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Glucose Tolerance Tests and Osteocalcin Responses in Healthy People

Aim: Osteocalcin and undercarboxylated osteocalcin are suggested to be endocrine messengers from the bones and have been shown to stimulate insulin secretion from pancreatic β-cells. Insulin is hypothesized to increase the osteoblastic production of osteocalcin. The aim of the study was to investiga...

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Autores principales: Starup-Linde, Jakob, Westberg-Rasmussen, Sidse, Lykkeboe, Simon, Handberg, Aase, Hartmann, Bolette, Holst, Jens J., Hermansen, Kjeld, Vestergaard, Peter, Gregersen, Søren
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6053521/
https://www.ncbi.nlm.nih.gov/pubmed/30057568
http://dx.doi.org/10.3389/fendo.2018.00356
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author Starup-Linde, Jakob
Westberg-Rasmussen, Sidse
Lykkeboe, Simon
Handberg, Aase
Hartmann, Bolette
Holst, Jens J.
Hermansen, Kjeld
Vestergaard, Peter
Gregersen, Søren
author_facet Starup-Linde, Jakob
Westberg-Rasmussen, Sidse
Lykkeboe, Simon
Handberg, Aase
Hartmann, Bolette
Holst, Jens J.
Hermansen, Kjeld
Vestergaard, Peter
Gregersen, Søren
author_sort Starup-Linde, Jakob
collection PubMed
description Aim: Osteocalcin and undercarboxylated osteocalcin are suggested to be endocrine messengers from the bones and have been shown to stimulate insulin secretion from pancreatic β-cells. Insulin is hypothesized to increase the osteoblastic production of osteocalcin. The aim of the study was to investigate whether the route of glucose administration influence the circulating levels of osteocalcin and undercarboxylated osteocalcin. Methods: Twelve healthy males were enrolled in an acute cross-over study where they underwent an oral glucose tolerance test (OGTT), an isoglycemic intravenous glucose infusion (IIGI) and a fasting period (control). Blood samples were collected throughout 180 min and analyzed for osteocalcin and undercarboxylated osteocalcin and compared to insulin, glucose, and gastro-intestinal hormone responses. Results: Neither osteocalcin levels nor undercarboxylated osteocalcin levels over time differed between the OGTT, IIGI, and fasting. Baseline insulin levels and glucose levels were not associated with osteocalcin or undercarboxylated osteocalcin levels. Increases in insulin and glucose levels were neither associated with altered osteocalcin nor undercarboxylated osteocalcin levels. Conclusion: The route of glucose administration does not influence the circulating levels of osteocalcin and undercarboxylated osteocalcin despite the differential insulin and incretin responses. In the acute setting this suggests that insulin does not increase osteoblastic production of osteocalcin in healthy human males.
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spelling pubmed-60535212018-07-27 Glucose Tolerance Tests and Osteocalcin Responses in Healthy People Starup-Linde, Jakob Westberg-Rasmussen, Sidse Lykkeboe, Simon Handberg, Aase Hartmann, Bolette Holst, Jens J. Hermansen, Kjeld Vestergaard, Peter Gregersen, Søren Front Endocrinol (Lausanne) Endocrinology Aim: Osteocalcin and undercarboxylated osteocalcin are suggested to be endocrine messengers from the bones and have been shown to stimulate insulin secretion from pancreatic β-cells. Insulin is hypothesized to increase the osteoblastic production of osteocalcin. The aim of the study was to investigate whether the route of glucose administration influence the circulating levels of osteocalcin and undercarboxylated osteocalcin. Methods: Twelve healthy males were enrolled in an acute cross-over study where they underwent an oral glucose tolerance test (OGTT), an isoglycemic intravenous glucose infusion (IIGI) and a fasting period (control). Blood samples were collected throughout 180 min and analyzed for osteocalcin and undercarboxylated osteocalcin and compared to insulin, glucose, and gastro-intestinal hormone responses. Results: Neither osteocalcin levels nor undercarboxylated osteocalcin levels over time differed between the OGTT, IIGI, and fasting. Baseline insulin levels and glucose levels were not associated with osteocalcin or undercarboxylated osteocalcin levels. Increases in insulin and glucose levels were neither associated with altered osteocalcin nor undercarboxylated osteocalcin levels. Conclusion: The route of glucose administration does not influence the circulating levels of osteocalcin and undercarboxylated osteocalcin despite the differential insulin and incretin responses. In the acute setting this suggests that insulin does not increase osteoblastic production of osteocalcin in healthy human males. Frontiers Media S.A. 2018-07-13 /pmc/articles/PMC6053521/ /pubmed/30057568 http://dx.doi.org/10.3389/fendo.2018.00356 Text en Copyright © 2018 Starup-Linde, Westberg-Rasmussen, Lykkeboe, Handberg, Hartmann, Holst, Hermansen, Vestergaard and Gregersen. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Endocrinology
Starup-Linde, Jakob
Westberg-Rasmussen, Sidse
Lykkeboe, Simon
Handberg, Aase
Hartmann, Bolette
Holst, Jens J.
Hermansen, Kjeld
Vestergaard, Peter
Gregersen, Søren
Glucose Tolerance Tests and Osteocalcin Responses in Healthy People
title Glucose Tolerance Tests and Osteocalcin Responses in Healthy People
title_full Glucose Tolerance Tests and Osteocalcin Responses in Healthy People
title_fullStr Glucose Tolerance Tests and Osteocalcin Responses in Healthy People
title_full_unstemmed Glucose Tolerance Tests and Osteocalcin Responses in Healthy People
title_short Glucose Tolerance Tests and Osteocalcin Responses in Healthy People
title_sort glucose tolerance tests and osteocalcin responses in healthy people
topic Endocrinology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6053521/
https://www.ncbi.nlm.nih.gov/pubmed/30057568
http://dx.doi.org/10.3389/fendo.2018.00356
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