# Maternal obesity and hormonally-mediated markers of fetal development

> **NIH NIH R03** · MICHIGAN STATE UNIVERSITY · 2020 · $85,435

## Abstract

PROJECT SUMMARY
Maternal obesity is a major public health crisis, as >50% of women enter pregnancy overweight or obese. This
is alarming, as children of obese women are more likely to develop risk factors for metabolic disease (including
obesity and insulin resistance) and reproductive disorders (such as earlier menarche in daughters and poor
sperm quality in sons). Important early-life predictors of metabolic disease include birth weight and ponderal
index (measured from birth weight and length), while early-life predictors of reproductive function include the
ratio of the 2nd-to-4th finger lengths (2:4D) and the distance between the anus and genitals (anogenital distance,
AGD). In humans, altered 2:4D is associated with various reproductive abnormalities, while early-life AGD,
specifically, correlates with long-term reproductive health and capacity. While standard measures of fetal
development, including birth weight and ponderal index, are altered in newborns of obese women, it is not known
whether maternal obesity affects neonatal AGD or 2:4D. Therefore, we will leverage an ongoing pregnancy
cohort that has already measured AGD and 2:4D, and that has various measures of maternal body
composition, to investigate whether maternal obesity is associated with these early-life markers of
perturbed reproductive development. Based on previous studies, we hypothesize that male infants of
overweight/obese women will be feminized (have shorter AGD and longer 2:4D), while female infants of obese
women will be masculinized (have longer AGD and shorter 2:4D).
 Altered fetal growth, as measured by birth weight or ponderal index, is a risk factors for later-life obesity,
while newborn AGD and 2:4D are risk factors for altered reproductive capacity. Maternal levels of estrogen and
testosterone, two important steroid hormones in pregnancy, are critical for fetal development and growth. For
example, estrogen controls placental angiogenesis, which regulates nutrient transfer to the fetus, while elevated
maternal testosterone in a sheep model of pregnancy was shown to cause intrauterine growth restriction. AGD
and 2:4D, which are associated with reproductive capacity, are also sex steroid hormone-mediated; in males
and females, both are markers of in utero testosterone or estrogen exposures, and are sensitive to hormonal
disruption by maternal environmental factors. Findings from our pregnancy cohort suggest that maternal obesity
is also an endocrine disruptor, as estrogen and testosterone were lower in overweight/obese pregnant women
compared to normal-weight women, and associations with testosterone were only seen in women carrying
males. It is not known whether these hormonal shifts in obese women are partially responsible for the
well-known associations of maternal obesity with fetal developmental outcomes (birth weight and
ponderal index), or for the proposed associations with 2:4D ratio and AGD. Therefore, we will investigate
this important biological mecha...

## Key facts

- **NIH application ID:** 9876266
- **Project number:** 1R03HD100775-01
- **Recipient organization:** MICHIGAN STATE UNIVERSITY
- **Principal Investigator:** Rita S. Strakovsky
- **Activity code:** R03 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $85,435
- **Award type:** 1
- **Project period:** 2020-06-05 → 2022-05-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/9876266

## Citation

> US National Institutes of Health, RePORTER application 9876266, Maternal obesity and hormonally-mediated markers of fetal development (1R03HD100775-01). Retrieved via AI Analytics 2026-05-23 from https://api.ai-analytics.org/grant/nih/9876266. Licensed CC0.

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