Effects of different levels of iodine concentration on insulin-like growth factors Ⅰ mRNA expression of thyroid and breast in lactating rats

Objective To study the effects of different levels of iodine concentration on insulin-like growth factors Ⅰ (IGF-1) mRNA expression of thyroid and breast in lactating rats. Methods Thirty Wistar female rats, having been weaned for 1 month, were randomly divided into three groups according to their body weights, i. e. :low iodine(LI) group,adequate iodine(AI) group, high iodine(HI) group, 10 rats in each group. Synthetic fodder and deionized water containing iodine of 0,150,3000 μg/L was respectively fed to these rats. After fed for 3 months, the rats mated and had offspring. Their mammary glands, thyroids and serum were sampled at lactation day 5. The serum iodine of lactating rats were determined by moderate acid digestion method, level of T3 and T4 were determined by radioimmunoassay method, and the expressions of IGF-1 mRNA of mammary glands and thyroids were determined by real-time fluorescence quantitative PCR assay. Results The value of serum iodine of LI group [(17.38±3.27) μg/L] was lower than that of AI group [(43.42±6.92) μg/L, P<0.05], and the value of serum iodine of HI group[(350.10±38.46)μg/L] was higher than that of AI group (P<0.05). The level of T3 of LI group and HI group[ (1.11±0.25), (1.61±0.33)μg/L] reduced obviously compared with that of AI group[(2.18±0.46) μg/L, P<0.05]. The mean of T4 of LI group and HI group[(33.40±11.11),(56.54±10.38)μg/L] had no statistical significance compared with AI group(44.02±12.51)μg/L, P>0.05), but the level of T4 of LI group was lower than that of HI group(P<0.05). The level of IGF-1 mRNA expression of thyroid in LI group and HI group (0.34±0.08, 0.23±0.08) was higher than that of AI group(0.15±0.03, P<0.05). The level of IGF-1 mRNA expression of lactating mammary in LI group(0.59±0.18) was higher than that of AI group(0.40±0.10, P<0.05). The level of IGF-1 mRNA expression of thyroid was lower than that of breast between the same group(t=3.54, 6.44,2.62, all P<0.05). Conclusion Iodine could affect IGF-1 mRNA expression of thyroid and lactating mammary, and IGF-1 mRNA expression of lactating mammary was stronger than that of the thyroid.     

低硒、低碘及联合对亲代和子代大鼠骨、软骨生长的影响

Objective To study the effects of selenium deficiency,iodine deficiency and combined selenium and iodine deficiency on bone and cartilage growth in the parental and the first filial generation rats. Methods Forty-eight weanling healthy SD rats were randomly divided into selenium deficieney, iodine deficiency, combined selenium and iodine deficiency and control groups according to their body mass. These rats were fed with selenium deficiency, iodine deficiency, combined selenium and iodine deficiency, and normal fodder, respectively. The parental rats (about 3 months old) were mated in each group 8 weeks after the beginning of the experiment. Right tibias and left knee joints were collected when the parental generation rats were about 6 months and the first filial generation rats were about 3 months old. Tibial length, mid-shaft tibial diameter, and articular cartilage diameters of the right tibias were measured by vernier caliper. Left knee joints were embedded and cut into sections and the thickness of the growth plate cartilage, layers of proliferative and hypertrophic chondrocytes in growth plate cartilage were observed under the light microscope. Results The selenium deficiency had significant effect on serum selenium level of the parental and the first filial generation rats(F value were 239.56,232.68, P< 0.01), and also on serum T4 level of the first filial generation rats(F value were 6.95, P < 0.05). The iodine deficiency had significant effect on serum T3 and T4 level in the two generations rats(F value were 14.11,14.05,30.29,34.53, P < 0.01 ). There were interactions between selenium deficiency and iodine deficiency on serum T4 level in the first filial generation rats (F= 5.99, P< 0.05). The serum selenium of selenium deficiency group[ (30.28 ± 6.34), (43.95 ± 9.75)μg/L],combined selenium and iodine deficiency group[ (30.33 ± 5.18), (35.40 ± 3.16)μg/L] were significantly lower than iodine deficiency group[(345.83 ± 29.55), (245.24 ± 9.95)μg/L] and the controls[ (358.64 ± 30.50), (236.50 ±9.75) μg/L] in the two generations. The serum T3 of combined selenium and iodine deficiency group [(0.55 ± 0.05 ),(0.88 ± 0.14)nmol/L] were significantly lower than the controls[(0.75 ± 0.08), (1.26 ± 0.26)nmol/L] in the two generations. The serum T4 of iodine deficiency [ (24.11 ± 2.29), (42.10 ± 8.92) nmol/L ] and combined selenium and iodine deficiency group[ (20.66 ± 1.93), (26.55 ± 5.98)nmol/L] were significantly lower than the controls[ (36.15 ±2.74), (52.79 ± 8.84)nmol/L] and selenium deficiency group[ (28.12 ± 3.33), (52.02 ± ll.99)nmol/L] in the two generations. The selenium deficiency and iodine deficiency had significant effect on tibial length, thickness of the growth plate cartilage, layers of proliferative and hypertrophic chondrocytes in first filial generation rats(F values were 24.31,6.98,40.76,56.15,25.24,82.82, 10.07,5.57, P <0.05 or <0.01). There were interactions between selenium deficiency and iodine deficiency on tibial length, thickness of the growth plate cartilage, layers of proliferative and hypertrophic chondrocytes (F values were 5.68,24.86,41.82,9.12, P <0.05 or <0.01 ). The tibial length of the selenium deficiency group[ (33.17 ± 0.34)mm] and combined selenium and iodine deficiency group[ (31.30 ± 0.87)mm] were significantly lower than the controls[ (34.12 ± 0.32)mm, P< 0.05]. Thickness of the growth plate cartilage [ (1.60 ± 0.18)mm ], layers of proliferative chondrocyte (8.54 ± 0.81), and hypertrophic chondrocyte (4.95 ± 0.37)of the combined selenium and iodine deficiency group were significantly decreased when compared to the selenium deficiency group[ (3.03 ± 0.10)mm, 14.68 ± 0.84,6.60 ± 0.31], iodine deficiency group[ (2.90 ± 0.09)mm, 13.75 ±0.33,6.61 ± 0.84 ] and the controls [ (3.19 ± 0.09) mm, 14.94 ± 0.36, 6.64 ± 0.26, P <0.05]. Thickness of the growth plate cartilage, layers of proliferative chondrocyte of the iodine deficiency group were lower than the controls(P<0.05). Conclusions Selenium deficiency impair tibial growth in first filial generation rats, iodine deficiency retarded the chondroncyte proliferation and decreases the thickness of growth plate cartilage in first filial generation rats, and combined selenium and iodine deficiency significantly impair the growth of bone and cartilage in first filial generation rats.     

