title: Iodine excess induces hepatic steatosis through disturbance of thyroid hormone metabolism involving oxidative stress in BALB/c mice.
abstract: Iodine excess is emerging as a new focus. A better understanding of its hazardous effects on the liver will be of great benefit to health. The aim of this study is to illustrate the effects of iodine excess on hepatic lipid homeostasis and explore its possible mechanisms. One hundred twenty BaLB/c mice were given iodine at different levels (0, 0.3, 0.6, 1.2, 2.4, and 4.8 mg I/L) in drinking water for 1 or 3 months. Lipid parameters and serum thyroid hormones were measured. Hepatic type 1 deiodinase activity and oxidative stress parameters were evaluated. The mRNA expression of sterol regulatory element-binding protein-1c (SREBP-1c) and fatty acid synthase (FAS) was detected by real-time polymerase chain reaction. Dose-dependent increase of hepatic triglyceride content was detected (r = 0.680, P < 0.01) in iodine-loaded groups. Evident hepatic steatosis was observed in 2.4 and 4.8 mg I/L iodine-loaded groups. The activities of antioxidant enzymes (glutathione peroxidase and superoxide dismutase) were decreased, and the malondialdehyde level was increased by excessive iodine in both serum and liver in a dose-dependent manner, accompanying the decrease of hepatic D1 activity. That resulted in the increase of serum total thyroxine and the decrease of serum total triiodothyronine in iodine-loaded groups. The mRNA expression of SREBP-1c and FAS was increased in iodine-loaded groups in response to the change of serum triiodothyronine. Present findings demonstrated that iodine excess could dose dependently induce hepatic steatosis. Furthermore, our data suggested that the disturbance of thyroid hormone metabolism involving oxidative stress may play a critical role in iodine excess-induced hepatic steatosis.
authors.affiliation: Department of General Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, Hubei, China.
authors.forename: Yun
authors.initials: Y
authors.lastname: Xia
authors.forename: Wei
authors.initials: W
authors.lastname: Qu
authors.forename: Li-Na
authors.initials: LN
authors.lastname: Zhao
authors.forename: Hao
authors.initials: H
authors.lastname: Han
authors.forename: Xue-Feng
authors.initials: XF
authors.lastname: Yang
authors.forename: Xiu-Fa
authors.initials: XF
authors.lastname: Sun
authors.forename: Li-Ping
authors.initials: LP
authors.lastname: Hao
authors.forename: Jian
authors.initials: J
authors.lastname: Xu
mesh_terms: D000818:Animals; D005234:Fatty Liver / Q000139:chemically induced*; D005260:Female; D007455:Iodine / Q000633:toxicity* / Q000652:urine; D008099:Liver / Q000473:pathology; D051379:Mice; D008807:Mice, Inbred BALB C; D018384:Oxidative Stress / Q000187:drug effects*; D016133:Polymerase Chain Reaction; D013963:Thyroid Hormones / Q000378:metabolism*
chemical_list: D013963:Thyroid Hormones; D007455:Iodine