Evidence map›Paper›PMID 26562417›Full record

ArticlePloS one2015

Early Life Exposure to Fructose Alters Maternal, Fetal and Neonatal Hepatic Gene Expression and Leads to Sex-Dependent Changes in Lipid Metabolism in Rat Offspring.

Zoe E Clayton, Mark H Vickers, Angelica Bernal, Cassandra Yap, Deborah M Sloboda

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
5.1field-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

25 citing papers in PubMed, 53 citations in OpenAlex.

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  11. Ovariectomy, but not orchiectomy, exacerbates metabolic syndrome after maternal high-fructose intake in adult offspring.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2021
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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 2 countries.

Zoe E ClaytonLiggins Institute and Gravida: National Centre for Growth and Development, University of Auckland, Aukland, New Zealand.
Mark H VickersLiggins Institute and Gravida: National Centre for Growth and Development, University of Auckland, Aukland, New Zealand.
Angelica BernalLiggins Institute and Gravida: National Centre for Growth and Development, University of Auckland, Aukland, New Zealand.
Cassandra YapLiggins Institute and Gravida: National Centre for Growth and Development, University of Auckland, Aukland, New Zealand.
Deborah M SlobodaDepartments of Biochemistry and Biomedical Sciences, McMaster University, Hamilton, Canada.
University of Auckland · NZMcMaster University · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimFructose consumption is associated with altered hepatic function and metabolic compromise and not surprisingly has become a focus for perinatal studies. We have previously shown that maternal fructose intake results in sex specific changes in fetal, placental and neonatal outcomes. In this follow-up study we investigated effects on maternal, fetal and neonatal hepatic fatty acid metabolism and immune modulation.

methodsPregnant rats were randomised to either control (CON) or high-fructose (FR) diets. Fructose was given in solution and comprised 20% of total caloric intake. Blood and liver samples were collected at embryonic day 21 (E21) and postnatal day (P)10. Maternal liver samples were also collected at E21 and P10. Liver triglyceride and glycogen content was measured with standard assays. Hepatic gene expression was measured with qPCR.

resultsMaternal fructose intake during pregnancy resulted in maternal hepatic ER stress, hepatocellular injury and increased levels of genes that favour lipogenesis. These changes were associated with a reduction in the NLRP3 inflammasome. Fetuses of mothers fed a high fructose diet displayed increased hepatic fructose transporter and reduced fructokinase mRNA levels and by 10 days of postnatal age, also have hepatic ER stress, and elevated IL1β mRNA levels. At P10, FR neonates demonstrated increased hepatic triglyceride content and particularly in males, associated changes in the expression of genes regulating beta oxidation and the NLRP3 inflammasome. Further, prenatal fructose results in sex-dependant changes in levels of key clock genes.

conclusionsMaternal fructose intake results in age and sex-specific alterations in maternal fetal and neonatal free fatty acid metabolism, which may be associated in disruptions in core clock gene machinery. How these changes are associated with hepatic inflammatory processes is still unclear, although suppression of the hepatic inflammasome, as least in mothers and male neonates may point to impaired immune sensing.

Indexed as

AnimalsAnimals, NewbornBody WeightCircadian Rhythm Signaling Peptides and ProteinsEndoplasmic Reticulum StressFatty Acids, NonesterifiedFemaleFollow-Up StudiesFructoseGene Expression Regulation, DevelopmentalGlycogenLipid MetabolismLiverMaleMaternal Nutritional Physiological PhenomenaPregnancyCircadian Rhythm Signaling Peptides and ProteinsFatty Acids, NonesterifiedFructoseGlycogen

Identifiers

PMID26562417
PMCPMC4643022
OpenAlexW2243575085

What OpenQuestion holds

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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.