低硒、低碘及联合对亲代和子代大鼠骨、软骨生长的影响

Objective To study the effects of selenium deficiency,iodine deficiency and combined selenium and iodine deficiency on bone and cartilage growth in the parental and the first filial generation rats. Methods Forty-eight weanling healthy SD rats were randomly divided into selenium deficieney, iodine deficiency, combined selenium and iodine deficiency and control groups according to their body mass. These rats were fed with selenium deficiency, iodine deficiency, combined selenium and iodine deficiency, and normal fodder, respectively. The parental rats (about 3 months old) were mated in each group 8 weeks after the beginning of the experiment. Right tibias and left knee joints were collected when the parental generation rats were about 6 months and the first filial generation rats were about 3 months old. Tibial length, mid-shaft tibial diameter, and articular cartilage diameters of the right tibias were measured by vernier caliper. Left knee joints were embedded and cut into sections and the thickness of the growth plate cartilage, layers of proliferative and hypertrophic chondrocytes in growth plate cartilage were observed under the light microscope. Results The selenium deficiency had significant effect on serum selenium level of the parental and the first filial generation rats(F value were 239.56,232.68, P< 0.01), and also on serum T4 level of the first filial generation rats(F value were 6.95, P < 0.05). The iodine deficiency had significant effect on serum T3 and T4 level in the two generations rats(F value were 14.11,14.05,30.29,34.53, P < 0.01 ). There were interactions between selenium deficiency and iodine deficiency on serum T4 level in the first filial generation rats (F= 5.99, P< 0.05). The serum selenium of selenium deficiency group[ (30.28 ± 6.34), (43.95 ± 9.75)μg/L],combined selenium and iodine deficiency group[ (30.33 ± 5.18), (35.40 ± 3.16)μg/L] were significantly lower than iodine deficiency group[(345.83 ± 29.55), (245.24 ± 9.95)μg/L] and the controls[ (358.64 ± 30.50), (236.50 ±9.75) μg/L] in the two generations. The serum T3 of combined selenium and iodine deficiency group [(0.55 ± 0.05 ),(0.88 ± 0.14)nmol/L] were significantly lower than the controls[(0.75 ± 0.08), (1.26 ± 0.26)nmol/L] in the two generations. The serum T4 of iodine deficiency [ (24.11 ± 2.29), (42.10 ± 8.92) nmol/L ] and combined selenium and iodine deficiency group[ (20.66 ± 1.93), (26.55 ± 5.98)nmol/L] were significantly lower than the controls[ (36.15 ±2.74), (52.79 ± 8.84)nmol/L] and selenium deficiency group[ (28.12 ± 3.33), (52.02 ± ll.99)nmol/L] in the two generations. The selenium deficiency and iodine deficiency had significant effect on tibial length, thickness of the growth plate cartilage, layers of proliferative and hypertrophic chondrocytes in first filial generation rats(F values were 24.31,6.98,40.76,56.15,25.24,82.82, 10.07,5.57, P <0.05 or <0.01). There were interactions between selenium deficiency and iodine deficiency on tibial length, thickness of the growth plate cartilage, layers of proliferative and hypertrophic chondrocytes (F values were 5.68,24.86,41.82,9.12, P <0.05 or <0.01 ). The tibial length of the selenium deficiency group[ (33.17 ± 0.34)mm] and combined selenium and iodine deficiency group[ (31.30 ± 0.87)mm] were significantly lower than the controls[ (34.12 ± 0.32)mm, P< 0.05]. Thickness of the growth plate cartilage [ (1.60 ± 0.18)mm ], layers of proliferative chondrocyte (8.54 ± 0.81), and hypertrophic chondrocyte (4.95 ± 0.37)of the combined selenium and iodine deficiency group were significantly decreased when compared to the selenium deficiency group[ (3.03 ± 0.10)mm, 14.68 ± 0.84,6.60 ± 0.31], iodine deficiency group[ (2.90 ± 0.09)mm, 13.75 ±0.33,6.61 ± 0.84 ] and the controls [ (3.19 ± 0.09) mm, 14.94 ± 0.36, 6.64 ± 0.26, P <0.05]. Thickness of the growth plate cartilage, layers of proliferative chondrocyte of the iodine deficiency group were lower than the controls(P<0.05). Conclusions Selenium deficiency impair tibial growth in first filial generation rats, iodine deficiency retarded the chondroncyte proliferation and decreases the thickness of growth plate cartilage in first filial generation rats, and combined selenium and iodine deficiency significantly impair the growth of bone and cartilage in first filial generation rats.     

高碘地区妊娠晚期妇女与育龄妇女甲状腺功能的比较

探讨妊娠和高碘对妇女甲状腺功能及甲状腺自身免疫功能的影响.选择高碘地区(27.69±4.73)岁孕妇210例和(30.62±6.01)岁育龄妇女290例;采集空腹晨尿及静脉血,砷-铈催化分光光度法测定尿碘浓度,化学发光法测定血清游离三碘甲腺原氨酸(FT3)、游离甲状腺素(FT4)及灵敏促甲状腺激素(sTSH),放射免疫法测定血清甲状腺过氧化物酶抗体(TPOAb)和甲状腺球蛋白抗体(TGAb).孕妇和育龄妇女尿碘中位数分别为1 240.70μg/L和949.21μg/L,有94.3%的孕妇和81.0%的育龄妇女碘过量.孕妇和育龄妇女甲状腺疾病总患病率为22.9%和30.3%,孕妇甲状腺功能亢进症(甲亢)、亚临床甲亢、甲状腺功能减退症(甲减)、亚临床甲减的患病率分别为0.5%、1.9%、0.5%和20.0%.育龄妇女的甲亢、亚临床甲亢、甲减及亚临床甲减的患病率分别为2.8%、0.3%、0.3%和26.9%.孕妇的FT3、FT4水平低于育龄妇女[(4.03±0.59对4.71±1.04)pmol/L,(13.35±1.59对14.27±3.63)pmol/L,均P＜0.01],TGAb阳性率低于育龄妇女(7.1%对14.1%,P=0.014).高碘地区妇女甲状腺疾病患病率及甲状腺自身抗体阳性率较高,妊娠使孕妇甲状腺激素水平及TGAb阳性率较育龄妇女降低,建议育龄妇女及孕妇控制碘摄入,并加强甲状腺功能和甲状腺自身抗体的监测.

Abstract：

To explore the influences of pregnancy and iodine intake on thyroid function and immune functions, 210 pregnant women and 290 fertile women were chosen from iodine excess area, and the average ages of them were (27. 69±4. 73 )and (30. 62±6. 01 )years respectively. Fasting blood and urine were collected in the morning. The urinary iodine level was determined by arsenic-cerium catalytic contact. Serum free triiodothyronine ( FT3 ), free thyroxine ( FT4 ), and sensitive thyroid-stimulating hormone ( sTSH ) levels were measured by chemiluminescence.Thyroid peroxidase antibody (TPOAb)and thyroglobulin antibody (TGAb)were measured by radioimmunoassay. The median urinary iodine in the pregnant and fertile women were I 240. 70 and 949. 21 μg/L, respectively. There were 84. 3% pregnant women and 81.0% fertile women admitting excess iodine intake. The prevalence of overall thyroid diseases was 22. 9% in the pregnant women and 30. 3% in the fertile women. The prevalence of hyperthyroidism,subclinical hyperthyroidism, hypothyroidism, and subclinical hypothyroidism was0. 5%, 1.9%, 0. 5%, and 20. 0% in the former group, and 2. 8%, 0. 3%, 0. 3%, and 26. 9% in the latter. Both FT3 and FT4 levels of the pregnant women were lower than those of fertile women [(4. 03±0. 59 vs 4. 71 ± 1.04)pmol/L, ( 13. 35 ± 1.59 vs 14. 27 ±3.63 )pmol/L,both P＜0. 01], and the positive rate of TGAb of pregnant women was also lower than that of fertile women (7. 1% vs14. 1%, P=0. 014). The prevalence of thyroid diseases and positive rate of thyroid autoantibodies is high in women with excess iodine intake. Compared with fertile women, pregnancy may lead to decreas~s in level of thyroid hormones and positive rate of TGAb. Their iodine intake should be controlled, and the thyroid function and autoimmunity antibodies should be monitored.     

