Familial longevity is associated with lower baseline bone turnover but not differences in bone turnover in response to rhTSH

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Familial longevity is associated with lower baseline bone turnover but not differences in bone turnover in response to rhTSH. / Zutinic, Ana; Roelfsema, Ferdinand; Pijl, Hanno; Ballieux, Bart E.; Westendorp, Rudi G.J.; Blauw, Gerard J.; van Heemst, Diana.

In: Aging, Vol. 13, No. 17, 2021, p. 21029-21039.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

Zutinic, A, Roelfsema, F, Pijl, H, Ballieux, BE, Westendorp, RGJ, Blauw, GJ & van Heemst, D 2021, 'Familial longevity is associated with lower baseline bone turnover but not differences in bone turnover in response to rhTSH', Aging, vol. 13, no. 17, pp. 21029-21039. https://doi.org/10.18632/aging.203511

APA

Zutinic, A., Roelfsema, F., Pijl, H., Ballieux, B. E., Westendorp, R. G. J., Blauw, G. J., & van Heemst, D. (2021). Familial longevity is associated with lower baseline bone turnover but not differences in bone turnover in response to rhTSH. Aging, 13(17), 21029-21039. https://doi.org/10.18632/aging.203511

Vancouver

Zutinic A, Roelfsema F, Pijl H, Ballieux BE, Westendorp RGJ, Blauw GJ et al. Familial longevity is associated with lower baseline bone turnover but not differences in bone turnover in response to rhTSH. Aging. 2021;13(17):21029-21039. https://doi.org/10.18632/aging.203511

Author

Zutinic, Ana ; Roelfsema, Ferdinand ; Pijl, Hanno ; Ballieux, Bart E. ; Westendorp, Rudi G.J. ; Blauw, Gerard J. ; van Heemst, Diana. / Familial longevity is associated with lower baseline bone turnover but not differences in bone turnover in response to rhTSH. In: Aging. 2021 ; Vol. 13, No. 17. pp. 21029-21039.

Bibtex

@article{c744a1ddd3644a5cb7ddef4a9ff92e5c,
title = "Familial longevity is associated with lower baseline bone turnover but not differences in bone turnover in response to rhTSH",
abstract = "Context: Offspring from long-lived families have a different thyroid status than controls, characterised by higher circulating levels of thyroid stimulating hormone (TSH) and similar levels of thyroid hormone. Expression of the TSH receptor has previously been observed on various extrathyroidal tissues, including bone. However, potential physiological consequences of differences in circulating TSH as observed in familial longevity on bone tissue remain unclear. Objective: Based on the hypothesis that TSH may inhibit bone resorption, we explored whether offspring of long-lived families have lower bone turnover than controls at baseline as well as following a challenge with recombinant human TSH (rhTSH). Methods: Bone turnover markers CTX and P1NP were measured in fasted morning samples from 14 offspring and 12 controls at baseline and at 24 hour intervals following 0.1 mg rhTSH i.m. administration for four consecutive days. Results: At baseline, mean (SEM) CTX was 0.32 (0.03) ng/ml in offspring and 0.50 (0.04) ng/ml in controls, p < 0.01, whereas mean (SEM) P1NP was 39.6 (3.2) ng/ml in offspring and 61.8 (6.6) ng/ml in controls, p < 0.01. Following rhTSH administration, both CTX and P1NP levels transiently increased over time and normalized towards baseline after 72 h (general linear modelling: CTX time p = 0.01, P1NP time p < 0.01); the response was similar between offspring and controls. Conclusions: Bone turnover markers were lower at baseline in offspring from long-lived families than in controls but increased similarly following an rhTSH challenge.",
keywords = "bone metabolism, longevity, rhTSH, thyroid",
author = "Ana Zutinic and Ferdinand Roelfsema and Hanno Pijl and Ballieux, {Bart E.} and Westendorp, {Rudi G.J.} and Blauw, {Gerard J.} and {van Heemst}, Diana",
note = "Publisher Copyright: {\textcopyright} 2021 Zutinic et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited",
year = "2021",
doi = "10.18632/aging.203511",
language = "English",
volume = "13",
pages = "21029--21039",
journal = "Aging",
issn = "1945-4589",
publisher = "Impact Journals LLC",
number = "17",

}

RIS

TY - JOUR

T1 - Familial longevity is associated with lower baseline bone turnover but not differences in bone turnover in response to rhTSH

AU - Zutinic, Ana

AU - Roelfsema, Ferdinand

AU - Pijl, Hanno

AU - Ballieux, Bart E.

