碘/钠摄入量对小鼠血脂代谢影响的实验研究

Objective The present study has been designed to investigate the impact of dietary iodine/sodium intake on blood lipid metabolism in mice. Methods According to body weight and gender, two hundred and sixty Balb/c mice were randomly divided into 2 groups including normal sodium group(Na) and low sodium group(LNa), with 130 animals per group. Each group were then randomly further divided into 5 sub-groups according to the amount of iodine intake: ① severe iodine deficiency(SID); ② mild iodine deficiency(MID); (③normal iodine (NI); ④ 10-fold high iodine ( 10HI ); (⑤ 50-fold high iodine (50HI), 10 groups in total, 26 per group.Eight months later, the body weight and the levels of urinary iodine, thyroid hormones and total cholesterol (TC),Results In Na group, the levels of TG and TC in male mice of SID group[ (1.64 ± 0.35), (3.88 ± 0.35 )mmol/L]and MID group[ ( 1.67 ± 0.31 ), (3.41 ± 0.66)mmol/L] were significantly higher than that of NI group[ ( 1.49 ± 0.42), (3.25 ± 0.47)mmol/L] and the levels of TG in female mice of SID group[(1.52 ± 0.22)mmol/L] were significantly higher than that of NI group[ (1.23 ± 0.22)mmol/L]. In addition, the levels of TG in male mice of 10HI and 50HI groups [ ( 1.16 ± 0.23 ), ( 1.21 ± 0.27 ) mmol/L ] were significantly lower than that of NI group [ ( 1.49 ± 0.42)mmol/L, all P ＜ 0.05], the levels of TC in female mice of 10HI and 50HI groups[(2.37 ± 0.49), (2.48 ± 0.37)mmol/L] were significantly lower than that of NI group[ (2.84 ± 0.37) mmol/L, all P ＜ 0.05 ]. In LNa group,the levels of TG and TC in male mice of SID group[ (1.39 ± 0.40), (3.33 ± 0.46 )mmol/L] were significantly lower than that of NI group [(1.30 ± 0.28), (3.00 ± 0.53) mmol/L, all P ＜ 0.05], the levels of TG, TC and LDL in female mice of SID group[ (1.48 ± 0.26), (2.76 ± 0.43), (0.62 ± 0.22)mmol/L], the levels of LDL in female mice of MID group[ (0.60 ± 0.17 )mmol/L] were significantly lower than that of NI group[(l.22 ± 0.36), (2.51 ± 0.38),(0.48 ± 0.08), (0.48 ± 0.08)mmol/L, all P ＜ 0.05], the levels of TG in male mice of 10HI and 50HI group [ (1.12 ± 0.22), (0.90 ± 0.11 )mmol/L] were significantly lower than that of NI group (all P ＜ 0.05 ), the levels of TC in female mice of 10HI and 50HI groups[ (2.35 ± 0.34), (2.37 ± 0.37)mmol/L], the levels of LDL in female mice of 50HI group[(0.65 ± 0.18)mmol/L], were significantly lower than that of NI group(all P ＜ 0.05). In Na group, the levels of thyroid hormones were distinctively decreased in SID group[TT4(0.00 ± 0.00)nmol/L, FT4 (0.93 ± 0.42)pmol/L, TT3(0.49 ± 0.07)nmol/L, FT3(2.86 ± 0.37)pmol/L] and MID group [TT4 (17.15 ± 15.26)nmol/L, FT4( 18.46 ± 4.31 )pmol/L, TT3(0.67 ± 0. 10)nmol/L, FT3(3.18 ± 0.24)pmol/L] compared with that of the NI group [TT4 (37.15 ± 15.26)nmol/L, FT4(28.46 ± 4.31)pmol/L, TT3(0.85 ± 0.10)pmol/L, FT3(3.87 ± 0.24)pmol/L, all P ＜ 0.05 ]. In LNa group, the levels of thyroid hormones were distinctively decreased in SID group [TT4 (0.00 ± 0.00) nmol/L,FT4(1.03 ± 0.78)pmol/L, TT3(0.51 ± 0.05)nmol/L, FT3(3.01 ± 0.17)pmol/L] and MID group[TT4(19.76 ± 12.22)nmol/L, FT4(21.46 ± 5.37)pmol/L, TT3(0.71 ± 0.21)nmol/L, FT3(3.56 ± 0.23)pmol/L] compared with that of the NI group[TT4(36.23 ± 14.72)nmol/L, FT4(30.96 ± 6.33)pmol/L, TT3(0.89 ± 0.20)nmol/L, FT3(4.05 ± 0.24)pmol/L, all P ＜ 0.05]. Conclusions Dietary iodine intake plays an important role in the blood lipid metabolism. Iodine deficiency could increase while iodine excess could decrease the levels of serum TG, TC or LDL in mice. Monitoring the amount of iodine intake during sodium restriction should have an important role in effective prevention and treatment of cardiovascular disease.     

