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HERO ID
1295243
Reference Type
Journal Article
Title
Dose and time-dependent hypercholesterolemic effects of iodine excess via TRbeta1-mediated down regulation of hepatic LDLr gene expression
Author(s)
Zhao, LN; Xu, J; Peng, XL; Tian, LY; Hao, LP; Yang, XF; Ying, CJ; Sun, XF
Year
2010
Is Peer Reviewed?
Yes
Journal
European Journal of Nutrition
ISSN:
1436-6207
EISSN:
1436-6215
Volume
49
Issue
5
Page Numbers
257-265
Language
English
PMID
19916081
DOI
10.1007/s00394-009-0081-3
Abstract
BACKGROUND:
With the global improvement of iodine nutrition, iodine excess is emerging as a new concern.
AIM OF STUDY:
The aim of this study is to illustrate the physiological effects and potential molecular mechanisms of excessive iodine intake on lipid metabolism.
METHODS:
Balb/c mice were given drinking water containing different levels of iodine for 1 month and treated with 1.2 microg/mL iodine for different periods of time, respectively. Plasma lipid parameters and serum thyroid hormones were measured. Expressions of hepatic genes were detected by real-time polymerase chain reactions and Western blot.
RESULTS:
Dose-dependent hypercholesterolemic effects were detected in mice (TC, r = 0.615; p < 0.01). Drinking 1.2 microg/mL iodine water for 1 month had no significant effect on serum lipid metabolism, while prolonged exposure induced an increase of serum cholesterol. Serum thyroid hormones were not affected by iodine throughout the study. At the molecular level, we detected a dose-dependent attenuation of hepatic low density lipoprotein receptor (LDLr) and thyroid hormone receptor beta1 (TRbeta1) expression in parallel to the change of serum cholesterol. Treatment with 1.2 microg/mL iodine water for 1 month did not affect LDLr and TRbeta1 expression, while 3 or 6 months exposure resulted in a decrease of their expression.
CONCLUSION:
Present findings demonstrated dose- and time-dependent hypercholesterolemic effects of iodine excess. Furthermore, our data suggests that TRbeta1-mediated down regulation of hepatic LDLr gene may play a critical role in iodine excess-induced hypercholesterolemic effects.
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