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目的观察过量碘摄入对肝脏脂代谢的影响,并探讨其相关分子机制。方法清洁级雌性断乳Balb/c小鼠60只,按体重随机均分为6组。碘剂量分组为:A组0;B组,300μg/L;C组,600μg/L;D组,1200μg/L;E组2400μg/L;F组4800μg/L。第3月末,放射免疫法测定甲状腺激素水平,测定血清及肝脏总胆固醇(TC)、甘油三酯(TG)水平。通过实时聚合酶链反应(real-time PCR)方法测定肝脏固醇结合原件调节蛋白-1C(sterol regulatory element binding proteins1c,SREBP-1c)、脂肪酸合成酶(fatty acid synthase,FAS)基因表达水平。结果各剂量组小鼠的尿碘水平呈碘剂量依赖性升高。过量碘摄入导致血清总三碘甲状腺氨酸(TT3)水平降低,血清总甲状腺素(TT4)、促甲状腺激素(TSH)水平增加。在碘剂量≥2400μg/L时与对照组相比差异具有显著性。与对照组相比,血清TC、TG增加,肝脏TC、TG含量显著性增加,在碘剂量≥2400μg/L差异具有显著性。肝脏SREBP-1C、FAS基因表达水平增加在碘剂量≥2400μg/L差异具有显著性。结论过量碘摄入导致肝脏发生脂肪变性,SREBP-1c、FAS基因表达上调可能是过量碘摄入导致肝脏脂肪变性的机制之一。
Objective To observe the effect of excessive iodine intake on hepatic lipid metabolism and to explore its molecular mechanism. Methods Sixty clean female Balb / c mice were randomly divided into 6 groups according to body weight. The iodine dose was divided into group A, group 0, group B, 300μg / L, group C, 600μg / L, group D, 1200μg / L, group E 2400μg / L, group F 4800μg / L. At the end of the third month, the levels of thyroid hormones were determined by radioimmunoassay, and the serum and liver total cholesterol (TC) and triglyceride (TG) levels were measured. The gene expression of sterol regulatory element binding proteins 1c (SREBP-1c) and fatty acid synthase (FAS) were determined by real-time PCR. Results The urinary iodine level of mice in each dose group increased in a dose-dependent manner. Excessive iodine intake led to a decrease in serum total triiodothyronine (TT3) levels and an increase in serum total thyroxine (TT4) and thyrotropin (TSH) levels. The iodine dose ≥2400μg / L compared with the control group, the difference was significant. Compared with the control group, serum TC, TG increased liver TC, TG significantly increased, in the iodine dose ≥ 2400μg / L difference was significant. Liver SREBP-1C, FAS gene expression increased in iodine dose ≥ 2400μg / L difference was significant. Conclusions Excessive iodine intake leads to fatty degeneration in the liver. Upregulation of SREBP-1c and FAS gene may be one of the mechanisms of hepatic steatosis caused by excess iodine intake.