3,5-二碘酪氨酸在大鼠体内的吸收代谢研究

目的 :　研究 3,5-二碘酪氨酸 ( DIT) DIT在动物体内吸收代谢的方式与碘离子的异同 ,为科学补碘提供资料。方法 :　经口灌胃分别给予去甲状腺 Wistar大鼠 DIT或 KI溶液 ,不同时间测血清中 DIT含量变化。结果 :　去甲状腺大鼠和正常大鼠直接摄入 DIT后 ,血清中 DIT含量明显增高 ,至 3h达最高值 ,6h后基本恢复正常 ,而摄入 KI者 ,血清 DIT含量几乎不随时间变化。结论 :　DIT是以分子形式吸收参加代谢的 ,而不是先转化成 I-形式后再吸收。     

高碘对大鼠实验性甲状腺肿的影响

目的：观察高碘对已形成甲状腺肿大鼠的影响。方法：复制Wistar大鼠甲状腺肿模型，分2组，实验组及实验对照组，实验组又分5组，常规饲料中投放不同浓度的碘。饲养7个月后处死，将甲状腺组织常规方法固定并包埋，切片，HE染色，核仁组织区嗜银蛋白（AgNOR)染色，用图象分析系统测量甲状腺滤泡上皮高度与甲状腺滤泡腔面积。结果：实验组出现胶质性甲状腺肿，不典型增生出现的百分率增加。甲状腺细胞的高度随饲料含量碘量的增加而逐渐降低，其泡腔面积逐渐增大，实验组不同共型增生区域的AgNOR颗粒数目增多，结论：高碘可使药物性甲磁谣胀变成高碘性甲状腺肿，并使某些区域增殖活跃，有变的可能。     

不同浓度的碘对大鼠实验性甲状腺肿的影响

目的 观察高碘对已形成甲状腺肿大鼠的影响。方法 复制Wistar大鼠甲状腺肿模型，分成两组：即实验组及实验对照组，实验组又分成5组，常规饲料中投放不同浓度的碘，饲养7个月后处死，将甲状腺组织常规方法固定并包埋，切片，HE染色核仁组织区嗜银蛋白（AgNOR)染色，用图像分析系统测量甲状腺滤泡上皮高度与甲状腺滤泡腔面积。结果 实验组出现了胶质性甲状腺肿，不典型增生出现的百分率增加，甲状腺细胞的高度随饲料含碘量的增加而逐渐降低；其滤泡腔面积逐渐增大，实验组不典型增生区域的AgNOR颗粒数目增多。结论 高碘可使药物性甲状腺肿变成高碘性甲状腺肿，并使某些区域增殖活跃，有恶变的可能。     

单纯性甲状腺肿

1概述单纯性甲状腺肿是一种常见的甲状腺疾病,其基本特征是非炎症性和非肿瘤性甲状腺肿大,不伴甲状腺功能减退和亢进的表现。引起单纯性甲状腺肿的原因很多,因缺碘或高碘所致者,常呈地方性分布,称为地方性甲状腺肿;因甲状腺激素合成障碍或致甲状腺肿物质引起者,多为散发分布,称为散发性甲状腺肿。2诊断标准2·1诊断依据①患者居住于碘缺乏地区,或具有高碘饮食史。部分患者呈现典型甲状腺肿大家族史。②甲状腺肿大,但无明显的甲状腺功能异常征象。③血清游离T3(FT3)、游离T4(FT4)一般在正常水平,甲状腺刺激激素无异常。④甲状腺摄131I率正…     

有机碘和无机碘对人甲状腺细胞凋亡的影响

目的 研究有机碘和无机碘对体外培养的人甲状腺细胞形态和凋亡相关蛋白Bcl-2和Bax表达的影响.方法 取正常人甲状腺细胞进行培养,分别设对照(培养液)组和KI组(碘浓度分别为10-7、10-5、10-3 mol/L)及3,5-二碘酪氨酸(DIT)组(碘浓度分别为10-7、10-5、10-3 mol/L),分别加入相应浓度用培养液稀释的DIT和KI溶液,继续培养48 h.采用免疫组织化学技术测定细胞凋亡相关蛋白表达的情况.结果 与对照组相比,10-5、10-3 mol/L KI组和10-3 mol/L DIT组甲状腺细胞Bcl-2表达量较低,10-5、10-3 mol/L KI及DIT暴露甲状腺细胞Bax表达量较高,差异均有统计学意义(P＜0.05,P＜0.01);且随着KI或DIT暴露浓度的升高,甲状腺细胞Bcl-2表达量呈下降趋势,Bax表达量呈上升趋势.与相同剂量KI组相比,10-5、10-3 mol/L DIT组甲状腺细胞Bcl-2表达量较高,Bax表达量较低,差异均有统计学意义(P＜0.05,P＜0.01).结论 高碘可引起甲状腺细胞形态的改变并增强其细胞凋亡的发生,且DIT对甲状腺细胞的影响弱于KI.     

