# Maternal regulation of diet-induced obesity in offspring.

> **NIH NIH R21** · MASSACHUSETTS GENERAL HOSPITAL · 2021 · $203,497

## Abstract

Project Summary
The incidence of obesity is rising globally and remains one of the biggest threats to adults and children.
Obesity rates are rapidly increasing among the young. Approximately 12.7 million, or 17% children in the US,
were reported to be either overweight or obese in 2015. Rising obesity rates have significant health
consequences, contributing to increased rates of metabolic diseases such as diabetes, steatosis,
hypertension, and heart disease. Obesity imposes a large economic burden on the individual, and on families
and nations. In 2014 the global economic impact of obesity was estimated to be US $2.0 trillion or 2.8% of the
global gross domestic product (GDP). In 2014, more than 2.1 billion people, nearly 30% of the global
population, were overweight or obese and 5% of the deaths worldwide were attributable to obesity. If the
incidence continues at this rate, almost half of the world's adult population will be overweight or obese by 2030.
Reducing obesity is a public health priority that has substantial health and economic benefits. As obesity is
accompanied by chronic low-grade inflammation in adipose tissues, mainly due to accumulated inflammatory
cells (Th1/Th17 cells, macrophages, etc) (2), recent studies, including our own work, provided evidence to
indicate that helminth-induced immunomodulation may prevent obesity onset and ameliorate the disease
severity. Our preliminary experiments have determined the potential maternal impact on developmental
programming affecting weight gain and adiposity in the offspring. We fed offspring of both normal control and
helminth-infected mother mice with HFD, and observed that offspring from helminth-infected mothers gained
significantly less body weight comparing with those from uninfected mothers. In addition to helminth-induced
maternal Th2 immune status, recent 16S rRNA gene sequencing analysis revealed that H. polygyrus infection
in mother mice significantly alters the composition of gut microbiome composition of offspring. Based on our
preliminary results, we hypothesize that the maternal helminth-induced Th2 immune response and associated
altered microbiota at critical periods of development may contribute to altered obesity in offspring through (a)
Th2-dependent conditioning of the developing immune system in the offspring or (b) helminth-induced
alterations of the maternal microbiota, which are then transmitted to the offspring to cause changes in
response to dietary treatment. The experiments proposed in this application will explore the mechanisms by
which maternal immune signals and microbiota modulate the development of obesity in offspring, and will
provide new insights that will be applicable to our understanding of the pathogenesis of obesity in children. A
clearer understanding of the immunoregulatory effects of maternal factors on the offspring may suggest new
therapeutic approaches for the prevention and treatment of metabolic disorders and obesity in both children
and a...

## Key facts

- **NIH application ID:** 10101620
- **Project number:** 5R21AI144738-02
- **Recipient organization:** MASSACHUSETTS GENERAL HOSPITAL
- **Principal Investigator:** Chien Wen Su
- **Activity code:** R21 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2021
- **Award amount:** $203,497
- **Award type:** 5
- **Project period:** 2020-02-07 → 2024-01-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10101620

## Citation

> US National Institutes of Health, RePORTER application 10101620, Maternal regulation of diet-induced obesity in offspring. (5R21AI144738-02). Retrieved via AI Analytics 2026-05-22 from https://api.ai-analytics.org/grant/nih/10101620. Licensed CC0.

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