高碘致甲状腺功能减退症患者血浆中去甲肾上腺素和5-羟吲哚乙酸含量变化

甲状腺功能减退症(hypothyroidism,简称甲减)是碘摄入过量引起的甲状腺疾病之一.研究显示,在高碘摄入地区甲减的患病率和亚甲减的5年累积发病率显著增高[1].单胺类神经递质是人体中枢神经重要的信息传递物质,包括去甲肾上腺素(noradrenaline bitartrate,NE)、肾上腺素、多巴胺和5-羟色胺(5-hydroxytryptamine,5-HT)等,其中5-羟吲哚乙酸(5-hydroxyindile acetic acid,5-HIAA)是5-HT的主要代谢产物.现已证实,促甲状腺素释放激素(thyrotropin releasing hormone,TRH)的垂体外作用与单胺类神经递质有关[2],上述神经递质可能参与甲减内分泌调节作用.笔者采用高效液相-电化学检测法测定高水碘地区甲减患者血浆中NE和5-HIAA含量,观察、分析其含量的变化,旨在探讨单胺类神经递质与甲减发生、发展的关系.     

天津市部分市售食品碘含量分析

目的 测定天津市区部分市售食品中碘含量,为天津市区碘营养水平的安全评价以及碘与硒联合作用的研究提供基础数据.方法 从天津市内6区的农贸市场中采集部分市售食品,用砷铈氧化还原法进行碘含量测定.结果 各类食品的碘含量分别为:蔬菜类(4.2±3.16)μg/100g;谷物干豆类(7.6±6.15)μg/100g;动物性食品(20.1±20.54)μg/100g;干海带的碘含量为(4263.6±1895.05)μg/100g.结论 不同种类食物的碘含量不同.不同来源的同类食品样品其碘含量可能有较大的差别.食盐加碘是补充碘的重要措施.     

壳聚糖衍生物对营养性肥胖大鼠的减肥作用

目的 评价2种壳聚糖衍生物对大鼠营养性肥胖的治疗效果。方法喂饲高脂饲料建立营养性肥胖模型后．通过膳食添加不同剂量氧羧和醇化壳聚糖。6周后处死动物，通过体重、体脂含量、相关生化指标及病理学检查衡量其减肥疗效。结果2种壳聚糖衍生物均能够明显降低大鼠体重、体脂含量、肝重、肝脏脂肪含量及胆固醇含量，不同程度地降低血脂及血糖，增加粪便中脂肪的排出量。病理结果显示，修饰后的壳聚糖能够显著改善肥胖所引发的肝脂肪变。结论2种壳聚糖衍生物对于大鼠的营养性肥胖具有一定的治疗作用。     

适应21世纪人才发展需求的本科教学体系的建设与改革

营养与食品卫生学是预防医学和其它医学领域的一门重要课程,在医学院校课程体系中占有极其重要的地位,预防医学、临床医学、康复医学、护理等不同专业的研究生、七年制、本科生、专科生均设有《营养与食品卫生学》课程。进入21世纪后,由于膳食结构的改     

关于成人碘安全摄入量的探讨

目的探讨成人碘的安全摄入量。方法选择甲状腺功能正常的(22.54±2.65岁)健康志愿者。随机分为7组,各组每人每日分别服用500,750,1000,1250,1500,1750,2000μg的碘剂,为期4w。于实验前、实验第2w以及实验结束时分别采集志愿者空腹血、晨尿。用化学发光免疫分析法测定血清FT4、灵敏促甲状腺激素(sTSH),定量放免法测定甲状腺过氧化物酶抗体(thyroid peroxidase antibody,TPOAb)、甲状腺球蛋白抗体(thyroglobulin antibody,TGAb)浓度,用砷铈氧化还原法测定尿碘水平。对被调查者进行为期7 d的膳食调查。采集天津市市售食物、饮用水样品,以及食盐样品,测定其碘含量。结果补碘前人群碘摄入水平充足,尿碘中位数为272.25μg/L,被调查者膳食碘摄入的平均值(含碘盐)为346.24μg/d。与补充碘剂前相比,补碘后各组人群尿碘水平明显增加;血清FT4在正常值范围内下降;各组人群在补充碘剂2 w后血清sTSH明显上升,与补碘前相比增加近1倍多,至4 w后增加近2倍。各剂量组间相比血清sTSH变化幅度基本一致。正常人群补充500～2000μg碘剂2 w后出现了亚临床甲状腺功能减退,各剂量组的发病率在15.00%~47.37%之间。试验结束时未见临床甲减患者。结论正常人群补充500μg/d碘即可引起亚临床甲状腺功能减退。因此,对于生活在碘营养充足地区的人群每日碘的补充剂量不宜超过500μg,结合每日膳食碘的摄入量,我们建议碘的可耐受的最高摄入量(UL)的上限值应低于900μg。     