海带有机碘与无机碘对甲亢大鼠血清FT_3和FT_4及尿碘的影响

目的研究海带有机碘(3,5-二碘酪氨酸,DIT)与无机碘(碘化钾,KI)对甲亢形成中的Wistar大鼠血清游离三碘甲状腺原氨酸(FT_3)、血清游离甲状腺素(FT_4)和尿碘水平的影响。方法将72只SPF级Wistar雄性大鼠随机分成8组,分别为正常对照组、甲亢模型组、DIT组(低、中、高剂量)和KI组(低、中、高剂量),其中低、中、高剂量(以碘计)分别为25.0、166.7、500.1μg/kg。正常对照组灌胃生理盐水,甲亢模型组灌胃甲状腺片悬浊液,其余组同时灌胃甲状腺片悬浊液及其相应的碘剂量。自由摄食饮水,连续喂养30 d,检测各组大鼠血清FT_3、FT_4和尿碘水平。结果与正常对照组比较,甲亢模型组大鼠末期体重下降,血清FT_3和FT_4、尿碘升高(P0.05)。与甲亢模型组比较,DIT各组末期体重较甲亢模型组高,血清FT_3、FT_4水平降低,尿碘水平明显上升(P0.05),KI各组末期体重、血清FT_3、FT_4水平无明显差异,尿碘水平明显上升(P0.05);DIT各组末期体重较对应的KI剂量组高,其中低、中剂量组有统计学意义(P0.05),DIT各组与对应的KI剂量组比较,血清FT_3、FT_4水平都显著降低(P0.05),尿碘水平明显上升,其中中、高剂量组有统计学意义(P0.05)。结论 DIT在甲状腺片诱导大鼠甲亢过程中,一定程度上可降低血清FT_3、FT_4水平,对甲状腺片所致甲亢产生一定的拮抗作用;而无机碘组仅有尿碘排出增加,KI对血清FT_3、FT_4水平无影响。     

有机碘和无机碘对人甲状腺细胞分泌功能影响的体外实验研究

目的 研究有机碘(DIT)和无机碘(KI)对体外培养的人甲状腺细胞(TEC)分泌三碘甲腺原氨酸(T3)、甲状腺素(T4)及甲状腺球蛋白(Tg)功能的影响.方法 取正常甲状腺细胞进行原代细胞培养,将细胞密度调整为2×105/ml,加入DIT和KI溶液(含碘最终浓度分别为0、10-8、10-7、10-6、10-5、10-4...     

核黄素对受冷大鼠甲状腺激素的影响

低温(4±0.5℃)饲养的大鼠与室温者相比;1.受冷大鼠甲状腺肥大,其重量与体重之比值增加,血清甲状腺素(简称T_4)下降,3,5,3′一三碘甲腺原氨酸(简称T_3)升高,摄食量增加,两周后直肠温度回升到正常水平。2.补充核黄素(6.0mg/kg饲料)可使受冷大鼠血清T_4升高,并有缩短T_4恢复到正常水平时间之趋势。3.增加核黄素供给量对受冷大鼠血清T_3浓度无明显影响。提示,增加核黄素供给量可能对促进机体冷适应有一定作用。     

锰离子对大鼠甲状腺功能的影响

作者用MnSO_4·H_2O(1mg/100g/天)给大鼠皮下注射5周,用放射免疫法测定甲状腺中的甲状腺素(T_4)和三碘甲腺原氨酸(T_3),以及血清中的T_4、T_3和促甲状腺激素(TSH)。对部分组织中锰含量也作了定量分析,结果见表1,表2。     

耳聋——甲状腺肿综合征1例

患者男,22岁。自幼发现耳聋,语言障碍。6岁时发现甲状腺肿大,并逐渐增大,曾在某医院按甲状腺机能亢进药物治疗未见好转。查体:身高165厘米,体重56公斤,智力稍差,无突眼。甲状腺呈弥漫性肿大,未扪及结节,无压痛,随吞咽而上下移动,无血管杂音。心肺未见异常。肝脾未触及。病理反射未引出。实验室检查:甲状腺吸(131)~碘率2小时43％;4小时54％;24小时58％。过氯酸钾释放试验:30分钟49％;60分钟54％;120分钟55％。甲状腺扫描:甲状腺呈弥漫性肿大。血清总T_4值3.4微克％,总T_3值1.2毫微克/毫升;TSH值102微单位/毫升。甲状腺球蛋白抗体:固相放射免疫法阴性。电测听力检查:感觉神     

