# Physiological and molecular metabolic consequences of fetal hyperglycemia

> **NIH NIH P20** · UNIVERSITY OF MISSISSIPPI MED CTR · 2020 · $276,388

## Abstract

Fetal hyperglycemia occurs when the developing fetus is exposed to high levels of glucose. For example
in humans, this is the case when the mother has diabetes. Fetal hyperglycemia is linked to health
complications for the fetus, including preeclamsia, fetal macrosomia and even fetal death. In addition,
fetal hyperglycemia also increases the risk for the individual to develop a variety of diseases later in life.
Adults exposed to fetal hyperglycemia are more susceptible to obesity, insulin resistance, type 2 diabetes,
cardiovascular diseases and several metabolic syndromes. To date, the physiological and molecular
mechanisms that underlie the link between fetal hyperglycemia and the adult sequelae are poorly
understood. The central goal of this project is to examine the physiological and molecular basis of
metabolic diseases in adults exposed to high levels of glucose only during embryogenesis. To accomplish
this goal, we have recently developed a zebrafish model of fetal hyperglycemia. Zebrafish offers several
advantages to complete this project. From a biological point of view, zebrafish embryos have the unique
feature of being a “closed system” i.e for the first 5 days of development, the embryo solely relies on the
yolk sac reserved deposited by the mother during ovulation and no energy exchange happens with the
exterior world prior the end of embryogenesis. Therefore, in zebrafish we can directly expose the embryos
to known concentration of glucose. Thus, specific aim 1 will test the hypothesis that fetal hyperglycemia
leads to an increase in BMI, fat mass and insulin resistance in adults fed normal diet. Specific aim 2 will
test the hypothesis that embryonic hyperglycemia increases glycolysis while decreasing β-oxidation in
embryos and in adults. Specific aim 3 will test the hypothesis that fetal hyperglycemia causes
hyperlipidemia and non-alcoholic fatty liver disease in adults. Specific aim 4 will test the hypothesis that
embryonic hyperglycemia increases the levels of circulating lipids and causes atherosclerosis later in life.
Successful completion of this proposal will lead to a better understanding of the physiological and
molecular consequences of fetal hyperglycemia and will help in defining strategic therapeutic
interventions to prevent the development of metabolic diseases in adults exposed to glucose during
embryogenesis.

## Key facts

- **NIH application ID:** 10154054
- **Project number:** 5P20GM104357-08
- **Recipient organization:** UNIVERSITY OF MISSISSIPPI MED CTR
- **Principal Investigator:** Yann Gibert
- **Activity code:** P20 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $276,388
- **Award type:** 5
- **Project period:** — → —

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10154054

## Citation

> US National Institutes of Health, RePORTER application 10154054, Physiological and molecular metabolic consequences of fetal hyperglycemia (5P20GM104357-08). Retrieved via AI Analytics 2026-05-28 from https://api.ai-analytics.org/grant/nih/10154054. Licensed CC0.

---

*[NIH grants dataset](/datasets/nih-grants) · CC0 1.0*