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The Role of Insulin Resistance/Hyperinsulinism on the Rising Trend of Thyroid and Adrenal Nodular Disease in the Current Environment

Thyroid follicular cells, as well as adrenocortical cells, are endowed by an intrinsic heterogeneity regarding their growth potential, in response to various stimuli. This heterogeneity appears to constitute the underlying cause for the focal cell hyperplasia and eventually the formation of thyroid...

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Autor principal: Tsatsoulis, Agathocles
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5867563/
https://www.ncbi.nlm.nih.gov/pubmed/29495350
http://dx.doi.org/10.3390/jcm7030037
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author Tsatsoulis, Agathocles
author_facet Tsatsoulis, Agathocles
author_sort Tsatsoulis, Agathocles
collection PubMed
description Thyroid follicular cells, as well as adrenocortical cells, are endowed by an intrinsic heterogeneity regarding their growth potential, in response to various stimuli. This heterogeneity appears to constitute the underlying cause for the focal cell hyperplasia and eventually the formation of thyroid and adrenal nodules, under the influence of growth stimulatory factors. Among the main stimulatory factors are the pituitary tropic hormones, thyroid-stimulating hormone (TSH) or thyrotropin and adrenocorticotropic hormone (ACTH), which regulate the growth and function of their respective target cells, and the insulin/insulin-like growth factor system, that, through its mitogenic effects, can stimulate the proliferation of these cells. The predominance of one or the other of these growth stimulatory factors appears to determine the natural history of thyroid and adrenal nodular disease. Thus, iodine deficiency was, in the past, the main pathogenic factor responsible, through a transient rise in TSH secretion, for the endemic nodular goiter with the characteristic colloid thyroid nodules among the inhabitants in iodine deficient areas. The correction of iodine deficiency was followed by the elimination of endemic colloid goiter and the emergence of thyroid autoimmunity. The recent epidemic of obesity and metabolic syndrome (MS), or insulin resistance syndrome, has been associated with the re-emergence of nodular thyroid disease. A parallel rise in the incidence of benign, nonfunctional adrenocortical tumors, known as adrenal incidentalomas, has also been reported in association with the manifestations of the MS. It is likely that the compensatory to insulin resistance hyperinsulinemia may be responsible for the rising trend of thyroid and adrenal nodular disease in the current environment.
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spelling pubmed-58675632018-04-09 The Role of Insulin Resistance/Hyperinsulinism on the Rising Trend of Thyroid and Adrenal Nodular Disease in the Current Environment Tsatsoulis, Agathocles J Clin Med Review Thyroid follicular cells, as well as adrenocortical cells, are endowed by an intrinsic heterogeneity regarding their growth potential, in response to various stimuli. This heterogeneity appears to constitute the underlying cause for the focal cell hyperplasia and eventually the formation of thyroid and adrenal nodules, under the influence of growth stimulatory factors. Among the main stimulatory factors are the pituitary tropic hormones, thyroid-stimulating hormone (TSH) or thyrotropin and adrenocorticotropic hormone (ACTH), which regulate the growth and function of their respective target cells, and the insulin/insulin-like growth factor system, that, through its mitogenic effects, can stimulate the proliferation of these cells. The predominance of one or the other of these growth stimulatory factors appears to determine the natural history of thyroid and adrenal nodular disease. Thus, iodine deficiency was, in the past, the main pathogenic factor responsible, through a transient rise in TSH secretion, for the endemic nodular goiter with the characteristic colloid thyroid nodules among the inhabitants in iodine deficient areas. The correction of iodine deficiency was followed by the elimination of endemic colloid goiter and the emergence of thyroid autoimmunity. The recent epidemic of obesity and metabolic syndrome (MS), or insulin resistance syndrome, has been associated with the re-emergence of nodular thyroid disease. A parallel rise in the incidence of benign, nonfunctional adrenocortical tumors, known as adrenal incidentalomas, has also been reported in association with the manifestations of the MS. It is likely that the compensatory to insulin resistance hyperinsulinemia may be responsible for the rising trend of thyroid and adrenal nodular disease in the current environment. MDPI 2018-02-26 /pmc/articles/PMC5867563/ /pubmed/29495350 http://dx.doi.org/10.3390/jcm7030037 Text en © 2018 by the author. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Review
Tsatsoulis, Agathocles
The Role of Insulin Resistance/Hyperinsulinism on the Rising Trend of Thyroid and Adrenal Nodular Disease in the Current Environment
title The Role of Insulin Resistance/Hyperinsulinism on the Rising Trend of Thyroid and Adrenal Nodular Disease in the Current Environment
title_full The Role of Insulin Resistance/Hyperinsulinism on the Rising Trend of Thyroid and Adrenal Nodular Disease in the Current Environment
title_fullStr The Role of Insulin Resistance/Hyperinsulinism on the Rising Trend of Thyroid and Adrenal Nodular Disease in the Current Environment
title_full_unstemmed The Role of Insulin Resistance/Hyperinsulinism on the Rising Trend of Thyroid and Adrenal Nodular Disease in the Current Environment
title_short The Role of Insulin Resistance/Hyperinsulinism on the Rising Trend of Thyroid and Adrenal Nodular Disease in the Current Environment
title_sort role of insulin resistance/hyperinsulinism on the rising trend of thyroid and adrenal nodular disease in the current environment
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5867563/
https://www.ncbi.nlm.nih.gov/pubmed/29495350
http://dx.doi.org/10.3390/jcm7030037
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