Effects of the long-term (17-19 months) feeding of high-iodine eggs on lipid metabolism and thyroid function in rats

The present paper describes the effects of long-term (17-19 months) feeding of high-iodine eggs on lipid metabolism and thyroid function of rats, and also the effects of inorganic iodine on lipid metabolism. Rats were meal-fed on a diet containing 1% (w/w) of ordinary egg powder (OE diet as control: 35 micrograms I/100 g) or high-iodine egg powder (IE diet: 392 micrograms I/100 g). After the 19-month dietary treatment, rats fed on the IE diet, compared with the controls, showed a higher tissue lipoprotein lipase activity, a lower lipid peroxide level in the brain and a trend toward lower serum triacylglycerol levels and body fat storage without alterations in serum levels of thyroid-related hormones (TSH, T3 and T4). From the results of cold exposure and anti-thyroid drug-treatment conducted on rats fed on the OE and IE diets for 17 months, high-iodine eggs seemed to improve the age-related defects in thermogenic and thyroid hormone responses to cold, and also to result in a resistance to the anti-thyroid drug. The effects of the IE diet on lipid metabolism of rats were partly exhibited by feeding of the OE diet with an equivalent amount of iodine added as KI or KIO3. Thus, it is suggested that iodine ingestion through high-iodine eggs modulates both lipid metabolism and thyroid function in rats.     

Type I iodothyronine deiodinase activity after high selenium intake, and relations between selenium and iodine metabolism in rats.

Type I iodothyronine deiodinase (I-D), which catalyzes the production of the thyroid hormone 3,3',5-triiodothyronine from thyroxine, has recently been identified as a selenoenzyme. It is therefore of interest to investigate the relationships between selenium and iodine metabolism. In the livers of Se-deficient rats I-D activity was inhibited; the production of 3,3',5-triiodothyronine and 3,3'-diiodothyronine from added thyroxine was decreased by greater than 95% relative to Se-adequate controls. The hepatic I-D activity was also reduced in rats fed a diet with a low iodine concentration. Unaltered glutathione peroxidase activities in liver and plasma of these rats suggest, however, that with normal Se intake this metabolic pathway of Se is not affected by iodine depletion. When rats were administered 75Se-labeled selenium at levels equal to the amounts ingested from diets with Se concentrations of 0.3 or 2 mg Se/kg, greater Se concentrations were found in the thyroid and liver of the animals receiving the higher dosage. The thyroidal 3,3',5-triiodothyronine and thyroxine concentrations, however, were comparable in rats fed diets with 0.3 mg Se/kg diet as selenite and 2 mg Se/kg as selenite or L-selenomethionine. The measurement of the hepatic I-D and glutathione peroxidase activities in these animals showed that excessive Se supply does not elevate the activities of the two enzymes but might even have the opposite effect. At high Se intake tissue Se concentration cannot therefore be used as indicator of the selenoenzyme activities.     

碘缺乏和碘过多对大鼠甲状腺细胞膜脂流动性的影响

目的 探讨碘缺乏和碘过多对甲状腺细胞膜脂流动性的影响及其作用机理。方法 观察不同碘摄入水平的３组Ｗｉｓｔａｒ大鼠血清Ｔ４、Ｔ３水平,甲状腺组织超氧化物歧化酶（ＳＯＤ）和谷胱甘肽过氧化物酶（ＧＰＳ）的活力以及脂质过氧化产物丙二醛（ＭＤＡ）含量,应用荧光偏振方法测量了甲状腺细胞膜脂的荧光偏振度和平均微黏度,以反映膜脂的流动性,结果：低碘组大鼠血清Ｔ４、Ｔ３水平显低于适碘对照组及高碘组ＳＯＤ和ＧＰｘ活     

