# Fetal Cardiomyocyte Fatty Acid Metabolism is impaired in Intrauterine Growth Restriction

> **NIH NIH F30** · OREGON HEALTH & SCIENCE UNIVERSITY · 2020 · $50,520

## Abstract

Project Summary
Babies who have suffered from placental insufficiency resulting in intrauterine growth restriction (IUGR) are
more vulnerable for metabolic and cardiovascular disease postnatally. However, the mechanisms underlying
this increased risk are poorly understood. Adaptations made by the fetus in response to placental insufficiency
changes the trajectory for cellular function with lifelong consequences. Fetal organs and systems must develop
and prepare for an extrauterine environment which involves an abrupt change in oxygen and nutritional
substrates. The fetal heart utilizes primarily glucose and lactate as fuel and transitions to primarily fatty acid
metabolism postnatally. This shift to fatty acid oxidation occurs concomitant with a doubling in oxygen levels at
birth. The physiological preparation of the myocardium for this transition to fatty acid oxidation is poorly
understood and the consequences of a suboptimal intrauterine environment on these processes is not known.
Umbilicoplacental embolization is a well-established, clinically relevant model of placental insufficiency in
sheep. This model leads to fetal hypoxemia, hypoglycemia and intrauterine growth restriction and has been
used to investigate the effect of IUGR on several organ systems. With respect to the heart, growth and
maturation is slowed, though little is known about the effects on metabolic pathways. Postnatally, IUGR sheep
have altered glucose tolerance and sensitivity. This metabolic change is likely to have been initiated in utero as
IUGR fetal sheep have impaired glucose oxidation. To the best of our knowledge, nothing is known about the
effect of IUGR on fatty acid processing. However, IUGR sheep have a tendency to be more obese compared
to control sheep, suggesting lipid handling may also be altered by placental insufficiency. Alterations to lipid
handling in utero could have lifelong consequences on cardiac function due to alterations in energy production.
The goal of this project is to determine whether fatty acid metabolism is impacted by placental insufficiency
using the umbilicoplacental embolization model in sheep. The mechanisms involved in fatty acid uptake and
metabolism will be systematically examined using an array of techniques including live cell imaging, lipidomics,
mitochondrial stress tests and gene and protein expression analysis. This study will determine how this
prenatal stress alters cardiomyocyte metabolism and may guide future therapies for improving nutrition
practices and/or cardiovascular health.

## Key facts

- **NIH application ID:** 9920004
- **Project number:** 5F30HD096812-02
- **Recipient organization:** OREGON HEALTH & SCIENCE UNIVERSITY
- **Principal Investigator:** Rachel Drake
- **Activity code:** F30 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $50,520
- **Award type:** 5
- **Project period:** 2019-04-01 → 2023-03-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/9920004

## Citation

> US National Institutes of Health, RePORTER application 9920004, Fetal Cardiomyocyte Fatty Acid Metabolism is impaired in Intrauterine Growth Restriction (5F30HD096812-02). Retrieved via AI Analytics 2026-05-22 from https://api.ai-analytics.org/grant/nih/9920004. Licensed CC0.

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