AU - Westendorp, Rudi G.J.

AU - Blauw, Gerard J.

AU - van Heemst, Diana

N1 - Publisher Copyright: © 2021 Zutinic et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited

PY - 2021

Y1 - 2021

N2 - Context: Offspring from long-lived families have a different thyroid status than controls, characterised by higher circulating levels of thyroid stimulating hormone (TSH) and similar levels of thyroid hormone. Expression of the TSH receptor has previously been observed on various extrathyroidal tissues, including bone. However, potential physiological consequences of differences in circulating TSH as observed in familial longevity on bone tissue remain unclear. Objective: Based on the hypothesis that TSH may inhibit bone resorption, we explored whether offspring of long-lived families have lower bone turnover than controls at baseline as well as following a challenge with recombinant human TSH (rhTSH). Methods: Bone turnover markers CTX and P1NP were measured in fasted morning samples from 14 offspring and 12 controls at baseline and at 24 hour intervals following 0.1 mg rhTSH i.m. administration for four consecutive days. Results: At baseline, mean (SEM) CTX was 0.32 (0.03) ng/ml in offspring and 0.50 (0.04) ng/ml in controls, p < 0.01, whereas mean (SEM) P1NP was 39.6 (3.2) ng/ml in offspring and 61.8 (6.6) ng/ml in controls, p < 0.01. Following rhTSH administration, both CTX and P1NP levels transiently increased over time and normalized towards baseline after 72 h (general linear modelling: CTX time p = 0.01, P1NP time p < 0.01); the response was similar between offspring and controls. Conclusions: Bone turnover markers were lower at baseline in offspring from long-lived families than in controls but increased similarly following an rhTSH challenge.

AB - Context: Offspring from long-lived families have a different thyroid status than controls, characterised by higher circulating levels of thyroid stimulating hormone (TSH) and similar levels of thyroid hormone. Expression of the TSH receptor has previously been observed on various extrathyroidal tissues, including bone. However, potential physiological consequences of differences in circulating TSH as observed in familial longevity on bone tissue remain unclear. Objective: Based on the hypothesis that TSH may inhibit bone resorption, we explored whether offspring of long-lived families have lower bone turnover than controls at baseline as well as following a challenge with recombinant human TSH (rhTSH). Methods: Bone turnover markers CTX and P1NP were measured in fasted morning samples from 14 offspring and 12 controls at baseline and at 24 hour intervals following 0.1 mg rhTSH i.m. administration for four consecutive days. Results: At baseline, mean (SEM) CTX was 0.32 (0.03) ng/ml in offspring and 0.50 (0.04) ng/ml in controls, p < 0.01, whereas mean (SEM) P1NP was 39.6 (3.2) ng/ml in offspring and 61.8 (6.6) ng/ml in controls, p < 0.01. Following rhTSH administration, both CTX and P1NP levels transiently increased over time and normalized towards baseline after 72 h (general linear modelling: CTX time p = 0.01, P1NP time p < 0.01); the response was similar between offspring and controls. Conclusions: Bone turnover markers were lower at baseline in offspring from long-lived families than in controls but increased similarly following an rhTSH challenge.

KW - bone metabolism

KW - longevity

KW - rhTSH

KW - thyroid

U2 - 10.18632/aging.203511

DO - 10.18632/aging.203511

M3 - Journal article

C2 - 34491903

AN - SCOPUS:85115660049

VL - 13

SP - 21029

EP - 21039

JO - Aging

JF - Aging

SN - 1945-4589

IS - 17

ER -

ID: 306972556