Palmitic Acid Downregulates Thyroglobulin (Tg), Sodium Iodide Symporter (NIS), and Thyroperoxidase (TPO) in Human Primary Thyrocytes: A Potential Mechanism by Which Lipotoxicity Affects Thyroid?

Our previous studies suggested that the thyroid might be a target organ affected by lipotoxicity, which might be partially related to the increasing prevalence of subclinical hypothyroidism. However, the underlying molecular mechanism is not yet clearly established. This study aimed to assess the ef...

Full description

Saved in:
Bibliographic Details
Main Authors: Meng Zhao, Xiaohan Zhang, Ling Gao, Yongfeng Song, Chao Xu, Chunxiao Yu, Shanshan Shao, Jiajun Zhao
Format: Article
Language:English
Published: Wiley 2018-01-01
Series:International Journal of Endocrinology
Online Access:http://dx.doi.org/10.1155/2018/4215848
Tags: Add Tag
No Tags, Be the first to tag this record!
_version_ 1832560498563874816
author Meng Zhao
Xiaohan Zhang
Ling Gao
Yongfeng Song
Chao Xu
Chunxiao Yu
Shanshan Shao
Jiajun Zhao
author_facet Meng Zhao
Xiaohan Zhang
Ling Gao
Yongfeng Song
Chao Xu
Chunxiao Yu
Shanshan Shao
Jiajun Zhao
author_sort Meng Zhao
collection DOAJ
description Our previous studies suggested that the thyroid might be a target organ affected by lipotoxicity, which might be partially related to the increasing prevalence of subclinical hypothyroidism. However, the underlying molecular mechanism is not yet clearly established. This study aimed to assess the effect of palmitic acid stimulation on thyrocyte function. Upon palmitic acid stimulation, intracellular contents of lipids, as well as the expression and activity of three key molecules in thyroid hormone synthesis (i.e., thyroglobulin, sodium iodide symporter, and thyroperoxidase), were determined in human primary thyrocytes. The contents of BODIPY® FL C16 (the fluorescently labeled palmitic acid analogue) entering into the thyrocytes were gradually increased with time extending. Accordingly, the intracellular accumulation of both triglyceride and free fatty acids increased in dose- and time-dependent manners. The effect of palmitic acid stimulation on thyroid hormone synthesis was then determined. Both the mRNA and protein levels of thyroglobulin, sodium iodide symporter, and thyroperoxidase were decreased following palmitic acid stimulation. Consistently, upon palmitic acid stimulation, the secreted thyroglobulin levels in supernatants, 131I uptake, and extracellular thyroperoxidase activity were all decreased in a dose-dependent manner. Our results demonstrated that upon palmitic acid stimulation, the expressions of the key molecules (thyroglobulin, sodium iodide symporter, and thyroperoxidase) were reduced and their activities were suppressed, which might lead to impaired thyroid hormone synthesis.
format Article
id doaj-art-f76ba5a98cc64a43bd54f2962fba8716
institution Kabale University
issn 1687-8337
1687-8345
language English
publishDate 2018-01-01
publisher Wiley
record_format Article
series International Journal of Endocrinology
spelling doaj-art-f76ba5a98cc64a43bd54f2962fba87162025-02-03T01:27:26ZengWileyInternational Journal of Endocrinology1687-83371687-83452018-01-01201810.1155/2018/42158484215848Palmitic Acid Downregulates Thyroglobulin (Tg), Sodium Iodide Symporter (NIS), and Thyroperoxidase (TPO) in Human Primary Thyrocytes: A Potential Mechanism by Which Lipotoxicity Affects Thyroid?Meng Zhao0Xiaohan Zhang1Ling Gao2Yongfeng Song3Chao Xu4Chunxiao Yu5Shanshan Shao6Jiajun Zhao7Department of Endocrinology, Shandong Provincial Hospital Affiliated to Shandong University, Jinan, Shandong 250021, ChinaDepartment of Endocrinology, Shandong Provincial Hospital Affiliated to Shandong University, Jinan, Shandong 250021, ChinaShandong Provincial Key Laboratory of Endocrinology and Lipid Metabolism, Jinan, Shandong 250021, ChinaDepartment of Endocrinology, Shandong Provincial Hospital Affiliated to Shandong University, Jinan, Shandong 250021, ChinaDepartment of Endocrinology, Shandong Provincial Hospital Affiliated to Shandong University, Jinan, Shandong 250021, ChinaDepartment of Endocrinology, Shandong Provincial Hospital Affiliated to Shandong University, Jinan, Shandong 250021, ChinaDepartment of Endocrinology, Shandong Provincial Hospital Affiliated to Shandong University, Jinan, Shandong 250021, ChinaDepartment of Endocrinology, Shandong Provincial Hospital Affiliated to Shandong University, Jinan, Shandong 250021, ChinaOur previous studies suggested that the thyroid might be a target organ affected by lipotoxicity, which might be partially related