妊娠期大鼠不同程度碘缺乏对胎鼠碘代谢和甲状腺功能的影响

Objective To study the effects of iodine deficiency during pregnancy on fetal iodine metabolism and thyroid function. Methods Wistar dams were randomly divided into four groups: severe iodine deficiency(SID), moderate iodine deficiency(MoID), mild iodine deficiency(MiID) and normal iodine(NI). All the dams were fed with iodine deficient food(iodine contents: 50 μg/kg) and drinking water with different doses of KI (0,54.9,163.8,381.7 μg/L) for 3 months till mating. Iodine was supplied at the dose of 1.24 μg/d(SID), 2.50 μg/d(MoID), 5.00 μg/d(MiID) and 10.00 μg/d(NI), respectively. The dams and their fetuses on gestation of 20 days were studied. Urine iodine of dams and iodine contents in fetal amniotic fluid were measured by As3+-Ce4+catalytic spectrophotometry using ammonium persulfate digestion. And blood iodine in pregnant rats and iodine contents in placental tissue were measured by As3+-Ce4+catalytic spectrophotometry in dry ash of samples in KClO3-ZnSO4-K2CO3-NaCl. Thyroid hormone levels in mother serum and in fetal amniotic fluid were detected by chemiluminascent assay, and their thyroid glands were weighted and carefully observed. Results ①Iodine content in urine and blood of pregnant rats and amniotic fluid of fetal rats reduced along with their decrease of iodine supply. Urine iodine median of rats in 4 groups(NI: 353.7 μg/L; MiID: 115.9 μg/L; MoID: 26.9 μg/L; SID: 0 μg/L) were statistically significant(χ2=32.884, P < 0.01). Blood iodine level in MoID and SID[(29.4±18.6), (11.7± 7.0)μg/L]was significantly lower than that in NI[(49.1±23.0)μg/L, P < 0.05 or < 0.01]. In iodine deficiency groups, there was a decreasing trend in iodine contents of fetal amniotic fluid[MiID: (48.3±23.1)μg/L; MoID: (29.2±14.7)μ/L; SID:(19.5±6.7)μg/L]and an increasing tendency in iodine contents of placental tissue [MiID: (0.57±0.26)μg/g, MoID: (0.53±0.34)μg/g; SID: (0.53±0.15)μg/g], but there was no statistical significance(P>0.05). ②In SID, TT4[(14.3±4.1)nmol/L]and FT4[(10.8±3.6)pmol/L]were lower than that in NI[(28.4±19.3)nmol/L, (20.2±8.0)pmol/L, P < 0.05 or < 0.01], while that in MoID[(22.1±6.1)nmol/L, (18.5±4.1)pmol/L]and MiID[(25.5±13.1)nmol/L, (18.6±8.4)pmol/L]were decreased without statistical significance(P > 0.05). And FT3/FT4 ratio(0.34±0.16), absolute[(48.4±22.7)mg]and relative weights[(144± 76)mg/kg]of thyroid gland in pregnant rats were respectively higher than that in NI[0.16±0.02, (19.5±3.1)mg, (66±10)mg/kg, P<0.01]. But that in MoID[0.19±0.04, (27.0±5.7)mg, (84±19)mg/kg]and MiID[0.17± 0.06, (25.0±8.9)mg, (78±25)mg/kg]were increased without statistical significance(P > 0.05). A visibly congestive enlargement thyroid was found in SID, while thyroid mildly enlarged in MoID and MiID. ③Compared with NI [(2.38±1.55)pmol/L,0.50±0.18], the FT4 levels [(1.07±0.87) pmol/L]in amniotic fluid were significantly decreased (P < 0.05) and the FT3/FT4 ratio (1.96±0.61) was significantly increased (P < 0.01) in SID. There were no statistical significances(P > 0.05) in other 3 groups[MiID: (2.77±0.90)pmol/L,0.46±0.15; MoID: (2.35±0.76)pmoL/L,0.61±0.21]. A visible thyroid enlargement with hyperemia was observed in SID fetus while in other 2 experiment groups their thyroids were only mildly congested. Conclusions Severe iodine deficiency during pregnancy can result in both mother and fetus overt hypothyroidism. The fetal thyroid hormone levels in mild iodine deficiency status is close to normal levels because of maternal and placental compensation. Moreover, both the dam and the fetus suffer from the negative effects in moderate iodine deficiency during pregnancy.     

妊娠期大鼠不同程度碘缺乏对胎鼠碘代谢和甲状腺功能的影响

Objective To study the effects of iodine deficiency during pregnancy on fetal iodine metabolism and thyroid function. Methods Wistar dams were randomly divided into four groups: severe iodine deficiency(SID), moderate iodine deficiency(MoID), mild iodine deficiency(MiID) and normal iodine(NI). All the dams were fed with iodine deficient food(iodine contents: 50 μg/kg) and drinking water with different doses of KI (0,54.9,163.8,381.7 μg/L) for 3 months till mating. Iodine was supplied at the dose of 1.24 μg/d(SID), 2.50 μg/d(MoID), 5.00 μg/d(MiID) and 10.00 μg/d(NI), respectively. The dams and their fetuses on gestation of 20 days were studied. Urine iodine of dams and iodine contents in fetal amniotic fluid were measured by As3+-Ce4+catalytic spectrophotometry using ammonium persulfate digestion. And blood iodine in pregnant rats and iodine contents in placental tissue were measured by As3+-Ce4+catalytic spectrophotometry in dry ash of samples in KClO3-ZnSO4-K2CO3-NaCl. Thyroid hormone levels in mother serum and in fetal amniotic fluid were detected by chemiluminascent assay, and their thyroid glands were weighted and carefully observed. Results ①Iodine content in urine and blood of pregnant rats and amniotic fluid of fetal rats reduced along with their decrease of iodine supply. Urine iodine median of rats in 4 groups(NI: 353.7 μg/L; MiID: 115.9 μg/L; MoID: 26.9 μg/L; SID: 0 μg/L) were statistically significant(χ2=32.884, P < 0.01). Blood iodine level in MoID and SID[(29.4±18.6), (11.7± 7.0)μg/L]was significantly lower than that in NI[(49.1±23.0)μg/L, P < 0.05 or < 0.01]. In iodine deficiency groups, there was a decreasing trend in iodine contents of fetal amniotic fluid[MiID: (48.3±23.1)μg/L; MoID: (29.2±14.7)μ/L; SID:(19.5±6.7)μg/L]and an increasing tendency in iodine contents of placental tissue [MiID: (0.57±0.26)μg/g, MoID: (0.53±0.34)μg/g; SID: (0.53±0.15)μg/g], but there was no statistical significance(P>0.05). ②In SID, TT4[(14.3±4.1)nmol/L]and FT4[(10.8±3.6)pmol/L]were lower than that in NI[(28.4±19.3)nmol/L, (20.2±8.0)pmol/L, P < 0.05 or < 0.01], while that in MoID[(22.1±6.1)nmol/L, (18.5±4.1)pmol/L]and MiID[(25.5±13.1)nmol/L, (18.6±8.4)pmol/L]were decreased without statistical significance(P > 0.05). And FT3/FT4 ratio(0.34±0.16), absolute[(48.4±22.7)mg]and relative weights[(144± 76)mg/kg]of thyroid gland in pregnant rats were respectively higher than that in NI[0.16±0.02, (19.5±3.1)mg, (66±10)mg/kg, P<0.01]. But that in MoID[0.19±0.04, (27.0±5.7)mg, (84±19)mg/kg]and MiID[0.17± 0.06, (25.0±8.9)mg, (78±25)mg/kg]were increased without statistical significance(P > 0.05). A visibly congestive enlargement thyroid was found in SID, while thyroid mildly enlarged in MoID and MiID. ③Compared with NI [(2.38±1.55)pmol/L,0.50±0.18], the FT4 levels [(1.07±0.87) pmol/L]in amniotic fluid were significantly decreased (P < 0.05) and the FT3/FT4 ratio (1.96±0.61) was significantly increased (P < 0.01) in SID. There were no statistical significances(P > 0.05) in other 3 groups[MiID: (2.77±0.90)pmol/L,0.46±0.15; MoID: (2.35±0.76)pmoL/L,0.61±0.21]. A visible thyroid enlargement with hyperemia was observed in SID fetus while in other 2 experiment groups their thyroids were only mildly congested. Conclusions Severe iodine deficiency during pregnancy can result in both mother and fetus overt hypothyroidism. The fetal thyroid hormone levels in mild iodine deficiency status is close to normal levels because of maternal and placental compensation. Moreover, both the dam and the fetus suffer from the negative effects in moderate iodine deficiency during pregnancy.     

