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Related Experiment Videos

Calcitonin and estrogens.

D Agnusdei1, R Civitelli, A Camporeale

  • 1Istituto di Semeiotica Medica, Università di Siena, Italy.

Journal of Endocrinological Investigation
|September 1, 1990
PubMed
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Estrogen therapy boosts calcitonin (CT) production and bone density in postmenopausal women. This suggests CT mediates estrogen

Area of Science:

  • Endocrinology
  • Bone Biology
  • Reproductive Medicine

Background:

  • Postmenopausal osteoporosis (PMO) is primarily linked to estrogen deficiency.
  • Calcitonin (CT) is hypothesized to mediate estrogen's effects on bone, but this remains debated.
  • Understanding the estrogen-CT relationship is crucial for PMO pathogenesis.

Purpose of the Study:

  • To investigate the impact of hormone therapy on calcitonin (CT) secretory reserve in postmenopausal women.
  • To clarify the role of CT as a mediator of estrogen action in the context of PMO.

Main Methods:

  • A one-year study involving 12 postmenopausal women receiving estro/progesterone therapy and 12 receiving a placebo.
  • Calcitonin (CT) secretory reserve was assessed using a calcium infusion test.

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  • Bone mineral density was measured at vertebral and femoral sites.

    • Main Results:

    • Hormone therapy led to a progressive increase in blood CT levels, reaching a plateau at 9 months.
    • The hormone-treated group showed improved CT response to calcium stimulation.
    • Vertebral bone mass increased, and femoral bone density was maintained in the hormone-treated group, unlike the placebo group.

    Conclusions:

    • Estrogens significantly regulate calcitonin (CT) secretion in postmenopausal women.
    • Calcitonin (CT) likely acts as a mediator of estrogen's beneficial effects on bone.
    • Hormone therapy demonstrates potential in managing bone loss associated with estrogen deficiency.