Go to JCI Insight
  • About
  • Editors
  • Consulting Editors
  • For authors
  • Publication ethics
  • Alerts
  • Advertising
  • Job board
  • Subscribe
  • Contact
  • Current issue
  • Past issues
  • By specialty
    • COVID-19
    • Cardiology
    • Gastroenterology
    • Immunology
    • Metabolism
    • Nephrology
    • Neuroscience
    • Oncology
    • Pulmonology
    • Vascular biology
    • All ...
  • Videos
    • Conversations with Giants in Medicine
    • Author's Takes
  • Reviews
    • View all reviews ...
    • Next-Generation Sequencing in Medicine (Upcoming)
    • New Therapeutic Targets in Cardiovascular Diseases (Mar 2022)
    • Immunometabolism (Jan 2022)
    • Circadian Rhythm (Oct 2021)
    • Gut-Brain Axis (Jul 2021)
    • Tumor Microenvironment (Mar 2021)
    • 100th Anniversary of Insulin's Discovery (Jan 2021)
    • View all review series ...
  • Viewpoint
  • Collections
    • In-Press Preview
    • Commentaries
    • Concise Communication
    • Editorials
    • Viewpoint
    • Top read articles
  • Clinical Medicine
  • JCI This Month
    • Current issue
    • Past issues

  • Current issue
  • Past issues
  • Specialties
  • Reviews
  • Review series
  • Conversations with Giants in Medicine
  • Author's Takes
  • In-Press Preview
  • Commentaries
  • Concise Communication
  • Editorials
  • Viewpoint
  • Top read articles
  • About
  • Editors
  • Consulting Editors
  • For authors
  • Publication ethics
  • Alerts
  • Advertising
  • Job board
  • Subscribe
  • Contact
Top
  • View PDF
  • Download citation information
  • Send a comment
  • Share this article
  • Terms of use
  • Standard abbreviations
  • Need help? Email the journal
  • Top
  • Abstract
  • Version history
  • Article usage
  • Citations to this article

Advertisement

Free access | 10.1172/JCI109578

Evidence for Skeletal Resistance to Parathyroid Hormone in Magnesium Deficiency: STUDIES IN ISOLATED PERFUSED BONE

Jeffrey J. Freitag, Kevin J. Martin, Mary B. Conrades, Ezequiel Bellorin-Font, Steven Teitelbaum, Saulo Klahr, and Eduardo Slatopolsky

Renal Division, Department of Internal Medicine, Jewish Hospital, Washington University School of Medicine, St. Louis, Missouri 63110

Renal Division, Department of Pathology, Jewish Hospital, Washington University School of Medicine, St. Louis, Missouri 63110

Find articles by Freitag, J. in: JCI | PubMed | Google Scholar

Renal Division, Department of Internal Medicine, Jewish Hospital, Washington University School of Medicine, St. Louis, Missouri 63110

Renal Division, Department of Pathology, Jewish Hospital, Washington University School of Medicine, St. Louis, Missouri 63110

Find articles by Martin, K. in: JCI | PubMed | Google Scholar

Renal Division, Department of Internal Medicine, Jewish Hospital, Washington University School of Medicine, St. Louis, Missouri 63110

Renal Division, Department of Pathology, Jewish Hospital, Washington University School of Medicine, St. Louis, Missouri 63110

Find articles by Conrades, M. in: JCI | PubMed | Google Scholar

Renal Division, Department of Internal Medicine, Jewish Hospital, Washington University School of Medicine, St. Louis, Missouri 63110

Renal Division, Department of Pathology, Jewish Hospital, Washington University School of Medicine, St. Louis, Missouri 63110

Find articles by Bellorin-Font, E. in: JCI | PubMed | Google Scholar

Renal Division, Department of Internal Medicine, Jewish Hospital, Washington University School of Medicine, St. Louis, Missouri 63110

