Literature DB >> 36115005

Physiological linkage of thyroid and pituitary sensitivities.

Stephen Paul Fitzgerald1,2, Nigel G Bean3, Henrik Falhammar4,5, Rudolf Hoermann6,7.   

Abstract

OBJECTIVES: The sensitivities of the pituitary to thyroxine feedback, and the thyroid to thyrotropin stimulation determine the free thyroxine /thyrotropin feedback loop and can be described mathematically by two curves. It is not well understood how the two curves combine in a healthy population with normal thyroid function to express the individual balance points that are observed. This study was directed at this issue testing the possibilities of random combination and directed linkage between the two curves.
METHODS: We reverse-engineered two sets of population data, on the assumption of independent combinations of thyroid and pituitary sensitivities, to obtain estimates of the curve describing thyroid sensitivity. Sensitivity studies were performed.
RESULTS: No analysis resulted in a physiologically feasible estimate of the curve describing thyroid sensitivity. There was evidence of linkage of the two curves in terms of their combination throughout the normal range. Thyroid response curves reflecting a low free thyroxine response to thyrotropin tended to be combined in individuals with thyrotropin curves reflecting a high thyrotropin response to free thyroxine, and vice versa.
CONCLUSIONS: Thyroid and pituitary sensitivities are linked, being combined in individuals in a non-random directed pattern. Direct mutual interaction may contribute to this linkage. This linkage precludes the derivation of the curves describing these sensitivities from population data of the free thyroxine and thyrotropin relationship and complicates their derivation by physiological experimentation. This linkage and probable interaction may also bestow evolutionary advantage by minimising inter-individual variation in free thyroxine levels and by augmenting homeostasis.
© 2022. The Author(s).

Entities:  

Keywords:  Thyroid function; Thyroid hormones; Thyroid physiology; Thyrotropin (TSH)

Year:  2022        PMID: 36115005     DOI: 10.1007/s12020-022-03184-8

Source DB:  PubMed          Journal:  Endocrine        ISSN: 1355-008X            Impact factor:   3.925


  6 in total

1.  Five new families with resistance to thyroid hormone not caused by mutations in the thyroid hormone receptor beta gene.

Authors:  J Pohlenz; R E Weiss; P E Macchia; S Pannain; I T Lau; H Ho; S Refetoff
Journal:  J Clin Endocrinol Metab       Date:  1999-11       Impact factor: 5.958

Review 2.  Thyroid hormone and the central control of homeostasis.

Authors:  Amy Warner; Jens Mittag
Journal:  J Mol Endocrinol       Date:  2012-06-26       Impact factor: 5.098

Review 3.  Paradigms of Dynamic Control of Thyroid Hormone Signaling.

Authors:  Antonio C Bianco; Alexandra Dumitrescu; Balázs Gereben; Miriam O Ribeiro; Tatiana L Fonseca; Gustavo W Fernandes; Barbara M L C Bocco
Journal:  Endocr Rev       Date:  2019-08-01       Impact factor: 19.871

4.  The role of functional thyroid capacity in pituitary thyroid feedback regulation.

Authors:  Rudolf Hoermann; John E M Midgley; Rolf Larisch; Johannes W Dietrich
Journal:  Eur J Clin Invest       Date:  2018-08-01       Impact factor: 4.686

5.  Resistance to thyroid hormone caused by two mutant thyroid hormone receptors beta, R243Q and R243W, with marked impairment of function that cannot be explained by altered in vitro 3,5,3'-triiodothyroinine binding affinity.

Authors:  H Yagi; J Pohlenz; Y Hayashi; A Sakurai; S Refetoff
Journal:  J Clin Endocrinol Metab       Date:  1997-05       Impact factor: 5.958

6.  Volume of sella turcica in normal subjects and in patients with primary hypothyroidism and hyperthyroidism.

Authors:  T Yamada; T Tsukui; K Ikejiri; Y Yukimura; M Kotani
Journal:  J Clin Endocrinol Metab       Date:  1976-05       Impact factor: 5.958

  6 in total

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