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.     

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.     

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.     

碘/钠摄入量对小鼠血脂代谢影响的实验研究

目的 探讨膳食碘摄入量对适钠和低钠饮食小鼠血脂代谢影响,为揭示碘与心血管疾病发病的相关性进行初步研究.方法 Balb/c小鼠260只,按体质量、性别随机分为适钠组(Na)和低钠组(Lna),每组130只;此两大组又分别按照碘摄入量分为①重度低碘组(SID);②轻度低碘组(MID);③适碘组(NI);④10倍碘过量组(10HI);⑤50倍碘过量组(50HI),总计为10组,每组26只.各组小鼠在饲养8个月时收集尿液和小鼠外周血,分离血清.测定小鼠尿碘、体质量、血脂[甘油三酯(TG)、总胆固醇(TC)、低密度脂蛋白(LDL)、高密度脂蛋白醇(HDL)]及甲状腺激素水平[总甲状腺素(TT4),总三碘甲腺原氨酸(TT3)、游离甲状腺素(FT4)、游离三碘甲腺原氨酸(FT3)].结果适钠组中,SID组、MID组雄性小鼠TG水平[(1.64±0.35)、(1.67±0.31)mmol/L]和SID组TC水平[(3.88±0.35)mmol/L]明显高于NI组[(1.49±0.42)、(3.25±0.47)mmol/L,P均＜0.05],SID组中雌性小鼠TG水平[(1.52±0.22)mmol/L]高于NI组[(1.23±0.22)mmol/L,P＜0.05].10HI和50HI组雄性小鼠外周血TG水平[(1.16±0.23)、(1.21±0.27)mmol/L]低于NI组(P均＜0.05),雌性小鼠TC水平[(2.37±0.49)、(2.48±0.37)mmol/L)低于NI组[(2.84±0.37)mmol/L,P均＜0.05].在低钠组,SID组雄性小鼠TG、TC水平[(1.39±0.40)、(3.33±0.46)mmol/L]均高于NI组[(1.30±0.28)、(3.00±0.53)mmol/L,P均＜0.05],SID组雌性小鼠TG、TC、LDL水平[(1.48±0.26)、(276±0.43)、(0.62±0.22)mmol/L]、MID组雌性小鼠LDL水平[(0.60±0.17)mmol/L]均高于NI组[(1.22±0.36)、(2.51±0.38)、(0.48±0.08)mmol/L,P均＜0.05].10HI和50HI组雄性小鼠TG水平[(1.12±0.22)、(0.90±0.11)mmol/L]均低于NI组(P均＜0.05),10HI和50HI组雌性小鼠TC水平[(2.35±0.34)、(2.37±0.37)mmol/L]、50HI组雌性小鼠LDL水平[(0.65±0.18)mmol/L]均低于NI组(P均＜0.05).适钠组中的SID和MID组血清TT4[(0.00±0.00)、(17.15±15.26)nmol/L]、FT4[(0.93±0.42)、(18.46±4.31)pmol/L]和TT3[(0.49±0.07)、(0.67±0.10)nmol/L]、FT3[(2.86±0.37)、(3.18±0.24)pmol/L]水平均低于NI组[(37.15±15.26)、(28.46±4.31)、(0.85±0.10)、(3.87±0.24)pmol/L,P＜0.01或P＜0.05].在低钠组,SID和MID组血清TT4、FT4和TT3、FT3水平[(0.00±0.00)nmol/L、(1.03±0.78)pmol/L、(0.51±0.05)nmol/L,(3.01±0.17)pmol/L,(19.76±12.22)nmol/L、(21.46±5.37)pmol/L、(0.71±0.21)nmol/L、(3.56±0.23)pmol/L]均低于NI组[(36.23±14.72)nmol/L、(30.96±6.33)pmol/L、(0.89±0.20)nmol/L、(4.05±0.24)pmol/L,P均＜0.05],10HI组的TT3水平[(1.06±0.23)nmol/L]高于NI组(P＜0.05).结论碘缺乏可致TG、TC和LDL升高,过量碘可致TG/TC水平降低.碘摄入量是影响血脂代谢的重要因素.限盐饮食的同时,严密监控碘的摄入量对当前有效防治心血管疾病应具有重要作用.     