Iron deficiency anemia reduces thyroid peroxidase activity in rats

Studies in animals and humans have shown that iron deficiency anemia (IDA) impairs thyroid metabolism. However, the mechanism is not yet clear. The objective of this study was to investigate whether iron (Fe) deficiency lowers thyroid peroxidase (TPO) activity. TPO is a heme-containing enzyme catalyzing the two initial steps in thyroid hormone synthesis. Male weanling Sprague-Dawley rats (n = 84) were randomly assigned to seven groups. Three groups (ID-3, ID-7, ID-11) were fed an Fe-deficient diet containing 3, 7 and 11 microg Fe/g, respectively. Because IDA reduces food intake, three control groups were pair-fed Fe-sufficient diets (35 microg Fe/g) to each of the ID groups and one control group consumed food ad libitum. After 4 wk, hemoglobin, triiodothyronine (T(3)) and thyroxine (T(4)) were lower in the Fe-deficient groups than in the ad libitum control group (P < 0.001). By multiple regression, food restriction had a significant, independent effect on T(4) (P < 0.0001), but not on T(3). TPO activity (by both guaiacol and iodine assays) was markedly reduced by food restriction (P < 0.05). IDA also independently reduced TPO activity (P < 0.05). Compared with the ad libitum controls, TPO activity per thyroid determined by the guaiacol assay in the ID-3, ID-7 and ID-11 groups was decreased by 56, 45 and 33%, respectively (P < 0.05). These data indicate that Fe deficiency sharply reduces TPO activity and suggest that decreased TPO activity contributes to the adverse effects of IDA on thyroid metabolism.     

Influences of feeding of high-iodine eggs on hypo- and hyperthyroid rats

The effects of the feeding of high-iodine eggs to rats with an abnormal thyroid status were investigated. Rats were fed for one week on a commercial diet supplemented with propylthiouracil (PTU) (10 mg/100 g diet) or thyroxine-Na (240 micrograms/100 g diet) respectively, to induce hypo- or hyperthyroidism, and then further fed for 4 weeks on the respective drug-supplemented diets, containing 1% (w/w) of either ordinary or high-iodine egg powder. Control (euthyroid) rats were maintained on the commercial diet. The induction of a hypothyroid state resulted in thyroid hyperplasia, with decreased thyroid iodine content, altered serum thyroid relating hormone levels (increased TSH and decreased T3 and T4), elevated serum total cholesterol and reduced serum triacylglycerol (TG) levels, and also increased muscle and adipose tissue lipoprotein lipase (LPL) activities. In contrast, in the hyperthyroid animals, thyroid atrophy, as well as decreased serum TSH and increased T3 and T4 levels, was associated with reduced serum total cholesterol level and muscle LPL activity. There were no essential differences between animals given high-iodine and ordinary eggs in either hypo- or hyperthyroid state, although the effects of PTU treatment on the thyroid and serum TG level appeared to be slightly lesser in rats given high-iodine eggs than in those given ordinary eggs. It is concluded that high-iodine eggs did not have any side-effect on either hypo- or hyperthyroid rat in this study.     

Dietary selenium intake controls rat plasma selenoprotein P concentration

The purpose of this study was to determine the effect of dietary selenium on selenoprotein P concentration. Selenoprotein P was quantitated in plasma by radioimmunoassay. Selenium-dependent glutathione peroxidase activity in plasma and liver 105,000 x g supernatant was measured for comparison. Weanling male rats were fed a selenium-deficient diet or a control diet that contained 0.5 mg selenium/kg as Na2SeO4. The concentration of selenoprotein P fell at approximately the same rate in the rats fed the selenium-deficient diet as did plasma glutathione peroxidase activity. Groups of weanling rats were fed different levels of selenium for 8 wk. Selenoprotein P concentration was proportional to dietary selenium level up to 0.1 mg/kg and was a greater percentage of control values than was glutathione peroxidase activity. No increment in selenoprotein P concentration occurred between 0.1 and 0.5 mg selenium/kg diet. These results indicate that the concentration of selenoprotein P in the plasma is directly dependent on selenium supply in the diet up to 0.1 mg/kg. There is overlap between the dietary selenium ranges in which selenoprotein P concentration and glutathione peroxidase activity increase, but the selenoprotein P range is lower than the glutathione peroxidase range.     

Influence of diet composition on serum triiodothyronine (T3) concentration, hepatic mitochondrial metabolism and shuttle system activity in rats

Two experiments were conducted to determine if variations in diet composition sufficient to alter circulating triiodothyronine (T3) concentration would influence hepatic mitochondrial metabolism. In experiment 1, mitochondrial respiration and the activity of succinate dehydrogenase (SDH), cytochrome oxidase (CO) and alpha glycerophosphate dehydrogenase (m alpha-GPD) were measured in 42-day-old male rats fed diets containing casein/carbohydrate/fat: 8/73/10% (low protein), 22/59/10% (control protein), and 45/36/10% (high protein) for 3 weeks. When compared to control, serum T3 was increased 2-3 times in the low and decreased 19% in the high protein-fed groups. Mitochondria isolated from low protein-fed rats consumed less oxygen in both state 4 and state 3 with succinate as substrate when compared to control or high protein fed rats. However, ADP/O and respiratory control (RC) ratios were similar in all groups. Activity of SDH and CO was decreased only in low protein-fed rats. M alpha-GPD activity was increased in the low and decreased in the high protein fed-rats. In experiment 2, alpha-glycerophosphate shuttle activity was increased 2-3 fold and malate-aspartate shuttle activity decreased 60% in intact mitochondria isolated from low protein-fed rats when compared to rats pair-fed control diet. These results suggest a role for diet composition as a regulator of hepatic intermediary metabolism mediated by thyroid hormones.     

