Evidence map›Paper›PMID 23690974›Full record

ArticlePloS one2013

Shared effects of genetic and intrauterine and perinatal environment on the development of metabolic syndrome.

Patricia M Vuguin, Kirsten Hartil, Michael Kruse, Harpreet Kaur, Chia-Lei Vivian Lin, Ariana Fiallo, Alan Scott Glenn, Avanee Patel, Lyda Williams, Yoshinori Seki and 2 more

Abstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
–field-weighted citation impact
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

17 citing papers in PubMed.

  1. Article
  2. Article
  3. Obesity Impairs Embryonic Myogenesis by Enhancing BMP Signaling within the Dermomyotome.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2021
    Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Effects of Maternal Obesity on Fetal Programming: Molecular Approaches.Cold Spring Harbor perspectives in medicine · 2015
    Review
  13. Article
  14. Critical periods of increased fetal vulnerability to a maternal high fat diet.Reproductive biology and endocrinology : RB&E · 2014
    Article
  15. Article
  16. Article
  17. Review
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

12 authors.

Patricia M VuguinDivision of Pediatric Endocrinology, Children's Hospital at Montefiore, Bronx, New York, United States of America. pvuguin@nshs.edu
Kirsten Hartil
Michael Kruse
Harpreet Kaur
Chia-Lei Vivian Lin
Ariana Fiallo
Alan Scott Glenn
Avanee Patel
Lyda Williams
Yoshinori Seki
Ellen B Katz
Maureen J Charron

Funding

GLUT4 AND CARDIAC METABOLISM AND PHYSIOLOGYR01HL058119 · NHLBI · YESHIVA UNIVERSITY · PI CHARRON, MAUREEN J · 1997 to 2004
$1.5M
Nutrition, Early Development and Glucose MetabolismK08HD042172 · NICHD · MONTEFIORE MEDICAL CENTER (BRONX, NY) · PI VUGUIN, PATRICIA MYRIAM · 2003 to 2007
$634k
Epigenetic Programming of Metabolic FlexibilityF31DK093332 · NIDDK · ALBERT EINSTEIN COLLEGE OF MEDICINE · PI WILLIAMS, LYDA · 2011 to 2013
$126k
NHLBI NIH HHS HL58119NHLBI NIH HHS R01 HL058119NICHD NIH HHS K08 HD042172NICHD NIH HHS K08-HD042172NIDDK NIH HHS DK47435NIDDK NIH HHS F31 DK093332NIDDK NIH HHS F31-DK093332
6 · The paper itself

Abstract

Genetic and environmental factors, including the in utero environment, contribute to Metabolic Syndrome. Exposure to high fat diet exposure in utero and lactation increases incidence of Metabolic Syndrome in offspring. Using GLUT4 heterozygous (G4+/-) mice, genetically predisposed to Type 2 Diabetes Mellitus, and wild-type littermates we demonstrate genotype specific differences to high fat in utero and lactation. High fat in utero and lactation increased adiposity and impaired insulin and glucose tolerance in both genotypes. High fat wild type offspring had increased serum glucose and PAI-1 levels and decreased adiponectin at 6 wks of age compared to control wild type. High fat G4+/- offspring had increased systolic blood pressure at 13 wks of age compared to all other groups. Potential fetal origins of adult Metabolic Syndrome were investigated. Regardless of genotype, high fat in utero decreased fetal weight and crown rump length at embryonic day 18.5 compared to control. Hepatic expression of genes involved in glycolysis, gluconeogenesis, oxidative stress and inflammation were increased with high fat in utero. Fetal serum glucose levels were decreased in high fat G4+/- compared to high fat wild type fetuses. High fat G4+/-, but not high fat wild type fetuses, had increased levels of serum cytokines (IFN-γ, MCP-1, RANTES and M-CSF) compared to control. This data demonstrates that high fat during pregnancy and lactation increases Metabolic Syndrome male offspring and that heterozygous deletion of GLUT4 augments susceptibility to increased systolic blood pressure. Fetal adaptations to high fat in utero that may predispose to Metabolic Syndrome in adulthood include changes in fetal hepatic gene expression and alterations in circulating cytokines. These results suggest that the interaction between in utero-perinatal environment and genotype plays a critical role in the developmental origin of health and disease.

Indexed as

AdiponectinAdiposityAnalysis of VarianceAnimalsBlood GlucoseBlood PressureBody CompositionCrosses, GeneticCytokinesDiet, High-FatFemaleFetal WeightGene Expression Regulation, DevelopmentalGenotypeGlucose Transporter Type 4HeterozygoteAdiponectinBlood GlucoseCytokinesGlucose Transporter Type 4Serpin E2Serpine2 protein, mouseSlc2a4 protein, mouse

Identifiers

PMID23690974
PMCPMC3656882

What OpenQuestion holds

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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.