Thyroid Nodules and Obesity

A widely discussed topic in the pathophysiology of thyroid nodules is the role of obesity, a state that leads to increased systemic inflammatory markers. Leptin plays a vital role in forming thyroid nodules and cancer through several mechanisms. Together with chronic inflammation, there is an augmen...

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Main Authors: Elpida Demetriou, Maria Fokou, Savvas Frangos, Panagiotis Papageorgis, Panayiotis A. Economides, Aliki Economides
Format: Article
Language:English
Published: MDPI AG 2023-05-01
Series:Life
Subjects:
Online Access:https://www.mdpi.com/2075-1729/13/6/1292
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author Elpida Demetriou
Maria Fokou
Savvas Frangos
Panagiotis Papageorgis
Panayiotis A. Economides
Aliki Economides
author_facet Elpida Demetriou
Maria Fokou
Savvas Frangos
Panagiotis Papageorgis
Panayiotis A. Economides
Aliki Economides
author_sort Elpida Demetriou
collection DOAJ
description A widely discussed topic in the pathophysiology of thyroid nodules is the role of obesity, a state that leads to increased systemic inflammatory markers. Leptin plays a vital role in forming thyroid nodules and cancer through several mechanisms. Together with chronic inflammation, there is an augmentation in the secretion of tumor necrosis factor (TNF) and the cytokine interleukin 6 (IL-6), which contributed to cancer development, progression and metastasis. In addition, leptin exerts a modulatory action in the growth, proliferation and invasion of thyroid carcinoma cell lines via activating various signal pathways, such as Janus kinase/signal transducer and activator of transcription, mitogen-activated protein kinase (MAPK) and/or phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt). Through several proposed mechanisms, aberrant endogenous estrogen levels have been suggested to play a vital role in the development of both benign and malignant nodules. Metabolic syndrome triggers the development of thyroid nodules by stimulating thyroid proliferation and angiogenesis due to hyperinsulinemia, hyperglycemia and dyslipidemia. Insulin resistance influences the distribution and structure of the thyroid blood vessels. Insulin growth factor 1 (IGF-1) and insulin affect the regulation of the expression of thyroid genes and the proliferation and differentiation of thyroid cells. TSH can promote the differentiation of pre-adipocytes to mature adipocytes but also, in the presence of insulin, TSH possesses mitogenic properties. This review aims to summarize the underlying mechanisms explaining the role of obesity in the pathophysiology of thyroid nodules and discuss potential clinical implications.
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spelling doaj.art-585135c9ba2e4e418a2acf017ab00fd32023-11-18T11:17:17ZengMDPI AGLife2075-17292023-05-01136129210.3390/life13061292Thyroid Nodules and ObesityElpida Demetriou0Maria Fokou1Savvas Frangos2Panagiotis Papageorgis3Panayiotis A. Economides4Aliki Economides5Department of Medicine, School of Medicine, European University Cyprus, 2404 Nicosia, CyprusDepartment of Medicine, School of Medicine, European University Cyprus, 2404 Nicosia, CyprusNuclear Medicine Department and Thyroid Cancer Clinic, Bank of Cyprus Oncology Center, 2404 Nicosia, CyprusDepartment of Life Sciences, European University Cyprus, 2404 Nicosia, CyprusDepartment of Medicine, School of Medicine, European University Cyprus, 2404 Nicosia, CyprusEconomides Thyroid and Endocrinology Center, Engomi, 2404 Nicosia, CyprusA widely discussed topic in the pathophysiology of thyroid nodules is the role of obesity, a state that leads to increased systemic inflammatory markers. Leptin plays a vital role in forming thyroid nodules and cancer through several mechanisms. Together with chronic inflammation, there is an augmentation in the secretion of tumor necrosis factor (TNF) and the cytokine interleukin 6 (IL-6), which contributed to cancer development, progression and metastasis. In addition, leptin exerts a modulatory action in the growth, proliferation and invasion of thyroid carcinoma cell lines via activating various signal pathways, such as Janus kinase/signal transducer and activator of transcription, mitogen-activated protein kinase (MAPK) and/or phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt). Through several proposed mechanisms, aberrant endogenous estrogen levels have been suggested to play a vital role in the development of both benign and malignant nodules. Metabolic syndrome triggers the development of thyroid nodules by stimulating thyroid proliferation and angiogenesis due to hyperinsulinemia, hyperglycemia and dyslipidemia. Insulin resistance influences the distribution and structure of the thyroid blood vessels. Insulin growth factor 1 (IGF-1) and insulin affect the regulation of the expression of thyroid genes and the proliferation and differentiation of thyroid cells. TSH can promote the differentiation of pre-adipocytes to mature adipocytes but also, in the presence of insulin, TSH possesses mitogenic properties. This review aims to summarize the underlying mechanisms explaining the role of obesity in the pathophysiology of thyroid nodules and discuss potential clinical implications.https://www.mdpi.com/2075-1729/13/6/1292thyroid nodulesobesityinflammationleptinestrogencytokines
spellingShingle Elpida Demetriou
Maria Fokou
Savvas Frangos
Panagiotis Papageorgis
Panayiotis A. Economides
Aliki Economides
Thyroid Nodules and Obesity
Life
thyroid nodules
obesity
inflammation
leptin
estrogen
cytokines
title Thyroid Nodules and Obesity
title_full Thyroid Nodules and Obesity
title_fullStr Thyroid Nodules and Obesity
title_full_unstemmed Thyroid Nodules and Obesity
title_short Thyroid Nodules and Obesity
title_sort thyroid nodules and obesity
topic thyroid nodules
obesity
inflammation
leptin
estrogen
cytokines
url https://www.mdpi.com/2075-1729/13/6/1292
work_keys_str_mv AT elpidademetriou thyroidnodulesandobesity
AT mariafokou thyroidnodulesandobesity
AT savvasfrangos thyroidnodulesandobesity
AT panagiotispapageorgis thyroidnodulesandobesity
AT panayiotisaeconomides thyroidnodulesandobesity
AT alikieconomides thyroidnodulesandobesity