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

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Preserved postprandial suppression of bone turnover markers, despite increased fasting levels, in postmenopausal women. / Abildgaard, Julie; Ploug, Thorkil; Pedersen, Anette Tonnes; Eiken, Pia; Pedersen, Bente Klarlund; Holst, Jens Juul; Hartmann, Bolette; Lindegaard, Birgitte.

In: Bone, Vol. 143, 115612, 2021.

Research output: Contribution to journalJournal articlepeer-review

Harvard

Abildgaard, J, Ploug, T, Pedersen, AT, Eiken, P, Pedersen, BK, Holst, JJ, Hartmann, B & Lindegaard, B 2021, 'Preserved postprandial suppression of bone turnover markers, despite increased fasting levels, in postmenopausal women', Bone, vol. 143, 115612. https://doi.org/10.1016/j.bone.2020.115612

APA

Abildgaard, J., Ploug, T., Pedersen, A. T., Eiken, P., Pedersen, B. K., Holst, J. J., Hartmann, B., & Lindegaard, B. (2021). Preserved postprandial suppression of bone turnover markers, despite increased fasting levels, in postmenopausal women. Bone, 143, [115612]. https://doi.org/10.1016/j.bone.2020.115612

Vancouver

Abildgaard J, Ploug T, Pedersen AT, Eiken P, Pedersen BK, Holst JJ et al. Preserved postprandial suppression of bone turnover markers, despite increased fasting levels, in postmenopausal women. Bone. 2021;143. 115612. https://doi.org/10.1016/j.bone.2020.115612

Author

Abildgaard, Julie ; Ploug, Thorkil ; Pedersen, Anette Tonnes ; Eiken, Pia ; Pedersen, Bente Klarlund ; Holst, Jens Juul ; Hartmann, Bolette ; Lindegaard, Birgitte. / Preserved postprandial suppression of bone turnover markers, despite increased fasting levels, in postmenopausal women. In: Bone. 2021 ; Vol. 143.

Bibtex

@article{45d45f23be4c4b07a1d4e665a70f4249,
title = "Preserved postprandial suppression of bone turnover markers, despite increased fasting levels, in postmenopausal women",
abstract = "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 periand 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.",
keywords = "Menopause, Bone turnover, Bone mineral density, Gut hormones, Glucose tolerance, DEPENDENT INSULINOTROPIC POLYPEPTIDE, MINERAL DENSITY, RISK-FACTOR, RESORPTION, MENOPAUSE, HORMONES, FRACTURES, METAANALYSIS, POPULATION",
author = "Julie Abildgaard and Thorkil Ploug and Pedersen, {Anette Tonnes} and Pia Eiken and Pedersen, {Bente Klarlund} and Holst, {Jens Juul} and Bolette Hartmann and Birgitte Lindegaard",
year = "2021",
doi = "10.1016/j.bone.2020.115612",
language = "English",
volume = "143",
journal = "Bone",
issn = "8756-3282",
publisher = "Elsevier",

}

RIS

TY - JOUR

T1 - Preserved postprandial suppression of bone turnover markers, despite increased fasting levels, in postmenopausal women

AU - Abildgaard, Julie

AU - Ploug, Thorkil

AU - Pedersen, Anette Tonnes

AU - Eiken, Pia

AU - Pedersen, Bente Klarlund

AU - Holst, Jens Juul

AU - Hartmann, Bolette

AU - Lindegaard, Birgitte

PY - 2021

Y1 - 2021

N2 - 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 periand 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.

AB - 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 periand 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.

KW - Menopause

KW - Bone turnover

KW - Bone mineral density

KW - Gut hormones

KW - Glucose tolerance

KW - DEPENDENT INSULINOTROPIC POLYPEPTIDE

KW - MINERAL DENSITY

KW - RISK-FACTOR

KW - RESORPTION

KW - MENOPAUSE

KW - HORMONES

KW - FRACTURES

KW - METAANALYSIS

KW - POPULATION

U2 - 10.1016/j.bone.2020.115612

DO - 10.1016/j.bone.2020.115612

M3 - Journal article

C2 - 32853851

VL - 143

JO - Bone

JF - Bone

SN - 8756-3282

M1 - 115612

ER -

ID: 255683061