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Population correlations do not support the existence of set points for blood levels of calcium or glucose – a new model for homeostasis

The prevailing teaching regarding homeostasis, and in particular endocrine homeostasis, includes the fundamental concept of a “set point,” which represents a target or optimum level defended by physiological control mechanisms. Analogies for the description and teaching of this concept have included...

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Autores principales: Fitzgerald, Stephen P., Bean, Nigel G.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5789653/
https://www.ncbi.nlm.nih.gov/pubmed/29333728
http://dx.doi.org/10.14814/phy2.13551
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author Fitzgerald, Stephen P.
Bean, Nigel G.
author_facet Fitzgerald, Stephen P.
Bean, Nigel G.
author_sort Fitzgerald, Stephen P.
collection PubMed
description The prevailing teaching regarding homeostasis, and in particular endocrine homeostasis, includes the fundamental concept of a “set point,” which represents a target or optimum level defended by physiological control mechanisms. Analogies for the description and teaching of this concept have included thermostats and cruise controls. We previously demonstrated that such a set‐point model of regulation implies that in population data of parameter set point/controlling hormone levels, correlations between the parameter and its controlling hormone must be in the direction of the response of the parameter to its controlling hormone, and that in thyroid homeostasis this relationship is not observed. In this work we similarly examined population correlations, extracted from the literature, for the parameters glucose and calcium, and their controlling hormones. We found 10 correlations. Most were highly significant (P < 0.01). All were in the direction of the response of the controlling hormone to the parameter. Therefore, none were consistent with the pattern implied by a set‐point model of regulation. Instead all were consistent with an “equilibrium point” model of regulation, whereby ambient levels have no particular connotation to the individual, and result passively from the interplay of physiological processes. We conclude that glucose and calcium regulation, like thyroid regulation, are not centered on set points. This may reflect a general property of homeostasis. We provide an alternative mechanistic analogy, without a set point, for the heuristic description and teaching, of homeostasis.
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spelling pubmed-57896532018-03-15 Population correlations do not support the existence of set points for blood levels of calcium or glucose – a new model for homeostasis Fitzgerald, Stephen P. Bean, Nigel G. Physiol Rep Original Research The prevailing teaching regarding homeostasis, and in particular endocrine homeostasis, includes the fundamental concept of a “set point,” which represents a target or optimum level defended by physiological control mechanisms. Analogies for the description and teaching of this concept have included thermostats and cruise controls. We previously demonstrated that such a set‐point model of regulation implies that in population data of parameter set point/controlling hormone levels, correlations between the parameter and its controlling hormone must be in the direction of the response of the parameter to its controlling hormone, and that in thyroid homeostasis this relationship is not observed. In this work we similarly examined population correlations, extracted from the literature, for the parameters glucose and calcium, and their controlling hormones. We found 10 correlations. Most were highly significant (P < 0.01). All were in the direction of the response of the controlling hormone to the parameter. Therefore, none were consistent with the pattern implied by a set‐point model of regulation. Instead all were consistent with an “equilibrium point” model of regulation, whereby ambient levels have no particular connotation to the individual, and result passively from the interplay of physiological processes. We conclude that glucose and calcium regulation, like thyroid regulation, are not centered on set points. This may reflect a general property of homeostasis. We provide an alternative mechanistic analogy, without a set point, for the heuristic description and teaching, of homeostasis. John Wiley and Sons Inc. 2018-01-12 /pmc/articles/PMC5789653/ /pubmed/29333728 http://dx.doi.org/10.14814/phy2.13551 Text en © 2018 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on behalf of The Physiological Society and the American Physiological Society This is an open access article under the terms of the Creative Commons Attribution (http://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Research
Fitzgerald, Stephen P.
Bean, Nigel G.
Population correlations do not support the existence of set points for blood levels of calcium or glucose – a new model for homeostasis
title Population correlations do not support the existence of set points for blood levels of calcium or glucose – a new model for homeostasis
title_full Population correlations do not support the existence of set points for blood levels of calcium or glucose – a new model for homeostasis
title_fullStr Population correlations do not support the existence of set points for blood levels of calcium or glucose – a new model for homeostasis
title_full_unstemmed Population correlations do not support the existence of set points for blood levels of calcium or glucose – a new model for homeostasis
title_short Population correlations do not support the existence of set points for blood levels of calcium or glucose – a new model for homeostasis
title_sort population correlations do not support the existence of set points for blood levels of calcium or glucose – a new model for homeostasis
topic Original Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5789653/
https://www.ncbi.nlm.nih.gov/pubmed/29333728
http://dx.doi.org/10.14814/phy2.13551
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