膳食碘对高脂血症小鼠甲状腺功能及脂代谢的影响

目的 研究碘摄入量对高脂血症小鼠甲状腺功能及血脂代谢的影响.方法 将4周龄雌性c57BL/6J小鼠50只随机分为重度低碘组(SID)、轻度低碘组(MID)、适碘组(NI)、10倍碘过量组(10HI)、50倍碘过量组(50HI),每组10只.均用高脂、高胆固醇、低碘(碘含量为20～40 μg/kg)饲料喂养.SID组饮用...     

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

目的 研究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.方法 40只Wistar雌性大鼠按体质量随机分为4组,每组10只,均食用低碘饲料(含碘量为50μg/kg);重、中、轻度缺碘(SID、MoID、MiID)组和正常碘(NI)组饮用含不同剂量碘化钾(0、54.9、163.8、381.7μg/L)的自来水(含碘量为8μg/L),每日总碘供给量分别为1.24、2.50、5.00、10.00μg.喂养3月后与按NI组条件饲养的Wistar雄性鼠交配,以妊娠20 d孕鼠和胎鼠为研究对象,过硫酸铵消化砷铈催化分光光度法测定孕鼠尿碘和胎鼠羊水含碘量,碱灰化砷铈催化分光光度法测定孕鼠血碘和胎盘组织含碘量,化学发光法测定孕鼠血清及胎鼠羊水甲状腺激素水平,检测并观察孕鼠和胎鼠的甲状腺质量及大体变化.结果 ①孕鼠尿碘、血碘,胎鼠羊水碘均随碘供给量减少呈降低趋势.NI、MiID、MoID、SID组孕鼠尿碘中位数分别为353.7、115.9、26.9、0μg/L,组间比较差异有统计学意义(χ2=32.884,P<0.01);MoID、SID组[(29.4±18.6)、(11.7±7.0)μg/L]孕鼠血碘明显低于NI组[(49.1±23.0)μg/L,P<0.05或<0.01).与NI组[(65.4±41.2)μg/L,(0.35±0.14)μg/g]比较,MiID、MoID、SID组胎鼠羊水碘[(48.3±23.1)、(29.2±14.7)、(19.5±6.7)μg/L]呈降低趋势,胎盘组织碘[(0.57±0.26)、(0.53±0.34)、(0.53±0.15)μg/g]呈升高趋势,但组间比较差异均无统计学意义(P>0.05).②SID组孕鼠血清TT4[(14.3±4.1)mmol/L]和FT4[(10.8±3.6)pmol/L]明显低于NI组[(28.4±19.3)nmol/L,(20.2±8.0)pmol/L,P<0.05或<0.01],而FT3/FT4比值(0.34±0.16),甲状腺绝对质量[(48.4±22.7)mg]和相对质量[(144±76)mg/kg]明显高于NI组[(0.16±0.02)、(19.5±3.1)mg,(66±10)mg/kg,P<0.01];MiID、MoID组TT4[(25.5±13.1)、(22.1±6.1)nmoL/L]和FT4[(18.6±8.4)、(18.5±4.1)pmol/L]与NI组比较,有降低趋势,FT3/FT4比值(0.17±0.06、0.19±0.04),甲状腺绝对质量[(25.0±8.9)、(27.0±5.7)mg]和相对质量[(78±25)、(84±19)mg/kg]与NI组比较,有增高趋势,但组间比较差异均无统计学意义(P>0.05);SID组孕鼠甲状腺明显充血肿大,MiID、MoID组轻度肿大.③SID组胎鼠羊水FT4[(1.07±0.87)pmol/L]低于NI组[(2.38±1.55)pmoVL],FT3/FT4比值(1.96±0.61)高于NI组(0.50±0.18),组间比较差异均有统计学意义(P<0.05或<0.01);MiID、MoID组FT4[(2.77±0.90)、(2.35±0.76)pmol/L]、FT3/FT4比值(0.46±0.15、0.61±0.21)与NI组比较,差异均无统计学意义(P>0.05);SID组胎鼠甲状腺有明显充血肿大,MiID、MoID组仅见轻度充血,其大小与NI组相似.结论 重度碘缺乏使孕鼠及其胎鼠均发生了明显甲状腺功能减退症,而轻度碘缺乏通过代偿可使胎儿甲状腺激素维持正常水平,中度碘缺乏对母亲和胎儿均有不同程度的负面影响.     