硒对碘过量EAT大鼠肝、脑抗氧化水平的影响

目的研究高碘及高碘条件下不同硒摄入水平对实验性自身免疫性甲状腺炎（experimental autoimmunethyroiditis,EAT）大鼠肝、脑SOD、GPX活性的影响。方法选择易感Lewis大鼠建立EAT模型,将动物随机分为5组,即对照组（C组）、模型组（M组）、造模＋高碘高硒组（M＋I＋Se＋组）、造模＋高碘适硒组（M＋I＋Se组）、造模＋高碘低硒组（M＋I＋Se-组）。按照实验设计对各组动物喂以不同硒、碘水平饲料。16周后,对大鼠的甲状腺组织进行病理学检查,测定甲状腺自身抗体（TGAb、TMAb）及大鼠肝、脑组织SOD、GPX活性。结果光镜下观察,M组大鼠甲状腺组织出现散在淋巴细胞浸润;M＋I＋Se＋组及M＋I＋Se组部分小叶受累,有淋巴细胞浸润;M＋I＋Se-组病变严重,几乎所有小叶受累。与C组相比,M组大鼠甲状腺自身抗体（TGAb、TMAb）水平明显升高,肝脏GPX活性显著降低。M＋I＋Se组与M组相比,脑组织GPX活性显著降低。与M＋I＋Se-组相比,M＋I＋Se＋组肝、脑GPX活性显著升高,M＋I＋Se组肝脏GPX活性显著升高。肝、脑GPX及SOD活性均有随硒摄入量增加而增强的趋势。结论EAT时大鼠机体抗氧化能力下降,高碘及低硒均可加重EAT大鼠甲状腺、肝、脑组织的氧化损伤,补硒可以提高组织GPX活性。     

碘过量对实验性自身免疫性甲状腺炎大鼠骨代谢的影响

目的 探讨碘过量对实验性自身免疫性甲状腺炎(EAT)大鼠骨代谢的影响.方法 雌性Lewis大鼠36只,体质量为(131±15)g,按体质量随机分为3组:对照组、EAT组和EAT+高碘组,每组12只.以不同含碘量(0.9、0.9、18.0 mg/kg)的饲料喂养各组大鼠,并用猪甲状腺球蛋白(pTG)和完全弗氏佐剂(CFA)对EAT组和EAT+高碘组大鼠进行免疫以建立EAT模型.2周后观察大鼠甲状腺病理改变,测定血清甲状腺自身抗体[甲状腺球蛋白抗体(TGAb)、甲状腺微粒体抗体(TMAb)]和甲状腺激素[三碘甲腺原氨酸(T3)、甲状腺素(T4)]以及骨代谢相关指标[骨钙素(BGP)、抗酒石酸盐酸性磷酸酶(TRAP)、Ⅰ型前胶原羧基末端前肽(PICP)、Ⅰ型胶原羧基吡啶并啉交联肽(ICTP)、胰岛素样生长因子-1(IGF-1)、护骨素(OPG)、核因子κB受体活化因子配体(RANKL)]水平.结果 EAT组和EAT+高碘组大鼠甲状腺组织均呈现炎细胞浸润,局部滤泡结构破坏,其中EAT+高碘组以甲状腺滤泡扩张、融合为主.EAT组和EAT+高碘组大鼠血清TGAb、TMAb、T3和T4水平[(63.01±12.36)%、(60.62±11.24)%,(3.78±1.43)、(125.12±16.00)pmol/L和(75.00±15.44)%、(72.15±15.00)%,(3.69±0.91)、(149.40±20.67)pmol/L]高于对照组[(4.47±1.04)%、(5.73±1.01)%,(0.75±0.12)、(76.91±9.30)pmol/L,P均＜0.05],EAT+高碘组大鼠血清TGAb、TMAb和T4水平较EAT组升高(P均＜0.05).EAT组大鼠血清BGP、PICP和IGF-1水平[(1.70±0.31)、(11.31±1.52)μg/L,(0.31±0.06)mg/L]较对照组[(8.60±0.33)、(14.28±3.10)μg/L,(1.16±0.02)mg/L]降低(P均＜0.05),血清TRAP、ICTP、OPG和RANKL水平[(19.88±3.60)ng/L,(2.43±0.82)、(22.36±2.80)、(1.35±0.23)μg/L]较对照组[(14.57±3.56)ng/L,(0.50±0.20)、(1.61±0.34)、(0.10±0.02)μg/L]升高(P均＜0.05);与EAT组比较,EAT+高碘组大鼠血清PICP和OPG水平[(8.03±1.84)、(16.80±3.79)μg/L]明显降低(P均＜0.05).结论 EAT时大鼠的破骨细胞分化与成熟增强,导致骨吸收增强.碘过量可抑制EAT大鼠成骨细胞和破骨细胞活性,呈现低转化型骨质疏松.