妊娠期大鼠不同程度碘缺乏对胎鼠碘代谢和甲状腺功能的影响

Objective To study the effects of iodine deficiency during pregnancy on fetal iodine metabolism and thyroid function. Methods Wistar dams were randomly divided into four groups: severe iodine deficiency(SID), moderate iodine deficiency(MoID), mild iodine deficiency(MiID) and normal iodine(NI). All the dams were fed with iodine deficient food(iodine contents: 50 μg/kg) and drinking water with different doses of KI (0,54.9,163.8,381.7 μg/L) for 3 months till mating. Iodine was supplied at the dose of 1.24 μg/d(SID), 2.50 μg/d(MoID), 5.00 μg/d(MiID) and 10.00 μg/d(NI), respectively. The dams and their fetuses on gestation of 20 days were studied. Urine iodine of dams and iodine contents in fetal amniotic fluid were measured by As3+-Ce4+catalytic spectrophotometry using ammonium persulfate digestion. And blood iodine in pregnant rats and iodine contents in placental tissue were measured by As3+-Ce4+catalytic spectrophotometry in dry ash of samples in KClO3-ZnSO4-K2CO3-NaCl. Thyroid hormone levels in mother serum and in fetal amniotic fluid were detected by chemiluminascent assay, and their thyroid glands were weighted and carefully observed. Results ①Iodine content in urine and blood of pregnant rats and amniotic fluid of fetal rats reduced along with their decrease of iodine supply. Urine iodine median of rats in 4 groups(NI: 353.7 μg/L; MiID: 115.9 μg/L; MoID: 26.9 μg/L; SID: 0 μg/L) were statistically significant(χ2=32.884, P < 0.01). Blood iodine level in MoID and SID[(29.4±18.6), (11.7± 7.0)μg/L]was significantly lower than that in NI[(49.1±23.0)μg/L, P < 0.05 or < 0.01]. In iodine deficiency groups, there was a decreasing trend in iodine contents of fetal amniotic fluid[MiID: (48.3±23.1)μg/L; MoID: (29.2±14.7)μ/L; SID:(19.5±6.7)μg/L]and an increasing tendency in iodine contents of placental tissue [MiID: (0.57±0.26)μg/g, MoID: (0.53±0.34)μg/g; SID: (0.53±0.15)μg/g], but there was no statistical significance(P>0.05). ②In SID, TT4[(14.3±4.1)nmol/L]and FT4[(10.8±3.6)pmol/L]were lower than that in NI[(28.4±19.3)nmol/L, (20.2±8.0)pmol/L, P < 0.05 or < 0.01], while that in MoID[(22.1±6.1)nmol/L, (18.5±4.1)pmol/L]and MiID[(25.5±13.1)nmol/L, (18.6±8.4)pmol/L]were decreased without statistical significance(P > 0.05). And FT3/FT4 ratio(0.34±0.16), absolute[(48.4±22.7)mg]and relative weights[(144± 76)mg/kg]of thyroid gland in pregnant rats were respectively higher than that in NI[0.16±0.02, (19.5±3.1)mg, (66±10)mg/kg, P<0.01]. But that in MoID[0.19±0.04, (27.0±5.7)mg, (84±19)mg/kg]and MiID[0.17± 0.06, (25.0±8.9)mg, (78±25)mg/kg]were increased without statistical significance(P > 0.05). A visibly congestive enlargement thyroid was found in SID, while thyroid mildly enlarged in MoID and MiID. ③Compared with NI [(2.38±1.55)pmol/L,0.50±0.18], the FT4 levels [(1.07±0.87) pmol/L]in amniotic fluid were significantly decreased (P < 0.05) and the FT3/FT4 ratio (1.96±0.61) was significantly increased (P < 0.01) in SID. There were no statistical significances(P > 0.05) in other 3 groups[MiID: (2.77±0.90)pmol/L,0.46±0.15; MoID: (2.35±0.76)pmoL/L,0.61±0.21]. A visible thyroid enlargement with hyperemia was observed in SID fetus while in other 2 experiment groups their thyroids were only mildly congested. Conclusions Severe iodine deficiency during pregnancy can result in both mother and fetus overt hypothyroidism. The fetal thyroid hormone levels in mild iodine deficiency status is close to normal levels because of maternal and placental compensation. Moreover, both the dam and the fetus suffer from the negative effects in moderate iodine deficiency during pregnancy.     

妊娠期大鼠不同程度碘缺乏对胎鼠碘代谢和甲状腺功能的影响

Objective To study the effects of iodine deficiency during pregnancy on fetal iodine metabolism and thyroid function. Methods Wistar dams were randomly divided into four groups: severe iodine deficiency(SID), moderate iodine deficiency(MoID), mild iodine deficiency(MiID) and normal iodine(NI). All the dams were fed with iodine deficient food(iodine contents: 50 μg/kg) and drinking water with different doses of KI (0,54.9,163.8,381.7 μg/L) for 3 months till mating. Iodine was supplied at the dose of 1.24 μg/d(SID), 2.50 μg/d(MoID), 5.00 μg/d(MiID) and 10.00 μg/d(NI), respectively. The dams and their fetuses on gestation of 20 days were studied. Urine iodine of dams and iodine contents in fetal amniotic fluid were measured by As3+-Ce4+catalytic spectrophotometry using ammonium persulfate digestion. And blood iodine in pregnant rats and iodine contents in placental tissue were measured by As3+-Ce4+catalytic spectrophotometry in dry ash of samples in KClO3-ZnSO4-K2CO3-NaCl. Thyroid hormone levels in mother serum and in fetal amniotic fluid were detected by chemiluminascent assay, and their thyroid glands were weighted and carefully observed. Results ①Iodine content in urine and blood of pregnant rats and amniotic fluid of fetal rats reduced along with their decrease of iodine supply. Urine iodine median of rats in 4 groups(NI: 353.7 μg/L; MiID: 115.9 μg/L; MoID: 26.9 μg/L; SID: 0 μg/L) were statistically significant(χ2=32.884, P < 0.01). Blood iodine level in MoID and SID[(29.4±18.6), (11.7± 7.0)μg/L]was significantly lower than that in NI[(49.1±23.0)μg/L, P < 0.05 or < 0.01]. In iodine deficiency groups, there was a decreasing trend in iodine contents of fetal amniotic fluid[MiID: (48.3±23.1)μg/L; MoID: (29.2±14.7)μ/L; SID:(19.5±6.7)μg/L]and an increasing tendency in iodine contents of placental tissue [MiID: (0.57±0.26)μg/g, MoID: (0.53±0.34)μg/g; SID: (0.53±0.15)μg/g], but there was no statistical significance(P>0.05). ②In SID, TT4[(14.3±4.1)nmol/L]and FT4[(10.8±3.6)pmol/L]were lower than that in NI[(28.4±19.3)nmol/L, (20.2±8.0)pmol/L, P < 0.05 or < 0.01], while that in MoID[(22.1±6.1)nmol/L, (18.5±4.1)pmol/L]and MiID[(25.5±13.1)nmol/L, (18.6±8.4)pmol/L]were decreased without statistical significance(P > 0.05). And FT3/FT4 ratio(0.34±0.16), absolute[(48.4±22.7)mg]and relative weights[(144± 76)mg/kg]of thyroid gland in pregnant rats were respectively higher than that in NI[0.16±0.02, (19.5±3.1)mg, (66±10)mg/kg, P<0.01]. But that in MoID[0.19±0.04, (27.0±5.7)mg, (84±19)mg/kg]and MiID[0.17± 0.06, (25.0±8.9)mg, (78±25)mg/kg]were increased without statistical significance(P > 0.05). A visibly congestive enlargement thyroid was found in SID, while thyroid mildly enlarged in MoID and MiID. ③Compared with NI [(2.38±1.55)pmol/L,0.50±0.18], the FT4 levels [(1.07±0.87) pmol/L]in amniotic fluid were significantly decreased (P < 0.05) and the FT3/FT4 ratio (1.96±0.61) was significantly increased (P < 0.01) in SID. There were no statistical significances(P > 0.05) in other 3 groups[MiID: (2.77±0.90)pmol/L,0.46±0.15; MoID: (2.35±0.76)pmoL/L,0.61±0.21]. A visible thyroid enlargement with hyperemia was observed in SID fetus while in other 2 experiment groups their thyroids were only mildly congested. Conclusions Severe iodine deficiency during pregnancy can result in both mother and fetus overt hypothyroidism. The fetal thyroid hormone levels in mild iodine deficiency status is close to normal levels because of maternal and placental compensation. Moreover, both the dam and the fetus suffer from the negative effects in moderate iodine deficiency during pregnancy.     

