Forskning
Udskriv Udskriv
Switch language
Region Hovedstaden - en del af Københavns Universitetshospital
Udgivet

Preserved postprandial suppression of bone turnover markers, despite increased fasting levels, in postmenopausal women

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

DOI

  1. The role of endogenous GIP and GLP-1 in postprandial bone homeostasis

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  2. High serum FSH is not a risk factor for low bone mineral density in infertile men

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  3. Consumption of nutrients and insulin resistance suppress markers of bone turnover in subjects with abdominal obesity

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  4. Bone resorption is unchanged by liraglutide in type 2 diabetes patients: A randomised controlled trial

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  1. A Neutralizing Monoclonal Antibody for Hospitalized Patients with Covid-19

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  2. Pharmacological but not physiological GDF15 suppresses feeding and the motivation to exercise

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  3. First wave of COVID-19 hospital admissions in Denmark: a Nationwide population-based cohort study

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

Vis graf over relationer

CONTEXT: Menopause leads to an increased bone turnover associated with a high risk of fractures. Bone turnover is inhibited by meal intake, to some extent mediated by gut hormones, and interventions based on these endocrine changes may have potential in future prevention of osteoporosis.

OBJECTIVE: To investigate whether postmenopausal women exhibit postprandial suppression of bone turnover markers to the same extent as premenopausal women, despite higher fasting levels. Furthermore, to assess whether menopausal differences in bone turnover markers are related to postmenopausal changes in plasma gut hormone levels.

METHODS: A cross-sectional study of 21 premenopausal, 9 perimenopausal, and 24 postmenopausal women between 45 and 60 years of age. Serum/plasma levels of bone turnover markers and gut hormones were investigated during a 120 min oral glucose tolerance test. Bone turnover markers included N-terminal propeptide of type-I procollagen (PINP, bone formation marker) and carboxyterminal collagen I crosslinks (CTX-I, bone resorption marker). Gut hormone secretion was evaluated from responses of glucagon-like peptide-1 (GLP-1), glucagon-like peptide-2 (GLP-2) and glucose-dependent insulinotropic polypeptide (GIP).

RESULTS: Fasting levels of s-CTX-I were increased in peri- and postmenopausal women compared to premenopausal women (p = 0.001). Despite higher fasting levels, the relative postprandial s-CTX-I suppression was comparable across menopausal status (p = 0.14). Fasting levels of s-PINP were also increased in postmenopausal women compared to premenopausal women (p < 0.001) with comparable and modest s-PINP suppression over menopause (p = 0.13). Postprandial plasma GLP-1 (p = 0.006) and GLP-2 (p = 0.01) were significantly increased in postmenopausal women compared to premenopausal women while GIP responses were slightly increased in the perimenopausal group (p = 0.02) but comparable between pre- and postmenopausal women. None of the postprandial gut hormone increases predicted postprandial bone turnover suppression in these women.

CONCLUSIONS: Glucose-induced suppression of bone turnover markers is preserved in postmenopausal women, despite significantly higher fasting values, indicating that CTX-I lowering treatments based on these postprandial mechanisms might be a feasible strategy to prevent postmenopausal osteoporosis.

OriginalsprogEngelsk
TidsskriftBone
Vol/bind143
Sider (fra-til)115612
ISSN8756-3282
DOI
StatusUdgivet - feb. 2021

Bibliografisk note

Copyright © 2020 Elsevier Inc. All rights reserved.

ID: 60799681