硒碘对大鼠谷胱甘肽过氧化物酶活力及甲状腺激素代谢的影响──Ⅱ．硒碘营养状态对大鼠甲状腺激素代谢的影响

用四种硒水平饲料和两种碘含量饮水饲养大鼠观察了其甲状腺激素（ＴＨ）代谢。硒组间肝脏、肾脏Ⅰ型脱碘酶（ＩＤⅠ）活力、血清Ｔａ含量差异显著；两碘组间甲状腺重量、甲状腺过氧化物酶（ＴＰＯ）活力。甲状腺碘含量、肾脏ＩＤⅠ及大脑Ⅱ型脱碘酶（ＩＤⅡ）活力差异明显；Ⅰ－（不加碘）组中甲状腺ＩＤⅠ活力与血清三碘甲腺原氨酸（Ｔａ）含量呈显著正相关。提示硒缺乏通过ＩＤⅠ影响ＴＨ代谢继而影响大脑ＩＤⅡ活力并可加重碘缺乏的效应；低碘时甲状腺ＩＤⅠ在维持循环Ｔａ含量中起重要作用；碘缺乏有可能增加硒缺乏的效应；硒、碘对ＴＨ代谢的影响可能在一定程度上取决于自身和对方的营养状态。     

Metabolic rate and thyroid status in rats fed diets of different protein-energy value: the importance of free T3

Oxygen consumption and thyroid hormone status have been investigated in relation to dietary protein and energy intake in young growing rats fed a control diet of 18% protein as well as diets containing 9 and 4.5% protein fed ad libitum and an 18% protein diet fed at a restricted intake for up to 14 days. Measurements of growth rate, food intake and oxygen consumption indicated that the rats fed a 4.5% protein diet ad libitum and those fed restricted amounts of an 18% protein diet have behaved similarly with severely arrested growth and reduced rates of oxygen consumption and food intake. However, the rats fed the 9% protein diet ad libitum differed from the control group only in terms of a reduced growth rate. Among all the rats thyroid hormone status was associated with the metabolic rate only in the case of the concentration of free L-3,3',5-triiodothyronine (T3), which was reduced in the groups fed 4.5% protein and 18% protein (restricted). Total T3 was actually increased in the rats fed 9% and 4.5% protein and unchanged in the restricted group. These differences in the concentrations of free and total T3 appeared to reflect the fact that the binding capacity for T3 increased with decreasing levels of dietary protein. It is concluded therefore that measurement of free rather than total T3 is the appropriate index of physiological thyroid status in protein-energy malnutrition, at least in the rat.     

Iodine deficiency mitigates growth retardation and osteopenia in selenium-deficient rats

Selenium deficiency is associated with impaired bone metabolism and osteopenia in rats. However, it is not known how combined selenium and iodine deficiency affects bone metabolism. Therefore, we investigated the effect of selenium and iodine deficiency on bone metabolism in 2nd-generation selenium- and iodine-deficient rats. Selenium-deficient (Se-), iodine-deficient (I-), selenium- and iodine-deficient (Se-/I-), and control rats (Se+/I+), were pair-fed their respective diets until they were 74 d old. Each pair-fed rat was fed a selenium-adequate diet in the same amount as that consumed the day before by its selenium-deficient counterpart, taking food spillage into account. The skeletal phenotype was analyzed by dual energy X-ray absorptiometry, histomorphometry, and bone metabolism markers. Erythrocyte glutathione peroxidase activity (Gpx) and plasma thyroid hormones were measured to assess selenium and iodine status, respectively. In both Se-/I+ and Se-/I- rats, Gpx was reduced by 99% compared with pair-fed Se+/I+ and Se+/I- rats (P < 0.001). Iodine deficiency reduced plasma thyroxine by 64% in the 2 iodine-deficient groups (P < 0.001). Body weight, tail length, plasma insulin-like growth factor, pituitary growth hormone concentration, and femur and tibia bone mineral density were significantly greater in the Se-/I- rats than in the Se-/I+ rats. This study shows that iodine deficiency mitigated growth retardation and osteopenia in 2nd-generation selenium-deficient rats and suggests that adequate selenium status should be ensured before measures are taken to correct iodine deficiency.