短期铁缺乏对大鼠甲状腺功能的影响

目的 研究短期铁缺乏对大鼠甲状腺功能的影响,并探讨其机制,为碘缺乏病的防治工作提供新的线索和思路.方法 选择健康SPF/VAF级初断乳SD雄性大鼠22只,按体质量随机分为对照组(饲料含铁量为65 mg/kg)和铁缺乏组(饲料含铁量为15 mg/kg),每组11只.喂养4周后,测定大鼠体质量和甲状腺质量,并计算甲状腺相对质量.取大鼠全血并分离血清,采用生化法检测血红蛋白、血清铁水平和总铁结合力;化学发光法检测血清游离三碘甲腺原氨酸(FT3)、游离甲状腺素(FT4)和促甲状腺激素(TSH)水平.甲状腺常规固定包埋切片后,免疫组化染色观察甲状腺过氧化物酶(TPO)蛋白表达情况.结果 铁缺乏组大鼠体质量[(214.3±18.1)g]比对照组[(243.8±16.4)g]减轻(t=4.002,P＜0.01),甲状腺绝对质量[(11.9±1.6)mg]比对照组[(13.4±1.3)mg]降低(t=2.369,P＜0.01),但甲状腺相对质量[(0.055±0.004)g/kg]与对照组[(0.055±0.006)g/kg]比较未见明显变化(t=0.162,P＞0.05).铁缺乏组大鼠血红蛋白水平[(100.4±8.9)g/L]和血清铁水平[(7.0±0.8)μmol/L]比对照组[(146.5±16.3)g/L、(26.1±5.1)μmol/L]降低(t值分别为8.233、12.277,P均＜0.01),总铁结合力[(124.8±6.3)μmol/L]比对照组[(74.0±4.6)μmol/L]升高(t=21.531,P＜0.01).铁缺乏组大鼠血清FT3、FT4和FT3/FT4[(4.71±0.53)、(29.69±2.63)pmol/L、0.16±0.02]均较对照组[(5.69±0.61)、(31.98±2.49)pmol/L、0.18±0.01]降低(t值分别为4.044、2.096、3.255,P＜0.01或＜0.05).铁缺乏组大鼠TPO蛋白表达强度较对照组减弱.结论 铁缺乏可导致甲状腺功能低下,可能与铁缺乏状态下TPO活性降低有关,碘铁联合补充可能会改善铁缺乏地区碘缺乏病防治的效果.

Abstract：

Objective To explore the effect of short-term iron deficiency on thyroid function of rat and its mechanism, and to provide new clues and ideas for prevention and control of iodine deficiency disorders. Methods Twenty-two healthy SPF/VAF level weaning male SD rats were randomly divided into control group(iron content in diet was 65 mg/kg) and iron deficiency group(iron content in diet was 15 mg/kg) by body weight, and 11 in each group respectively. After 4 weeks feeding, body weight and thyroid glands weight were measured, and the relative weight of thyroid gland was calculated. Rat whole blood was collected and serum was separated. Hemoglobin, serum iron levels and total iron binding capacity were tested using biochemical assay;serum free iodine thyroid three original acid (FT3), free thyroxine (FT4) and thyroid stimulating hormone (TSH) levels were detected by chemiluminescence;after thyroid were fixed in formalin, embedded with paraffin and sectioned regularly, and immunohistochemical stained, the protein expression of thyroid peroxidase(TPO) was observed. Results Compared with control group [(243.8 ± 16.4)g], iron deficiency group of animals had less body weight[(214.3 ± 18.1 )g, t = 4.002, P ＜ 0.01];there was a lower absolute thyroid weight in iron deficiency group[(11.9 ± 1.6)mg]than in control group[(13.4 ±1.3)mg, t = 2.369, P ＜ 0.01], but no significant changes of the relative weight of thyroid gland between the two groups[(0.055 ± 0.004),(0.055 ± 0.006)g/kg, t = 0.162, P ＞ 0.05]. Hemoglobin and serum iron in iron deficiency group were ( 100.4 ± 8.9)g/L and (7.0 ± 0.8)μmol/L, which were less than that in control group[( 146.5 ±16.3)g/L, (26.1 ± 5.1 )μmol/L, t = 8.233,12.277, all P ＜ 0.01]. Total iron binding capacity in control group was (74.0 ± 4.6)μ mol/L and that in iron deficiency group[(124.8 ± 6.3)μmol/L], and the difference was significant (t = 21.531, P＜ 0.01). At the same time, their serum hormones FT3, FT4 and FT3/FT4[(4.71 ± 0.53), (29.69 ±2.63)pmol/L, 0.16 ± 0.02]were lower than that in control group[(5.69 ± 0.61),(31.98 ± 2.49)pmol/L, 0.18 ±0.01, t = 4.044,2.096,3.255, P ＜ 0.01 or ＜ 0.05]. The expression of TPO protein decreased in iron deficiency group than in control group. Conclusions Iron deficiency reduces thyroid function, which perhaps is due to the reduction of TPO activity. Combined supplementation of iodine and iron will possibly improve the prevention effect on iodine deficiency disorder in iron deficiency areas.     

妊娠期大鼠不同程度碘缺乏对胎鼠碘代谢和甲状腺功能的影响

Objective To study the effects of iodine deficiency during pregnancy on fetal iodine metabolism and thyroid function. Methods Wistar dams were randomly divided into four groups: severe iodine deficiency(SID), moderate iodine deficiency(MoID), mild iodine deficiency(MiID) and normal iodine(NI). All the dams were fed with iodine deficient food(iodine contents: 50 μg/kg) and drinking water with different doses of KI (0,54.9,163.8,381.7 μg/L) for 3 months till mating. Iodine was supplied at the dose of 1.24 μg/d(SID), 2.50 μg/d(MoID), 5.00 μg/d(MiID) and 10.00 μg/d(NI), respectively. The dams and their fetuses on gestation of 20 days were studied. Urine iodine of dams and iodine contents in fetal amniotic fluid were measured by As3+-Ce4+catalytic spectrophotometry using ammonium persulfate digestion. And blood iodine in pregnant rats and iodine contents in placental tissue were measured by As3+-Ce4+catalytic spectrophotometry in dry ash of samples in KClO3-ZnSO4-K2CO3-NaCl. Thyroid hormone levels in mother serum and in fetal amniotic fluid were detected by chemiluminascent assay, and their thyroid glands were weighted and carefully observed. Results ①Iodine content in urine and blood of pregnant rats and amniotic fluid of fetal rats reduced along with their decrease of iodine supply. Urine iodine median of rats in 4 groups(NI: 353.7 μg/L; MiID: 115.9 μg/L; MoID: 26.9 μg/L; SID: 0 μg/L) were statistically significant(χ2=32.884, P < 0.01). Blood iodine level in MoID and SID[(29.4±18.6), (11.7± 7.0)μg/L]was significantly lower than that in NI[(49.1±23.0)μg/L, P < 0.05 or < 0.01]. In iodine deficiency groups, there was a decreasing trend in iodine contents of fetal amniotic fluid[MiID: (48.3±23.1)μg/L; MoID: (29.2±14.7)μ/L; SID:(19.5±6.7)μg/L]and an increasing tendency in iodine contents of placental tissue [MiID: (0.57±0.26)μg/g, MoID: (0.53±0.34)μg/g; SID: (0.53±0.15)μg/g], but there was no statistical significance(P>0.05). ②In SID, TT4[(14.3±4.1)nmol/L]and FT4[(10.8±3.6)pmol/L]were lower than that in NI[(28.4±19.3)nmol/L, (20.2±8.0)pmol/L, P < 0.05 or < 0.01], while that in MoID[(22.1±6.1)nmol/L, (18.5±4.1)pmol/L]and MiID[(25.5±13.1)nmol/L, (18.6±8.4)pmol/L]were decreased without statistical significance(P > 0.05). And FT3/FT4 ratio(0.34±0.16), absolute[(48.4±22.7)mg]and relative weights[(144± 76)mg/kg]of thyroid gland in pregnant rats were respectively higher than that in NI[0.16±0.02, (19.5±3.1)mg, (66±10)mg/kg, P<0.01]. But that in MoID[0.19±0.04, (27.0±5.7)mg, (84±19)mg/kg]and MiID[0.17± 0.06, (25.0±8.9)mg, (78±25)mg/kg]were increased without statistical significance(P > 0.05). A visibly congestive enlargement thyroid was found in SID, while thyroid mildly enlarged in MoID and MiID. ③Compared with NI [(2.38±1.55)pmol/L,0.50±0.18], the FT4 levels [(1.07±0.87) pmol/L]in amniotic fluid were significantly decreased (P < 0.05) and the FT3/FT4 ratio (1.96±0.61) was significantly increased (P < 0.01) in SID. There were no statistical significances(P > 0.05) in other 3 groups[MiID: (2.77±0.90)pmol/L,0.46±0.15; MoID: (2.35±0.76)pmoL/L,0.61±0.21]. A visible thyroid enlargement with hyperemia was observed in SID fetus while in other 2 experiment groups their thyroids were only mildly congested. Conclusions Severe iodine deficiency during pregnancy can result in both mother and fetus overt hypothyroidism. The fetal thyroid hormone levels in mild iodine deficiency status is close to normal levels because of maternal and placental compensation. Moreover, both the dam and the fetus suffer from the negative effects in moderate iodine deficiency during pregnancy.     

