# Epigenetic Regulation of fetal BAT Development via Maternal N-3 PUFA intake

> **NIH NIH R21** · UNIVERSITY OF MASSACHUSETTS AMHERST · 2020 · $199,375

## Abstract

PROJECT SUMMARY
Childhood obesity predisposes adults for metabolic susceptibility to obesity and type 2 diabetes. Therefore,
identifying early regulatory factors to prevent childhood obesity is critical for combating the current obesity
epidemic. Brown adipose tissue (BAT) is a specialized fat that dissipates excess energy into heat counteracting
obesity. Current research renews the metabolic function of BAT demonstrating that BAT is a crucial regulator in
maintaining energy balance by increasing thermogenic energy expenditure. Given that BAT is formed prenatally
and its retainment alters propensity for weight gain in later life, enhancement of BAT development during
pregnancy holds promise for prevention of childhood obesity. The long-term goal of this proposal is to develop
therapeutic strategies to combat obesity by boosting BAT activity. The objective of this application is to
evaluate the role of maternal supply of n-3 PUFA as a molecular driver to stimulate prenatal BAT formation and
mitigate metabolic susceptibility to obesity in offspring. Based on preliminary results, the central hypothesis to
test is that maternal supply of n-3 PUFA promotes the embryonic BAT development via histone acetylation and
microRNA (miRNA)-mediated epigenetic mechanisms, which results in increased postnatal BAT retainment and
decreased risk of obesity and T2D in later life. This project will pursue the two specific aims. Specific Aim1 will
determine the mechanism by which maternal n-3 PUFA intake modulates the transcriptional reprogramming of
fetal BAT. We will evaluate the impact of maternal n-3 PUFA nutrition on epigenetic modification including the
genome-wide H3K27Ac pattern and pri-miRNA processing efficiency. Specific Aim2 will identify the metabolic
significance of maternal n-3 PUFA supplementation in postnatal BAT retainment and long-term metabolic
ramification. The proposed work will explore a novel signaling pathway that links maternal n-3 PUFA intake to
prenatal BAT reprogramming. Results of this application will provide seminal evidence establishing the
innovative role of prenatal exposure of n-3 PUFA on BAT formation at the time of birth, post-natal retention, and
its long-term metabolic implications.

## Key facts

- **NIH application ID:** 10067215
- **Project number:** 7R21HD094273-02
- **Recipient organization:** UNIVERSITY OF MASSACHUSETTS AMHERST
- **Principal Investigator:** Soonkyu Chung
- **Activity code:** R21 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $199,375
- **Award type:** 7
- **Project period:** 2019-01-01 → 2021-12-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10067215

## Citation

> US National Institutes of Health, RePORTER application 10067215, Epigenetic Regulation of fetal BAT Development via Maternal N-3 PUFA intake (7R21HD094273-02). Retrieved via AI Analytics 2026-06-12 from https://api.ai-analytics.org/grant/nih/10067215. Licensed CC0.

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