Role of the placental intrinsic clock as a central regulator of endocrine function and offspring growth
Active Project Grant Awarded Last action
- Award ID
- F32HD122330
- Recipient
-
Regents Of The University Of Minnesota UEI KABJZBBJ4B54
- Awarding agency
-
National Institute of Child Health and Human Development
National Institutes of Health, Department of Health and Human Services
- Obligated
- $76,300
Award facts
- Assistance listing
- 93.865 Child Health and Human Development Extramural Research
- Completion date 0% complete
- Place of performance
- Minneapolis, MN 55455, USA
Award details come from USAspending.gov.
Description
- Abstract
- The dohad hypothesis proposes that pregnancy is a key time period for programming offspring disease risk, including obesity. Maternal obesity increases the risk of metabolic disease in offspring, making IT an intergenerational condition. However, the underlying mechanisms remain poorly understood. One potential mechanism linking maternal obesity to suboptimal offspring health is disruption of the circadian rhythm of the placenta. While the placenta expresses all core clock genes, IT is unknown whether their expression and rhythmicity are regulated by maternal status and how this influences placental function and offspring metabolic health. The long-term goal of this research is to define how placental circadian gene expression and rhythmic hormone production generate an optimal in utero environment for healthy offspring development. The central hypothesis is that maternal obesity disrupts the placental intrinsic clock, impairing hormone secretion and increasing offspring susceptibility to metabolic disease. The main objective of this proposal is to determine how maternal obesity, characterized by hyperinsulinemia, affect placental clock gene expression and to test the functional consequences of clock disruption. Specific aim 1 will assess how maternal obesity and hyperinsulinemia alter the circadian expression of core placental clock genes and hormone secretion using in vivo mouse models and EX vivo hormone secretion assays. Specific aim 2 will determine how loss of the placental clock impacts placental growth, hormone production, and offspring metabolic health using a placenta- specific BMAL1 knockout mouse model. This F32 fellowship is innovative because no current studies directly investigate the regulation of the placental clock or its role in placental function and the programming of offspring metabolic health. Successful completion of this project will fill a critical GAP in our understanding of how early-life circadian disruption contributes to generational metabolic disease risk. IT will also advance the field by informing new strategies to prevent metabolic disease beginning in utero, improving maternal and child health. I will gain new expertise in circadian biology, dynamic hormone secretion assays, and pregnancy physiology, under the guidance of dedicated mentorship and structured career development. Training in grantsmanship, communications, and mentorship will also prepare me for a successful transition to an independent investigator. The university of minnesota offers an outstanding research environment, with leading expertise in metabolism, circadian biology, and perinatal physiology. My primary sponsor, DR. Emilyn alejandro, and CO- sponsor, DR. Ruifeng (RAY) CAO at rutgers university, provide complementary strengths in the proposed field of studies. Together with my scientific advisory committee, including DR. Sarah wernimont and DR. Germaine cornelissen-guillaume, they will ensure rigorous scientific training and oversight. This fellowship will strongly support my readiness to launch a successful career as an independent investigator.
Quick answers
Who received award F32HD122330?
F32HD122330 was awarded to Regents Of The University Of Minnesota by National Institute of Child Health and Human Development (National Institutes of Health) on December 1, 2026.
How much is award F32HD122330 worth?
$76,300 has been obligated on F32HD122330.
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