不同碘营养水平对妊娠期大鼠胎盘激素分泌的影响

目的 探讨不同碘营养水平对妊娠期大鼠胎盘激素分泌的影响.方法 Wistar大鼠225只(雌鼠165只,雄鼠60只),体质量约80～ 100g.将雌鼠按体质量随机分为5组:低碘1组、低碘2组、适碘(对照)组、高碘1组、高碘2组,每组33只.2个低碘组大鼠食用病区粮食,含碘量为13.46 μg/kg,分别饮用含0、5μg/L碘酸钾的去离子水;对照组和2个高碘组大鼠食用普通粮食,含碘量为22.00 μg/kg,分别饮用含50、3000、10000 μg/L碘酸钾的去离子水.饲养3个月,雌鼠与雄鼠合笼交配,于孕早期(5±2)d、孕中期(12±2)d、孕晚期(17±2)d处死母鼠,取血清.采用酶联免疫吸附测定法(ELISA)测血清绒毛膜促性腺激素(HCG)、绒毛膜促甲状腺激素(HCT)、孕激素.结果 孕晚期大鼠血清HCG组间比较差异有统计学意义(F=4.16,P＜ 0.05);孕晚期低碘1组[(16.08±4.45)U/L]、低碘2组[(17.43±2.70)U/L]较对照组[(13.68±3.52)U/L]显著升高(P均＜ 0.01).孕中、孕晚期大鼠血清HCT组间比较差异有统计学意义(F值分别为3.59、3.40,P均＜0.05);孕中期高碘1组[(70.11±10.97 )μU/L]、孕晚期高碘2组[(74.93±13.22)μU/L]较对照组[(57.14±12.56)、(58.17±8.54) μU/L]显著升高(P均＜0.01).低碘1组、对照组大鼠血清孕激素组内比较差异有统计学意义(F值分别为4.06、4.43,P均＜0.05);低碘1组孕晚期[(1462.80±286.48)pmol/L]低于孕旱[(1929.93±158.37)pmol/L,P＜0.05]、孕中期[(1856.44±542.08)pmol/L,P＜0.05];对照组孕中期[(2046.45±475.67)pmol/L]高于孕早期[(1714.39±461.71 )pmol/L,P＜ 0.05].结论 妊娠期母体胎盘HCG分泌在缺碘条件下增加,HCT分泌在碘过量条件下增加.孕激素在重度低碘情况下,随孕期增加而分泌下降,与HCG在孕期的变化趋势相反,易造成不良妊娠结果.     

碘铁联合缺乏对大鼠血脂水平的影响

目的 通过控制碘、铁摄入量,造成缺铁、缺碘模型,研究碘、铁缺乏对大鼠血脂水平的影响.方法 将Sprauge-Dawley (SD)雄性大鼠随机分为4组:正常对照组(N组,饲料碘含量362.0 μg/kg,铁含量93.3 mg/kg),碘缺乏组(ID组,饲料碘含量61.4 μg/kg,铁含量93.3 mg/kg),铁缺乏...     

碘缺乏和碘过量对实验性甲状腺功能减退小鼠血脂代谢的影响

目的 观察碘缺乏和碘过量对实验性甲状腺功能减退(简称甲减)小鼠血脂代谢的影响,探讨碘不依赖于甲状腺激素的独立作用机制.方法 将雌性Balb/c小鼠按体质量随机分为6组:对照、重度低碘(SID)、轻度低碘(MID)、适碘(NI)、10倍碘过量(10HI)和50倍碘过量(50HI)组,每组10只.对照组饲以低碘饲料,其他各组饲以含0.2%甲基硫氧嘧啶的低碘饲料,同时饮用碘化钾(KI)配制的含碘量分别为326.79、0、196.08、326.79、3856.21、19 542.50 μg/L的去离子水.喂养3个月后,处死并收集小鼠外周血,分离血清.放射免疫分析法测定甲状腺激素水平,酶法检测血清中甘油三酯(TG)、总胆固醇(TC)、高密度脂蛋白胆固醇(HDL-C)及低密度脂蛋白胆固醇(LDL-C)水平.结果 ①SID[(21.27±9.63)μg/L]、MID[(23.41±3.93)μg/L]、NI[(22.57±4.66)μg/L]、10HI[(21.07±5.03)μg/L]和50HI组[(21.46±5.90)μg/L]血清TT4水平明显低于对照组[(42.15±8.26)μg/L,P均＜0.01],而各组间血清TT3水平比较,差异无统计学意义(F=0.99,P＞0.05).②10HI组TG水平[(1.17±0.16)mmol/L]与对照组[(1.39±0.22)mmol/L]和NI组[(1.51±0.22)mmol/L]比较,明显降低(P均＜0.05).50HI组TG和TC水平[(1.18±0.22)、(1.78±0.15)mmol/L]与对照组[(1.39±0.22)、(2.14±0.37)mmol/L]和NI组[(1.51±0.22)、(2.00±0.15)mmol/L]比较,明显降低(P均＜0.05).各组HDL-C、LDL-C水平比较,差异无统计学意义(F值分别为0.55、0.54,P均＞0.05).结论 碘可不依赖于甲状腺激素独立发挥调节甲减小鼠血脂的作用;监控碘的摄入量,对有效防治心血管疾病亦有重要作用.

Abstract：

Objective To observe the effects of iodine deficiency and iodine excess on the lipid metabolism in an experimental hypothyroid model of mice and to explore the roles of iodine independent of its role in thyroid hormones. Methods Female Balb/c mice were randomly divided into 6 groups: control, severe iodine deficiency (SID), mild iodine deficiency(MID), normal iodine (NI), 10-fold high iodine (10HI) and 50-fold high iodine(50HI), 10 in each group. The mice in control group were fed with low iodine forage, other mice were fed with low iodine forage containing 0.2% methylthiouracilum. All mice drank deionic water containing different concentrations of potassium iodide(KI). The iodine content in water was 326.79, 0, 196.08,326.79, 385621, 19 542.50 μg/L, respectively. After three months, thyroid hormones in the serum were determined by radioimmunoassay.Also, the blood samples were analyzed for total cholesterol (TC), triglyceride (TG), high density lipoprotein cholesteiol (HDL-C) and low density lipoprotein cholesterol (LDL-C) and measured enzymatically by automatic analyzer. Results ①The levels of Tr4 in SID[(21.27 ± 9.63)μg/L], MID[(23.41 ± 3.93)μg/L], NI[(22.57 ±4.66)μg/L], 10HI [(21.07 ± 5.03) μg/L] and 50HI groups [(21.46 ± 5.90) μg/L] were distinctively decreased compared with control group[(42.15 ± 8.26)μg/L, all P ＜ 0.01]. There were no statistical significant differences of TT3 between different groups (F = 0.99, P > 0.05 ). ②The level of TG in 10HI group [ ( 1.17 ± 0.16)mmol/L ] was obviously decreased compared with control [(1.39 ± 0.22 )mmol/L] and NI groups[(151 ± 0.22)mmol/L, all P＜ 0.05].Both TG and TC in 50HI group[(1.18 ± 0.22), (1.78 ± 0.15)mmol/L] were significantly decreased compared with control [( 1.39 ± 0.22), (2.14 ± 0.37)mmol/L] and NI groups [(1.51 ± 0.22), (2.00 ± 0.15)mmol/L, all P ＜ 0.05].The difference of serum HDL-C and LDL-C between the groups was not significant(F = 0.55,0.54, all P ＞ 0.05 ).Conclusions Dietary iodine plays a role in the metabolism of serum lipids independent of thyroid hormones.Thus, monitoring the amount of iodine intake during sodium restriction should also be taken extremely important for effectively prevention and cure of cardiovascular disease.     