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.     

碘过量对哺乳期母鼠乳腺钠碘转运体mRNA和蛋白表达的影响

目的 观察碘过量对哺乳期母鼠乳腺钠碘转运体(sodium-iodide symporter,NIS)mRNA及蛋白表达的影响.方法 断乳1个月健康Wistar大鼠60只,雌雄比为2:1.将大鼠按体质量随机分为适碘组(30只)、10倍碘组(15只)、100倍碘组(15只),通过饮食(含碘300μg/ks)和饮水(含碘5、1845、20 295μg/L)摄碘.喂养3个月后交配产仔鼠,在哺乳第10天,采用砷铈催化分光光度法测定母鼠尿碘和乳汁碘.取母鼠乳腺,用反转录聚合酶链反应(RT-PCR)测定NIS mRNA表达;用SABC法进行免疫组化染色观察NIS蛋白表达强度.结果 ①母鼠尿碘:适碘组344.7μg/L、10倍碘组3597.5μg/L、100倍碘组25 404.3μg/L,10倍碘组和100倍碘组分别是适碘组的10.4倍和73.7倍.②母鼠乳汁碘:适碘组6.0×103μg/L、10倍碘组27.1×103μg/L、100倍碘组191.0×103μg/L,10倍碘组和100倍碘组分别是适碘组的4.5倍和31.8倍,母鼠乳汁碘增加倍数低于尿碘.③母鼠乳腺NIS表达:NIS raRNA表达组间比较差异有统计学意义(F=24.19,P＜0.01);其中适碘组(1.532±0.044)较10倍碘组(1.250±0.034)、100倍碘组(1.272±0.039)明显增高(P＜0.01),而且哺乳期母鼠乳腺N1S mRNA表达(1.532±0.044)高于非哺乳期母鼠(0.879±0.018),二者比较差异有统计学意义(t=19.09,P＜0.01);母鼠乳腺NIS蛋白表达强度随碘摄入量增加而减弱.结论 过量碘摄入可抑制乳腺NISmRNA和蛋白表达,限制乳汁中的含碘量随碘摄入量增加的幅度,此机制对下一代有着重要的保护作用.     

高碘对大鼠甲状腺过氧化物酶和钠碘转运体基因mRNA表达的影响

目的 观察长期碘过量对大鼠甲状腺过氧化物酶(TPO)和钠碘转运体(NIS)mRNA表达的影响.方法 将SD大鼠按体质量随机分为对照(CI)组、高碘Ⅰ(HI Ⅰ)组、高碘Ⅱ(HIⅡ)组,分别饮用含碘5、5000、10000μg/L的自来水.6个月时取大鼠甲状腺,在光、电镜下观察甲状腺形态结构的变化;采用放射免疫法测定血清甲状腺激素水平;RT-PCR法检测甲状腺TPO、NIS mRNA的表达.结果 高碘组与CI组相比.部分甲状腺滤泡明显增大,滤泡腔内充满浓染胶质;血清TT4 、TT3水平,HI Ⅰ组[(73.82±16.48)、(1.34±0.31)nmol/L]和HIⅡ组[(70.65±11.43)、(1.15±0.39)nmol/L]与对照组[(75.68±13.99)、(1.45±0.49)nmol/L]相比呈逐渐下降趋势,但组间差异无统计学意义(F值分别为0.371、1.163,P＞0.05);TPO、NIS mRNA表达水平,组间比较差异有统计学意义(F值分别为30.863、62.675,P＜0.05).HI Ⅰ组(1.28±0.10、0.56±0.17)和HIⅡ组(1.14±0.04、0.39±0.06)均比对照组(1.39±0.08、0.71±0.13)明显降低(P＜0.05).结论 长期碘过量可造成甲状腺组织形态学改变,并且抑制甲状腺TPO、NIS mRNA表达.     

