# The lasting effect of maternal choline supplementation on lipid metabolism in mouse progeny affected by maternal obesity and gestational diabetes mellitus

> **NIH NIH SC3** · BROOKLYN COLLEGE · 2020 · $117,750

## Abstract

Project summary
 Maternal obesity affects more than one third of pregnant women in the U.S. and increases the risk of
gestational diabetes mellitus (GDM), defined by high blood glucose during pregnancy. Both maternal obesity
and GDM lead to fetal overgrowth, which subsequently increases the risk of obesity and cardio-metabolic
diseases of the offspring later in life. Despite the increase in overall adiposity, GDM-affected babies
demonstrate a paradoxical decrease in long-chain polyunsaturated fatty acids (LC-PUFAs) such as
docosahexaenoic acid (DHA) content in the cord blood, which likely affects DHA incorporation into the brain
and cognitive development. Choline is a semi-essential nutrient that affects different pathways of lipid
metabolism, such as mediating lipid transport and epigenetic control of lipid metabolic genes. Our prior studies
have demonstrated that maternal choline supplementation (MCS) prevented fetal overgrowth and enhanced
the expression of a LC-PUFA transporter in the placenta of mouse embryos from obese and GDM dams. In the
current study, we hypothesize that MCS in obese/GDM mice persistently reduces ectopic fat accumulation in
different organs while restoring LC-PUFA status in mouse progeny, thereby maintaining their metabolic health
later in life. Aim 1 will determine the persisting influence of MCS on lipid homeostasis in key organs regulating
metabolism. C57BL/6J female mice will be fed either a 60% high-fat (HF) diet to induce obesity and GDM or a
10% normal fat (NF) diet. Mice will be either supplemented with 25mM choline chloride in water or given
control plain drinking water 4 weeks prior to timed-mating until weaning of pups. We will dissect pups either at
weaning or after 6 weeks of post-weaning HF feeding (n=2 females and 2 males/dam and 10 dams/group) and
quantify lipoprotein-cholesterol, triglyceride, and fatty acid contents as well as lipid metabolic gene expression
in the liver, blood, skeletal muscle and gonadal fat pad. Aim 2 will determine the differential effect of MCS on
the metabolism of individual fatty acids, especially LC-PUFA in the offspring. A lipidomics approach will be
used to scan all fatty acid species. Aim 3 will delineate which pathway of choline metabolism participates in the
regulation of lipid homeostasis. We will use a deuterium labeled choline tracer to trace the metabolic fate of
choline in the body. We anticipate that MCS has long-lasting effects on promoting lipid catabolism and export,
while preserving LC-PUFA status in the offspring from obese/GDM dams and preventing them from HF diet-
induced obesity, fatty liver, and diabetes. This study will comprehensively determine the mechanism by which
MCS influences the lipid profile, distribution, and metabolism in mouse progeny affected by maternal
obesity/GDM. Results will provide insights into a cost-effective nutritional approach to counteract the lasting
adverse influence of maternal obesity /GDM on lipid homeostasis and metabolic heal...

## Key facts

- **NIH application ID:** 9903390
- **Project number:** 5SC3GM132010-02
- **Recipient organization:** BROOKLYN COLLEGE
- **Principal Investigator:** Xinyin Jiang
- **Activity code:** SC3 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $117,750
- **Award type:** 5
- **Project period:** 2019-04-01 → 2023-02-28

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/9903390

## Citation

> US National Institutes of Health, RePORTER application 9903390, The lasting effect of maternal choline supplementation on lipid metabolism in mouse progeny affected by maternal obesity and gestational diabetes mellitus (5SC3GM132010-02). Retrieved via AI Analytics 2026-05-23 from https://api.ai-analytics.org/grant/nih/9903390. Licensed CC0.

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