1759例甲状腺疾病患者TRAb，TGAb，TMAb联检结果分析

目的 通过对1759例甲状腺疾病患者TRAb,TGAb,TMAb联合检测结果的分析,探讨3种甲状腺自身抗体在甲状腺疾病鉴别诊断中的应用价值.方法 收集2002-2006年在山东省甲状腺疾病防治中心就诊的甲状腺疾病患者1759例,根据病史、症状、体征、化验及辅助检查结果分为6组.观察各组TRAb,TGAb,TMAb测定值的分布情况,各组间率的比较采用卡方检验.结果 (1)TRAb强阳性仅存在于甲亢患者(A、B两组),其他4组阳性率均很低,且测定值均小于50 u/L;(2)6组中TGAb,TMAb各档几乎均有分布,阳性率从高到低依次为D组(高达91.53%,94.92%)、C组、A组与B组、E组、F组;(3)A组与C组TGAb,TMAb强阳性率及TGAb阳性率差异均无统计学意义,仅TMAb阳性率c组略高于A组.结论 TRAb可作为甲状腺疾病的鉴别诊断依据;TGAb,TMAb强阳性对AITD及其他甲状腺疾病的鉴别有一定临床价值;不同类型甲状腺疾病患者的TGAb,TMAb存在异质性.     

桥本甲状腺功能亢进与Graves病鉴别诊断的临床观察

目的 探讨细针穿刺细胞学(FNAC)检查和甲状腺自身抗体检测在桥本甲状腺功能亢进(甲亢)与Graves病(GD)鉴别诊断中的临床应用价值.方法 本组资料362例中有3例因样本细胞数量少而未能诊断,根据FNAC分型将359例甲亢患者分为桥本甲亢组119例、GD-Ⅰ组(间质淋巴细胞浸润<10%)162例、GD-Ⅱ组(淋巴细胞浸润10%～20%)49例、GD-Ⅲ组(淋巴细胞浸润20%～40%)29例,观察4组甲状腺自身抗体及甲状腺激素水平的差异.结果 FNAC发现淋巴细胞破坏上皮细胞以及退行性变和(或)嗜酸性变的滤泡上皮细胞时仅见于桥本甲亢组,为其特征性表现.GD-Ⅰ、Ⅱ、Ⅲ3组FNAC检查可见淋巴细胞数量依次呈增加趋势,而滤泡上皮细胞增生呈降低趋势;3组平均血清甲状腺球蛋白抗体(TGAb)分别为(43.5±29.0)%、(61.3±24.4)%、(68.9±22.3)%,而平均甲状腺微粒体抗体(TMAb)分别为(38.0±26.1)%、(54.7±23.0)%、(60.8±22.7)%,与GD-Ⅰ组相比,GD-Ⅱ、GD-Ⅲ组升高均有显著性差异(P<0.05);3组的促甲状腺激素受体抗体(TRAb)水平分别为(57.7±71.0)U/L、(31.5±62.1)U/L、(21.2±47.0)U/L,与GD-Ⅰ组相比,GD-Ⅱ、GD-Ⅲ组显著降低(P<0.01).桥本甲亢组TGAb、TMAb均值显著高于GD-Ⅰ组(P<0.01),而TRAb、游离T_3(FT_3)、游离T_4(FT_4)均值显著低于GD-Ⅰ组(P<0.01);桥本甲亢组与GD-Ⅱ、Ⅲ组相比,各抗体均值差异均无统计学意义(P>0.05).GD-Ⅲ组病史均值显著长于其他3组(P<0.01),而其他3组间差异无显著性(P>0.05).结论 FNAC对鉴别桥本甲亢与GD各型具有重要的临床价值.血清TRAb、TGAb、TMAb水平对鉴别桥本甲亢与GD-Ⅰ型有一定临床价值,而对鉴别桥本甲亢与GD-Ⅱ型、Ⅲ型临床意义不大.     

不同碘营养水平对哺乳期大鼠甲状腺和乳腺TSHR mRNA表达的影响

目的观察不同碘营养水平对哺乳期大鼠甲状腺和乳腺促甲状腺激素受体（TSHR）mRNA表达水平的影响。方法30只雌性Wistar大鼠按体质量随机分成3组：低碘组（合成饲料,去离子水） 适碘组（合成饲料,含碘150μg/L的去离子水） 高碘组（合成饲料,含碘3 000μg/L的去离子水）。喂养3个月后,与雄鼠合笼交配,待母鼠哺乳5 d后将其处死、取母鼠乳腺、甲状腺及血清,温和酸消化法测定血清碘 放射免疫分析法测定T3、T4水平 实时荧光定量PCR法检测乳腺和甲状腺TSHR mRNA表达水平。结果低碘组血清碘低于适碘组（P〈0.05）,高碘组血清碘高于适碘组（P〈0.05） 低碘组、高碘组T3水平低于适碘组（P〈0.05） 低碘组、高碘组T4水平与适碘组比较差异均无统计学意义（P〉0.05）,低碘组T4水平低于高碘组（P〈0.05） 低碘组甲状腺TSHR mRNA表达水平明显高于适碘组（P〈0.05）,高碘组低于适碘组,但差异无统计学意义 低碘组、高碘组乳腺TSHR mRNA表达水平都低于适碘组（P〈0.05）。结论高碘时甲状腺和乳腺TSHR表达均减少,下调碘的摄入保护自身及子代免受碘过量的危害 轻度低碘时甲状腺提高TSHR表达以增加碘的摄入保护自身免受缺碘危害,但乳腺未增加摄碘能力,因此对子代没有保护作用或保护作用不明显。     

不同碘营养水平对哺乳期大鼠甲状腺和乳腺胰岛素样生长因子Ⅰ mRNA表达的影响

目的 观察不同碘营养水平对哺乳期大鼠甲状腺和乳腺胰岛素样生长因子Ⅰ(IGF-1)mRNA表达水平的影响.方法 30只雌性断乳1个月Wistar大鼠按体质量随机分成3组:低碘组、适碘组、高碘组,每组10只,食用合成饲料,分别饮用含碘0、150、3000 μg/L的去离子水.喂养3个月后,与雄鼠合笼交配,待母鼠哺乳5 d后将其处死、取母鼠乳腺、甲状腺及血清,温和酸消化法测定血清碘,放射免疫分析法测定T3、T4水平,实时荧光定量PCR法检测乳腺和甲状腺IGF-1 mRNA表达水平.结果 低碘组血清碘[(17.38±3.27)μg/L]低于适碘组[(43.42±6.92)μg/L,P<0.05],高碘组血清碘[(350.10±38.46)μg/L]高于适碘组(P<0.05);低碘组、高碘组T3水平[(1.11μ0.25)、(1.61±0.33)μg/L]低于适碘组[(2.18±0.46)μg/L,P均<0.05];低碘组、高碘组T4水平[(33.40±11.11)、(56.54±10.38)μg/L]与适碘组[(44.02±12.51)μg/L]比较差异无统计学意义(P>0.05),低碘组T4水平低于高碘组(P均<0.05);低碘组、高碘组甲状腺IGF-1 mRNA表达水平(0.34±0.08、0.23±0.08)均高于适碘组(0.15±0.03,P均<0.05);低碘组哺乳期乳腺IGF-1 mRNA表达水平(0.59±0.18)高于适碘组(0.40±0.10,P<0.05);3组甲状腺IGF-1 mRNA表达均低于同组的乳腺表达水平(t=3.54、6.44、2.62,P均<0.05).结论 碘能够影响哺乳期甲状腺和乳腺IGF-1 mRNA的表达,且哺乳期乳腺表达强于甲状腺.     