Abstract：

Objective To explore the effect of iodine excess on bone metabolism in experimental autoimmune thyroiditis (EAT) rats. Methods We selected 36 female Lewis rats with body weight of (131 ± 15)g,and divided them into 3 groups randomly: control group, EAT group and EAT + high iodine group, assuring 12 rats in every group. These rats were fed fodder with different concentration of iodine(0.9,0.9, 18.0 mg/kg), and rats in EAT group and EAT + high iodine group were immunized with pig thyroglobulin(pTG) and complete Freund's adjuvant(CFA) to create EAT model. After two weeks, the pathological changes of the thyroid tissues were observed,and the serum thyroid autoantibody[thyroglobulin antibody(TGAb) and thyroid microsomal antibody(TMAb)], the thyroid hormone levels[triiodo thyronine(T3) and thyrine(T4)] and some relevant data of bone metabolism[bone gla protein (BGP), tartrate-resistant acid phosphatase (TRAP), C-terminal propeptide of type Ⅰ procollagen (PICP),C-terminal telopeptide of type Ⅰ collagen (ICTP), insulin-like growth factor- 1 ( IGF- 1 ), osteoprotegerin (OPG) and receptor activator of NF-κB ligand (RANKL)] were measured. Results Inflammatory cell infiltration and local follicular structural damage were observed in the thyroid tissues of EAT rats in EAT group and EAT + high iodine group, and the pathological changes of EAT + high iodine group were mainly thyroid follicular expansion and integration. The level of serum TGAb, TMAb, T3 and T4 of EAT rats in EAT group and EAT + high iodine group[ (63.01 ± 12.36)%, (60.62 ± 11.24)%, (3.78 ± 1.43), (125.12 ± 16.00)pmol/L and (75.00 ± 15.44)%,(72.15 ± 15.00)%, (3.69 ± 0.91 ), (149.40 ± 20.67)pmol/L] were higher than those of the control group[ (4.47 ±1.04)%, (5.73 ± 1.01 )%, (0.75 ± 0.12), (76.91 ± 9.30)pmol/L, all P ＜ 0.05], and the level of serum TGAb,TMAb and T4 of EAT rats in EAT + high iodine group were higher than those of the EAT group(all P ＜ 0.05).The level of serum BGP, PICP and IGF- 1 in EAT group[ ( 1.70 ± 0.31 ), ( 11.31 ± 1.52) μg/L, (0.31 ± 0.06 ) mg/L]were lower than those of the control group[ (8.60 ± 0.33), (14.28 ± 3.10)μg/L, (1.16 ± 0.02)mg/L, all P ＜0.05], and the level of serum TRAP, ICTP, OPG and RANKL[ ( 19.88 ± 3.60)ng/L, (2.43 ± 0.82), (22.36 ± 2.80),( 1.35 ± 0.23 )μg/L] were higher than those of the control group[ ( 14.57 ± 3.56)ng/L, (0.50 ± 0.20), (1.61 ± 0.34),(0.10 ± 0.02)μg/L, all P ＜ 0.05]; compared with EAT group, the level of PCIP and OPG in EAT + high iodine group [ (8.03 ± 1.84), ( 16.80 ± 3.79)μg/L] were obviously decreased(all P ＜ 0.05). Conclusions The reinforcement of differentiation and maturation of osteoblast in the EAT rats results in the increasing of bone resorption. The activity of osteoblast and osteoclast of the EAT rats are inhibited by excessive iodine, showing a low conversion-type osteoporosis.     

