactorial and includes genetic, epigenetic and environmental influences. Evidence in rodents, humans and non-human primates support the scientific premise that exposure to maternal obesity or high-fat diet during pregnancy creates a long-lasting metabolic signature on the infant innate immune system and the juvenile microbiota, which predisposes the offspring to obesity and metabolic diseases. In neonates, gastrointestinal microbes introduced through the mother are noted for their ability to serve as direct inducers/regulators of the infant immune system. Neonates have a limited capacity to initiate an immune response. Thus, disruption of microbial colonization during the early neonatal period results in disrupted postnatal immune responses that highlight the neonatal period as a critical developmental window. Although the mechanisms are poorly understood, increasing evidence suggests that maternal obesity or poor diet influences the development and modulation of the infant liver and other end organs through direct communication via the portal system, metabolite production, alterations in gut barrier integrity and the hematopoietic immune cell axis. This review will focus on how maternal obesity and dietary intake influence the composition of the infant gut microbiota and how an imbalance or maladaptation in the microbiota, including changes in early pioneering microbes, might contribute to the programming of offspring metabolism with special emphasis on mechanisms that promote chronic inflammation in the liver. Comprehension of these pathways and mechanisms will elucidate our understanding of developmental programming and may expand the avenue of opportunities for novel therapeutics.

Indexed as

Gastrointestinal MicrobiomeAnimalsFemaleHumansInfantMetabolic DiseasesPregnancyPrenatal Exposure Delayed EffectsmetabolismNAFLDneonatalobesitypregnancy

Identifiers

PMID28751453
PMCPMC5568816
OpenAlexW2739563526

What OpenQuestion holds

Textmetadata
LicenceTDM
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.