不同碘营养水平大鼠妊娠期甲状腺和胎盘胰岛素样生长因子-Ⅰ及转化生长因子-β1mRNA表达水平的研究

目的 观察不同碘营养水平下大鼠妊娠期甲状腺和胎盘胰岛素样生长因子(IGF)-Ⅰ及转化生长因子(TGF)-β1 mRNA表达水平的变化.方法 雌性Wistar大鼠150只,体质量80～100g,按体质量随机分为5组,每组30只,分别饮用含碘50(对照组,NI)、0(低碘1组,LI1)、5(低碘2组,LI2)、3000(高碘1组,HI1)、10 000 μg/L(高碘2组,HI2)的去离子水.饲养12周将雌鼠同雄鼠合笼交配,分别于孕早期(第6、7天),孕中期(第12、13天)、孕晚期(第19、20天)处死,取甲状腺及胎盘.利用实时荧光定量PCR方法测定大鼠甲状腺和胎盘的IGF-Ⅰ及TGF-β1 mRNA表达水平.结果 ①LI1组和LI2组甲状腺绝对质量[(12.17±5.41)×10-2、(3.54±1.21)×10-2g]均高于NI组[(2.05±0.50)×10-2 g,P均＜0.05];HI1组、HI2组甲状腺绝对质量[(1.64±0.27)×10-2、(1.66±0.29)×10-2 g]与NI组比较,差异无统计学意义(P均＞0.05).②大鼠甲状腺IGF-Ⅰ mRNA表达:孕早期,LI1组、LI2组(1.98±0.35、1.47±0.22)均高于NI组(1.01±0.18,P均＜0.01),HI1组、HI2组(0.68±0.16、0.75±0.09)均低于NI组(P均＜0.05);孕中期,HI2组(1.14±0.17)低于NI组(1.58±0.33,P＜ 0.01);孕晚期,LI2组、HI2组(1.47±0.20、1.45±0.35)均低于NI组(2.20±0.37,P均＜0.01).NI组,孕早期、孕中期、孕晚期的IGF-Ⅰ mRNA表达水平(1.01±0.18、1.58±0.33、2.20±0.37)呈增高趋势,任意两组间比较差异均有统计学意义(P均＜ 0.01).③大鼠甲状腺TGF-β1 mRNA表达:孕早期,H1组(1.37±0.13)高于NI组(1.05±0.18,P＜ 0.01),HI1组、HI2组(0.50±0.09、0.44±0.11)均低于NI组(P均＜0.01);孕中期,LI1组LI2组(1.39±0.28、1.17±0.12)均高于NI组(0.63±0.22,P均＜0.01);孕晚期,LI1组、LI2组(1.57±0.30、1.23±0.20)均高于NI组(0.68±0.17,P均＜0.01).NI组孕中期、孕晚期(0.63±0.22、0.68±0.17)均低于孕早期(1.05±0.18,P均＜0.01).④大鼠胎盘IGF-Ⅰ mRNA表达:孕中期,HI1组、HI2组(1.48±0.16、1.45±0.25)均高于NI组(1.00±0.10,P均＜0.01);孕晚期,HI1组(1.75±0.15)高于NI组(1.54±0.29,P＜ 0.05);HI2组(1.94±0.31)高于NI组(P＜0.01).NI组孕晚期高于孕中期(P＜0.01).⑤大鼠胎盘TGF-β1 mRNA表达:孕中期、孕晚期各组间比较差异均无统计学意义(P均＞0.05);NI组孕晚期(0.83±0.16)低于孕中期(0.98±0.20,P＜ 0.05).结论 妊娠期碘缺乏条件下甲状腺上调IGF-ⅠmRNA表达,这种作用在孕早期尤为显著;同时增高TGF-β1 mRNA表达,且此抑制作用随碘缺乏程度加深逐渐显著.碘过量情况下甲状腺IGF-Ⅰ、TGF-β1作用则相对较弱.随着孕程增长胎盘组织中IGF-Ⅰ发挥促进组织生长分化的作用逐渐显著,相反TGF-β1的抑制作用则减弱.     

碘对小鼠产后甲状腺炎影响的实验研究

目的 探讨碘对小鼠产后甲状腺炎(postpartum thyroiditis,PPT)发生,发展的影响.方法 44只8周龄雌性C57BL/6J小鼠均饲以低碘饲料(含碘量≤35 μg/kg),按体质量随机分成4组:非妊娠实验性自身免疫性甲状腺炎(EAT)组 8只,采用猪甲状腺球蛋白加完全弗氏佐剂复制EAT模型,最终存活6只,NI-PPT组(正常碘),10HI-PPT组(10倍碘),50HI-PPT组(50倍碘)各12只,复制EAT模型(方法 同非妊娠EAT组)后,与性成熟雄鼠交配,分别有7,6,6只小鼠受孕.4 组鼠分别饮用含KI为0.3,0.3,3.0,15.0 mg/L的碘水.妊娠母鼠生产4周后,观察4组小鼠甲状腺组织病理改变,血清中甲状腺球蛋白抗体(Tg-Ab)和甲状腺过氧化物酶抗体(TPO-Ab)水平,血清中甲状腺激素(TT3,TT4)水平以及脾脏中IFN-γ,和IL-4 mRNA的表达水平.结果 甲状腺组织病理检查示甲状腺内炎细胞浸润,上皮细胞扁平,滤泡萎缩或破坏.非妊娠EAT组,NI-PPT组,10HI-PVT组小鼠的炎细胞浸润程度均低于50HI-PPT组,组间两两比较,差异有统计学意义(P＜0.05).非妊娠EAT组,NI-PPT组,10HI-PPT组和50HI-PPT组的血清TPO-Ab水平分别为(14.32±8.85)%,(64.45±10.52)%,(38.46±5.57)%,(90.09±9.98)%,任意两组组间比较,差异均有统计学意义(P＜0.05),血清Tg-Ab水平分别为(33.74±3.71)%,(29.65±2.06)%,(37.21±3.87)%,(33.87±4.17)%,组间比较差异无统计学意义(F＝0.484,P＞0.05),血清TT3水平分别为(2.47±0.69)%,(1.57±0.25)%,(1.60±0.28)%,(1.82±0.75)%,组间比较差异无统计学意义(F＝1.596,P＞0.05),非妊娠EAT组,NI-PPT组和10HI-PPT组血清中TT4水平[(99.87±5.97)%,(89.13±7.64)%,(91.05±5.82)%]与50HI-PPT组[(66.68±5.47)%]比较,差异均有统计学意义(P＜0.05).在非妊娠EAT组,NI-PPT组,10HI-PPT组和50HI-PPT组,小鼠脾脏IFN-γmRNA表达水平分别为1.02±0.10,1.37±0.10,1.39±0.12,1.68±0.06,除NI-PPT组和10HI-PVF组的组间比较之外,其他的任意两组组间比较.差异均有统计学意义(P＜0.05),IL-4 mRNA表达水平分别为0.24±0.05,0.35±0.05,0.49±0.04,0.53±0.06.10HI-PPT组,50HI-PPT组与非妊娠EAT组和NI-PPT组比较,差异均有统计学意义(P＜0.05).结论 妊娠及产后易诱发PPT,增加适量碘的摄入量,可降低PPT的炎症反应,而补碘过量也是诱发或增加产后甲状腺炎发生的重要因素.因此,妊娠及产后补碘应遵循合理和科学的原则.