碘充足地区孕妇碘水平及新生儿甲状腺功能分析

目的了解碘充足地区孕妇碘营养状况及新生儿甲状腺功能。方法选择天津市中心妇产科医院的174名妊娠晚期孕妇为调查对象,收集其空腹晨尿及新生儿脐带血,分别测定尿碘浓度及血清中游离三碘甲腺原氨酸(FT3)、游离甲状腺素(FT4)、敏感促甲状腺激素(sTSH)水平。结果 174名孕妇尿碘中位数为217.06μg/L9,.2%孕妇碘过量2,7.6%碘缺乏;新生儿FT3、FT4s、TSH水平为(2.31±0.28)(、16.50±1.34)pmol/L、4.71(3.96～6.04)μU/mL;整体孕妇尿碘水平与新生儿FT3、FT4s、TSH水平无相关性(P>0.05),不同碘营养状况孕妇所产新生儿FT3、FT4水平在各组间差异无统计学意义(P<0.05),碘不足组孕妇所产新生儿的sTSH水平高于碘超足量组;男婴的sTSH水平高于女婴,且男婴的sTSH更偏向于高值分布,经阴道产的新生儿sTSH水平高于剖宫产。结论碘充足地区孕妇整体碘水平适宜,但仍存在碘缺乏和碘过量个体,碘缺乏孕妇所产新生儿患甲减、亚甲减的风险较高;性别和生产方式影响新生儿的sTSH水平。     

高水碘摄入对成人空腹血糖影响的探讨

Objective:To investigate the blood glucose level in different iodine status, then explore the impact of excess-iodine-intake on fasting blood-glucose. Methods:Adults were chosen from Haixing County in Cangzhou, Hebei. Llimosis morning-urinary and venous blood were collected to measure the levels of urinary iodine. Chemilu-minescent immunoassay was used to perform free triiodothyronine (FT₃), free thyroxine (FT₄), and sensitive thyroid-stimulating hormone (sTSH) in serum. Fasting blood-glucose was also measured by glucometer. Results:The median of water iodine in the excess-iodine-intake area (841.4 μg/L) was higher than that in the control area (12.79 μg/L, P<0.05). For adults’ urine iodine, the excess-iodine-intake area was higher(P<0.05), with the value of 1 137.3（646.8～1 450.8）μg/L vs 216.6（146.5～366.9）μg/L. The level of FT₃ in the excess-iodine-intake area was lower (P<0.05), with the value of （4.72±0.48） pmol/L vs （4.96±0.36）pmol/L. No significant difference was found in the FT₄ level in the areas. The median of sTSH in the excess-iodine-intake area was higher than that in the control area, with the value of（3.07±2.17）μIU/ mL vs （2.30±1.07） μIU/mL . And the prevalence of thyroid disease in the excess-iodine-intake area was higher, with 43(22.75%) vs 8(10.13%). No significant difference in the level of the fasting blood-glucose was found in the areas (P>0.05). Age and FT₄ were found positively correlated with fasting blood-glucose by correlation analysis（r=0.258,P<0.001; r=0.154,P=0.013）, while the others were not related. Conclusion:Difference in fasting blood-glucose in water-iodine-excess area and the control area does not exist. Yet further study should be taken in a larger population-based epidemiological investigation to confirm the effects of excess-iodine-intake on glucose.      

碘对自身免疫性甲状腺炎大鼠抗氧化能力影响

目的 探讨不同碘水平对实验性自身免疫甲状腺炎(experimental autoimmune thyroiditis,EAT)大鼠抗氧化活性的影响.方法 选择雌性Lewis大鼠,随机分为4组;于实验第8周处死动物,观察大鼠甲状腺组织的病理变化,测定甲状腺球蛋白抗体(TGAb)、甲状组甲状腺腺微粒体抗体(TMAb),肝和脑组织中谷胱甘肽过氧化物酶(GSH-Px)、超氧化物歧化酶(SOD)活性.结果 各造模组织出现淋巴细胞浸润,高碘时以甲状腺滤泡扩张、融合为主,低碘时以增生为主;高碘+造模组大鼠的TGAb和TMAb水平分别为(75.00±15.44)%,(72.15±15.00)%,明显高于造模组的(63.01±12.36)%,(60.62±11.24)%和低碘+造模组的(58.87±9.57)%,(57.89±9.67)%(P<0.05);低碘组EAT大鼠肝组织GSH-Px和SOD活性最低,分别为(122.01±10.34),(522.81±54.62)U/(mg·prot)(P<0.05)碘过量时脑组织谷胱甘肽过氧化物酶(GPX)活性最低,为(412.09±115.71)U/(mg·prot(P<0.05).结论 碘缺乏和碘过量均能够加重EAT大鼠甲状腺的炎性损伤和氧化损伤,其中碘缺乏对EAT大鼠作用明显.