Evidence map›Paper›PMID 40437764›Full record

ArticleThe Journal of physiology2026

Fetal glucose availability: a key regulator of the metabolic, hormonal and contractility profiles of the fetal sheep heart.

Melanie R Bertossa, Jack R T Darby, Stacey L Holman, Steven K S Cho, Ashley S Meakin, Mitchell C Lock, Jordan A Minns, Michael D Wiese, Christopher K Macgowan, Mike Seed and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The Journal of physiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Review
  2. Article
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.

Melanie R BertossaEarly Origins of Adult Health Research Group, Health and Biomedical Innovation, UniSA: Clinical and Health Sciences, University of South Australia, Adelaide, South Australia, Australia.ORCID https://orcid.org/0000-0002-6598-1503
Jack R T DarbyEarly Origins of Adult Health Research Group, Health and Biomedical Innovation, UniSA: Clinical and Health Sciences, University of South Australia, Adelaide, South Australia, Australia.ORCID https://orcid.org/0000-0001-7114-3920
Stacey L HolmanEarly Origins of Adult Health Research Group, Health and Biomedical Innovation, UniSA: Clinical and Health Sciences, University of South Australia, Adelaide, South Australia, Australia.ORCID https://orcid.org/0000-0002-6326-4797
Steven K S ChoEarly Origins of Adult Health Research Group, Health and Biomedical Innovation, UniSA: Clinical and Health Sciences, University of South Australia, Adelaide, South Australia, Australia.ORCID https://orcid.org/0000-0002-4776-0192
Ashley S MeakinEarly Origins of Adult Health Research Group, Health and Biomedical Innovation, UniSA: Clinical and Health Sciences, University of South Australia, Adelaide, South Australia, Australia.ORCID https://orcid.org/0000-0003-2806-6274
Mitchell C LockEarly Origins of Adult Health Research Group, Health and Biomedical Innovation, UniSA: Clinical and Health Sciences, University of South Australia, Adelaide, South Australia, Australia.ORCID https://orcid.org/0000-0002-3594-1455
Jordan A MinnsEarly Origins of Adult Health Research Group, Health and Biomedical Innovation, UniSA: Clinical and Health Sciences, University of South Australia, Adelaide, South Australia, Australia.ORCID https://orcid.org/0000-0001-7353-1476
Michael D WieseEarly Origins of Adult Health Research Group, Health and Biomedical Innovation, UniSA: Clinical and Health Sciences, University of South Australia, Adelaide, South Australia, Australia.
Christopher K MacgowanTranslational Medicine, Hospital for Sick Children, Toronto, Canada.ORCID https://orcid.org/0000-0002-7016-0662
Mike SeedDivision of Cardiology, Hospital for Sick Children, Toronto, Canada.ORCID https://orcid.org/0000-0001-7330-234X
Janna L MorrisonEarly Origins of Adult Health Research Group, Health and Biomedical Innovation, UniSA: Clinical and Health Sciences, University of South Australia, Adelaide, South Australia, Australia.ORCID https://orcid.org/0000-0002-8602-8519

Funding

Australia Research Council Future Fellowship Level 3 FT170100431MRB is funded by an Australian Research Training Program Scholarship
6 · The paper itself

Abstract

There is an association between fetal growth restriction (FGR) and a poor lifetime cardiac health trajectory. Defining the underlying mechanisms will aid in developing interventions to decrease the contribution of FGR-born offspring to the global burden of cardiovascular disease. One cause of FGR is maternal undernutrition. In late-gestation undernutrition (LGUN) fetal glucose supply, a main energy source for the fetal heart, is reduced. This may be a key contributor to altered fetal cardiac development; thus restoration of fetal glucose availability in the LGUN setting may be a viable target for intervention. To investigate the role of glucose availability in fetal heart development, we utilized an established pregnant sheep model of LGUN (50% global nutrient restriction) with or without a continuous intrafetal glucose infusion. LGUN reduced fetal plasma glucose concentrations, resulting in brain sparing that was normalized by intrafetal glucose infusion. LGUN decreased the protein abundance of oxidative phosphorylation complexes 1 and 3; however glucose infusion returned complex 3 abundance to that of controls. LGUN increased the phosphorylation of contractility and hypertrophy marker CAMKII, which was associated with increased left ventricular cardiac output; however intrafetal glucose infusion normalized CAMKII. Our findings demonstrate that glucose plays a specific role in regulating cardiac development in utero, highlighting the importance of adequate maternal nutrition in late gestation. KEY POINTS: Maternal late-gestation undernutrition (LGUN) reduces fetal plasma glucose concentrations. To investigate the role of glucose availability in fetal left ventricle (LV) development, we assessed whether LGUN-induced alterations in the contractility, metabolic and hormonal profiles can be ameliorated in LGUN fetuses receiving glucose infusion (LGUN+G). Relative brain weight was increased in LGUN compared to controls and restored in LGUN+G despite fetal glucose infusion only partially normalizing fetal plasma glucose concentrations to that of controls. LGUN decreased cardiac oxidative phosphorylation (OXPHOS)complex 1 and 3 abundance, and LGUN+G restored complex 3 to that of controls. LGUN increased the activation of the contractility marker, Ca

Indexed as

Fetal Growth RetardationFetal HeartGlucoseMyocardial ContractionAnimalsBlood GlucoseCalcium-Calmodulin-Dependent Protein Kinase Type 2Developmental Origins of Health and DiseaseFemalePregnancySheepBlood GlucoseCalcium-Calmodulin-Dependent Protein Kinase Type 2Glucosecardiovascular diseasefetal growth restrictionfetuslate gestationleft ventriclematernal undernutrition

Identifiers

PMID40437764
PMCPMC13481007

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Registered trials

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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.