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Journal of Dairy Science Vol. 77 No. 7 1952-1963
© 1994 by American Dairy Science Association ®
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Parathyroid Hormone-Related Protein: A Regulated Calcium-Mobilizing Product of the Mammary Gland

Mark A. Thiede 1

1 Pfizer Central Research, Groton, CT 06340

Parathyroid hormone-related protein shares similarities in sequence and function with the endocrine hormone, parathyroid hormone. However, unlike parathyroid hormone, a product of the parathyroid glands, parathyroid hormone-related protein has a wide distribution in tissues, including the mammary gland. Although during pregnancy the expression of parathyroid hormone-related protein in the mammary gland is low, following birth, protein levels rise sharply in the gland in response to elevations in serum prolactin. Large amounts of parathyroid hormone-related protein are secreted into milk, suggesting a possible role in the neonate. Transient phosphaturia and elevations of parathyroid hormone-related protein in mammary vein plasma support a possible endocrine function for parathyroid hormone-related protein during lactation. Recent evidence suggests a local function for parathyroid hormone-related protein in the lactating mammary gland, and evidence exists that parathyroid hormone-related protein stimulates calcium secretion by the goat mammary gland. Parathyroid hormone-related protein, a putative vasodilator, is produced by the external nutrient vasculature of the mammary gland, and levels within this tissue are regulated during lactation. Infusion of parathyroid hormone-related protein into the ovine mammary artery increases gland blood flow, suggesting a role for the protein in modulation of mammary gland hemodynamics. Regulation of parathyroid hormone-related protein synthesis by the lactating gland, together with the protein's actions on regional blood flow and calcium secretion, support an important function in the mammary gland during lactogenesis.

Key Words: parathyroid hormone-related protein • mammary gland • calcium secretion • lactation

Submitted on June 16, 1993
Accepted on October 18, 1993




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