Renal Division, Department of Pathology, Jewish Hospital, Washington University School of Medicine, St. Louis, Missouri 63110

Find articles by Teitelbaum, S. in: JCI | PubMed | Google Scholar

Renal Division, Department of Internal Medicine, Jewish Hospital, Washington University School of Medicine, St. Louis, Missouri 63110

Renal Division, Department of Pathology, Jewish Hospital, Washington University School of Medicine, St. Louis, Missouri 63110

Find articles by Klahr, S. in: JCI | PubMed | Google Scholar

Renal Division, Department of Internal Medicine, Jewish Hospital, Washington University School of Medicine, St. Louis, Missouri 63110

Renal Division, Department of Pathology, Jewish Hospital, Washington University School of Medicine, St. Louis, Missouri 63110

Find articles by Slatopolsky, E. in: JCI | PubMed | Google Scholar

Published November 1, 1979 - More info

Published in Volume 64, Issue 5 on November 1, 1979
J Clin Invest. 1979;64(5):1238–1244. https://doi.org/10.1172/JCI109578.
© 1979 The American Society for Clinical Investigation
Published November 1, 1979 - Version history
View PDF
Abstract

Hypocalcemia during magnesium (Mg) depletion has been well described, but the precise mechanism(s) responsible for its occurrence is not yet fully understood. The hypocalcemia has been ascribed to decreased parathyroid hormone (PTH) secretion as well as skeletal resistance to PTH. Whereas the former is well established, controversy exists as to whether or not Mg depletion results in skeletal resistance to PTH. These studies examine the skeletal response to PTH in normal dogs and dogs fed a Mg-free diet for 4-6 mo. Isolated tibia from normal (serum Mg 1.83±0.1 mg/100 ml) and experimental dogs (serum Mg 1.34±0.15 mg/100 ml) were perfused with Krebs-Henseleit buffer during a constant infusion of 3 ng/ml of synthetic bovine PTH 1-34 (syn b-PTH 1-34). The arteriovenous (A-V) difference for immunoreactive PTH (iPTH) across seven normal bones was 37.5±3%. In contrast, the A-V difference for iPTH was markedly depressed to 10.1±1% across seven bones from Mg-depleted dogs. These findings correlated well with a biological effect (cyclic AMP [cAMP] production) of syn b-PTH 1-34 on bone. In control bones, cAMP production rose from a basal level of 5.8±0.2 to 17.5±0.7 pmol/min after syn b-PTH 1-34 infusion. In experimental bones, basal cAMP production was significantly lower than in controls, 4.5±0.1 pmol/min, and increased to only 7.1±0.4 pmol/min after syn b-PTH 1-34 infusion. Even when PTH concentrations were increased to 20 ng/ml, cAMP production by experimental bones was lower than in control bones perfused with 3 ng/ml. Histological examination of bones from Mg-deficient dogs showed a picture compatible with skeletal inactivity. These studies demonstrate decreased uptake of iPTH and diminished cAMP production by bone, which indicates skeletal resistance to PTH in chronic Mg deficiency.

Images.

Browse pages

Click on an image below to see the page. View PDF of the complete article

icon of scanned page 1238
page 1238
icon of scanned page 1239
page 1239
icon of scanned page 1240
page 1240
icon of scanned page 1241
page 1241
icon of scanned page 1242
page 1242
icon of scanned page 1243
page 1243
icon of scanned page 1244
page 1244
Version history
  • Version 1 (November 1, 1979): No description

Article tools

  • View PDF
  • Download citation information
  • Send a comment
  • Share this article
  • Terms of use
  • Standard abbreviations
  • Need help? Email the journal

Metrics

  • Article usage
  • Citations to this article

Go to

  • Top
  • Abstract
  • Version history
Advertisement
Advertisement

Copyright © 2022 American Society for Clinical Investigation
ISSN: 0021-9738 (print), 1558-8238 (online)

Sign up for email alerts