# THE ROLE OF 1,25 DIHYDOXYVITAMIN D DURING FETAL LIFE

> **NIH NIH R01** · UNIVERSITY OF CINCINNATI · 1988 · $108,494

## Abstract

Many premature infants develop hypocalcemia during the first 24 hours of
life.  Of these, twenty percent may have subsequent skeletal
demineralization (osteopenia, rickets, long bone fractures).  The
underlying mechanisms are unknown but may involve abnormal vitamin D
metabolism.  The present proposal is designed to help clarify the role of
the hormonal form of vitamin D, namely, 1,25 dihydroxyvitamin D
(1,25(OH)2D) in the mineral economy of the fetus during intrauterine life.
The following specific questions will be addressed:  1) What are the
relative contributions of the fetal kidney and the placenta to fetal
circulating 1,25(OH)2D concentrations during intrauterine life?  2) Are
normal fetal circulating 1,25(OH)2D concentrations necessary for normal
intrauterine mineral metabolism?  3) Are the placenta and fetal bone
responsive target organs for the action of 1,25(OH)2D during fetal life?
In phase I of our study, singleton sheep fetuses will be instrumented at
110 days of gestation (term 145) to determine the 1,25(OH)2D synthetic
capacity of the fetal-placental unit.  This will be done by measurement of
the fetal Production and Metabolic Clearance Rates of 1,25(OH)2D and by
measurement of the in vivo placental synthesis rate using an in vivo
placental perfusion technique.  Normal gestationally related changes in
serum minerals and calcium regulating hormones will also be assessed
longitudinally from 110 days to 138 days of gestation when normal placental
mineral transfer and fetal mineral utilization rates will be determined.
In phase II of our study, we will use bilaterally nephrectomized fetuses to
determine the impact of loss of fetal renal 1,25(OH)2D synthetic capacity
on fetal serum 1,25(OH)2D and mineral concentrations, placental mineral
transfer and fetal mineral utilization rates.  Based on our previous
studies, fetal nephrectomy will result in fetal hypocalcemia,
hyperphosphatemia and reduced fetal serum 1,25(OH)2D concentrations.  We
hypothesize that these changes result from reduced 1,25(OH)2D-mediated
placental mineral transfer and disruption of normal bone mineralization and
will be largely corrected by treatment with exogenous 1,25(OH)2D therapy.
These combined studies will provide valuable insight into the functional
role of 1,25(OH)2D during fetal life, as it relates to the etiology of
hypocalcemia and bone demineralization in prematurity.

## Key facts

- **NIH application ID:** 3157622
- **Project number:** 5R01AR036487-03
- **Recipient organization:** UNIVERSITY OF CINCINNATI
- **SAM.gov UEI:** DZ4YCZ3QSPR5
- **Principal Investigator:** RICHARDUS ROSS
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1988
- **Award amount:** $108,494
- **Award type:** 5
- **Project period:** 1986-01-01 → 1988-12-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3157622

## Citation

> US National Institutes of Health, RePORTER application 3157622, THE ROLE OF 1,25 DIHYDOXYVITAMIN D DURING FETAL LIFE (5R01AR036487-03). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/3157622. Licensed CC0.

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