to the increasing prevalence of subclinical hypothyroidism. However, the underlying molecular mechanism is not yet clearly established. This study aimed to assess the effect of palmitic acid stimulation on thyrocyte function. Upon palmitic acid stimulation, intracellular contents of lipids, as well as the expression and activity of three key molecules in thyroid hormone synthesis (i.e., thyroglobulin, sodium iodide symporter, and thyroperoxidase), were determined in human primary thyrocytes. The contents of BODIPY® FL C16 (the fluorescently labeled palmitic acid analogue) entering into the thyrocytes were gradually increased with time extending. Accordingly, the intracellular accumulation of both triglyceride and free fatty acids increased in dose- and time-dependent manners. The effect of palmitic acid stimulation on thyroid hormone synthesis was then determined. Both the mRNA and protein levels of thyroglobulin, sodium iodide symporter, and thyroperoxidase were decreased following palmitic acid stimulation. Consistently, upon palmitic acid stimulation, the secreted thyroglobulin levels in supernatants, 131I uptake, and extracellular thyroperoxidase activity were all decreased in a dose-dependent manner. Our results demonstrated that upon palmitic acid stimulation, the expressions of the key molecules (thyroglobulin, sodium iodide symporter, and thyroperoxidase) were reduced and their activities were suppressed, which might lead to impaired thyroid hormone synthesis.http://dx.doi.org/10.1155/2018/4215848
spellingShingle Meng Zhao
Xiaohan Zhang
Ling Gao
Yongfeng Song
Chao Xu
Chunxiao Yu
Shanshan Shao
Jiajun Zhao
Palmitic Acid Downregulates Thyroglobulin (Tg), Sodium Iodide Symporter (NIS), and Thyroperoxidase (TPO) in Human Primary Thyrocytes: A Potential Mechanism by Which Lipotoxicity Affects Thyroid?
International Journal of Endocrinology
title Palmitic Acid Downregulates Thyroglobulin (Tg), Sodium Iodide Symporter (NIS), and Thyroperoxidase (TPO) in Human Primary Thyrocytes: A Potential Mechanism by Which Lipotoxicity Affects Thyroid?
title_full Palmitic Acid Downregulates Thyroglobulin (Tg), Sodium Iodide Symporter (NIS), and Thyroperoxidase (TPO) in Human Primary Thyrocytes: A Potential Mechanism by Which Lipotoxicity Affects Thyroid?
title_fullStr Palmitic Acid Downregulates Thyroglobulin (Tg), Sodium Iodide Symporter (NIS), and Thyroperoxidase (TPO) in Human Primary Thyrocytes: A Potential Mechanism by Which Lipotoxicity Affects Thyroid?
title_full_unstemmed Palmitic Acid Downregulates Thyroglobulin (Tg), Sodium Iodide Symporter (NIS), and Thyroperoxidase (TPO) in Human Primary Thyrocytes: A Potential Mechanism by Which Lipotoxicity Affects Thyroid?
title_short Palmitic Acid Downregulates Thyroglobulin (Tg), Sodium Iodide Symporter (NIS), and Thyroperoxidase (TPO) in Human Primary Thyrocytes: A Potential Mechanism by Which Lipotoxicity Affects Thyroid?
title_sort palmitic acid downregulates thyroglobulin tg sodium iodide symporter nis and thyroperoxidase tpo in human primary thyrocytes a potential mechanism by which lipotoxicity affects thyroid
url http://dx.doi.org/10.1155/2018/4215848
work_keys_str_mv AT mengzhao palmiticaciddownregulatesthyroglobulintgsodiumiodidesymporternisandthyroperoxidasetpoinhumanprimarythyrocytesapotentialmechanismbywhichlipotoxicityaffectsthyroid
AT xiaohanzhang palmiticaciddownregulatesthyroglobulintgsodiumiodidesymporternisandthyroperoxidasetpoinhumanprimarythyrocytesapotentialmechanismbywhichlipotoxicityaffectsthyroid
AT linggao palmiticaciddownregulatesthyroglobulintgsodiumiodidesymporternisandthyroperoxidasetpoinhumanprimarythyrocytesapotentialmechanismbywhichlipotoxicityaffectsthyroid
AT yongfengsong palmiticaciddownregulatesthyroglobulintgsodiumiodidesymporternisandthyroperoxidasetpoinhumanprimarythyrocytesapotentialmechanismbywhichlipotoxicityaffectsthyroid
AT chaoxu palmiticaciddownregulatesthyroglobulintgsodiumiodidesymporternisandthyroperoxidasetpoinhumanprimarythyrocytesapotentialmechanismbywhichlipotoxicityaffectsthyroid
AT chunxiaoyu palmiticaciddownregulatesthyroglobulintgsodiumiodidesymporternisandthyroperoxidasetpoinhumanprimarythyrocytesapotentialmechanismbywhichlipotoxicityaffectsthyroid
AT shanshanshao palmiticaciddownregulatesthyroglobulintgsodiumiodidesymporternisandthyroperoxidasetpoinhumanprimarythyrocytesapotentialmechanismbywhichlipotoxicityaffectsthyroid
AT jiajunzhao palmiticaciddownregulatesthyroglobulintgsodiumiodidesymporternisandthyroperoxidasetpoinhumanprimarythyrocytesapotentialmechanismbywhichlipotoxicityaffectsthyroid