# HUMAN CALCITONIN PHYSIOLOGY AND BONE DISEASE

> **NIH NIH R01** · MAYO CLINIC ROCHESTER · 1987 · $113,949

## Abstract

The role of calcitonin (CT) in human physiology is unknown.  Pharmacologic
doses of CT lower plasma calcium (Ca) and phosphate concentrations by
inhibiting bone resorption, suggesting that CT might protect against
excessive bone resorption and thus preserve bone mass.  If so, Ct
deficiency should lead to bone loss.  Interest in this possibility has been
piqued by the observations that women of all ages have lower plasma
immunoreactive CT (iCT) values than do men; that Ca-stimulated iCT levels
may decrease with age; and that estrogen therapy may raise iCT
concentrations.  However, the validity of existing iCT measurements on
normal plasma is uncertain, and there have been no systematic studies of
whether Ct deficiency, natural or surgically-induced, leads to excessive
bone loss.  The lack of definitive research is attributable in part to
methodologic problems which are now solved.  The overall hypothesis to be
tested in the proposed research is that subnormal levels of CT result in
increased bone resorption relative to formation, aggravating age- and
sex-related bone loss.  These studies are made possible by:  the
development here of a new technique for extraction, concentration, and
assay of plasma Ct monomer (hCT-M) at concentrations as low as 0.5-1.0
pg/ml; the availability of methods for noninvasive measurement of axial and
appendicular bone mass; and the presence of a modern bone histomorphometry
laboratory.  The extractable CT assay for the first time permits definition
of subnormal plasma CT concentrations.  The studies will compare levels of
hCT-M, the biological active form of circulating Ct, in normal adults of
both sexes and all ages, as well as in totally and
partially-thyroidectomized persons and osteoporotic women.  Basal and
stimulated hCT-M levels will be correlated with axial and appendicular bone
mass.  Metabolic clearance rate determinations for hCT-M will allow the
first estimates of true CT secretion rates.  We will assess the effects of
hCT-M deficiency on bone by histomorphometry.  Finally, we will determine
if estrogen therapy or high-calcium diets augment hCT-M secretion.  The
proposed research will provide information about the physiological role of
CT in human skeletal homeostasis can never be obtained from animal or in
vitro studies, and may offer valuable guidance in planning the treatment of
osteoporosis.

## Key facts

- **NIH application ID:** 3156327
- **Project number:** 5R01AR032526-05
- **Recipient organization:** MAYO CLINIC ROCHESTER
- **SAM.gov UEI:** Y2K4F9RPRRG7
- **Principal Investigator:** HUNTER HEATH
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1987
- **Award amount:** $113,949
- **Award type:** 5
- **Project period:** 1983-08-01 → 1988-07-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3156327

## Citation

> US National Institutes of Health, RePORTER application 3156327, HUMAN CALCITONIN PHYSIOLOGY AND BONE DISEASE (5R01AR032526-05). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/3156327. Licensed CC0.

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