Serum total testosterone is associated with phosphate and calcium excretion in response to oral phosphate loading in healthy middle‐aged males

Author:

Sharma Jaya K.1ORCID,Turner Mandy E.1,Paynter Amanda S.1,Norman Patrick A.2,White Christine A.3,Ward Emilie C.1,Adams Michael A.1,Holden Rachel M.13

Affiliation:

1. Department of Biomedical and Molecular Sciences Queen's University Kingston Ontario Canada

2. Kingston General Health Research Institute Kingston Health Sciences Centre Kingston Ontario Canada

3. Department of Medicine Queen's University Kingston Ontario Canada

Abstract

AbstractAndrogen receptors are expressed in the kidney and serum testosterone is negatively associated with serum phosphate in males, suggesting a role of testosterone in renal phosphate handling. In this cross‐sectional study, we examined the association of serum total and free testosterone with acute phosphate and calcium excretion in males in response to an oral phosphate challenge. Thirty‐five healthy adult males with normal baseline testosterone levels consumed a 500 mg phosphorus drink and the urinary excretion of minerals, as well as levels of relevant circulating parameters, were assessed at baseline and hourly for 4 h. Serum total testosterone was positively associated with overall phosphate excretion (r = 0.35, p = 0.04) and calcium excretion (r = 0.44, p = 0.00) in response to the challenge. Serum free testosterone was positively associated with post‐challenge calcium excretion (r = 0.34, p = 0.048), but significance was not reached for phosphate excretion (r = 0.31, p = 0.07). Serum total and free testosterone were not associated with parathyroid hormone, fibroblast growth factor‐23, or vitamin D—key factors implicated in phosphate and calcium regulation. Overall, higher serum total testosterone levels in healthy middle‐aged males are associated with a greater capacity to acutely excrete phosphate and calcium after a single oral phosphate challenge, suggesting potential ramifications of testosterone deficiency related to mineral homeostasis.

Publisher

Wiley

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