维生素A对碘过量小鼠甲状腺细胞凋亡相关基因表达的影响

目的 观察维生素A对碘过量小鼠甲状腺细胞凋亡相关基因表达的影响.方法 将昆明种小鼠按体质量随机分成6组:对照(NI)组、高碘(HI)组、低维生素A(LVA)组、高碘低维生素A(HI+LVA)组、高碘补维生素A1(HI+VA1)组、高碘补维生素A2(HI+VA2)组.各组小鼠饲以合成饲料(维生素A分别为4000、4000、0、0、8000、16 000 U/kg),并饮用含不同剂量碘酸钾的去离子水(含碘量分别为50、3000、50、3000、3000、3000μg/L).分别在实验3、6个月时,采用原位末端标记(TUNEL)法检测甲状腺细胞凋亡水平,反转录-聚合酶链反应(RT-PCR)法检测甲状腺细胞凋亡相关基因Fas、FasL、Bcl-2 mRNA表达水平.结果甲状腺细胞凋亡指数随着月龄的增长呈逐渐上升的趋势.3个月时,HI组[(20.91±9.57)%]、HI+LVA组[(20.29±9.90)%]、HI+VA2组[(19.51±8.25)%]均明显高于NI组[(14.09±5.68)%,P均<0.05];6个月时,HI组[(23.22±8.58)%]、LVA组[(22.56±6.17)%]、HI+LVA组[(25.99±9.62)%]、HI+VA1组[(21.65±7.74)%]均明显高于Nl组[(16.80±9.90)%,P均<0.05].3、6个月时HI组Fas、FasL mRNA表达(Fas:1.57±0.36、1.49±0.35,FasL:1.85±0.46、1.84±0.32)与NI组(Fas:1.29±0.25、1.27±0.26,FagL:1.60±0.13、1.65±0.13)比较有增高趋势,但差异无统计学意义(P均>0.05);6个月时,HI+VA1、HI+VA2组Fas mRNA表达(1.33±0.35、1.30±0.26)与HI组比较有降低趋势,与NI组比较差异无统计学意义(P均>0.05);3、6个月时,HI+LVA组Fas、FagL mRNA表达(Fag:1.60±0.27、1.67±0.32,FagL:1.88±0.46、2.10±0.34)与HI组比较,差异均无统计学意义(P均>0.05).上述各组Bcl-2 mRNA表达水平3个月时分别为1.05±0.19、0.96±0.33、0.95±0.26、1.18±0.27、1.10±0.19、0.98±0.36,6个月时分别为1.35±0.28、1.60±0.25、1.48±0.18、1.71±0.26、1.66±0.29、1.56±0.35,组间比较差异均无统计学意义(P均>0.05).结论 高碘可引起小鼠甲状腺细胞凋亡;补充VA在一定程度上调控了凋亡相关基因的表达水平,部分拮抗了高碘引起的细胞凋亡.     

碘过量对NOD和Balb/c鼠甲状腺TRAIL和TRAIL-sR1表达的影响

目的 观察碘过量对自身免疫性疾病敏感品系NOD鼠和非敏感品系Balb/c鼠甲状腺细胞凋亡相关基因肿瘤坏死因子的相关凋亡诱导配体(tumor necrosis factor-related apoptosis-inducing ligand, TRAIL)和其受体TRAIL刺激性受体1(TRAIL-sR1)表达的影响,了解碘过量诱导实验性自身免疫性甲状腺炎(EAT)发病过程中TRAIL和TRAIL-sR1的作用机制.方法 6～7周龄雌性NOD鼠和Balb/c鼠各16只,按体质量各随机分为对照组和碘过量(HI)组,每组8只.对照组饮高压灭菌水,HI组饮0.05%NaI添加水,饲养8周后处死.测量甲状腺相对质量,进行甲状腺组织形态学观察,测量血清甲状腺素(TT4)和甲状腺刺激激素(TSH),检测甲状腺滤泡上皮细胞凋亡情况,应用实时定量PcR(real time PCR)方法检测TRAIL和TRAIL-sR1 mRNA表达情况.结果 NOD鼠HI组甲状腺相对质量[(104.8±14.5)mg/kg]高于对照组[(71.8±20.4)mg/kg],血清TT4水平[(30.77±3.59)mmol/L]低于对照组[(36.43±2.66)mmol/L],TSH水平[(6.98±0.66)μg/L]高于对照组[(5.55±0.56)μg/L],组间比较差异均有统计学意义(t值分别为7.773、-9.526、-4.458,P均<0.05).HI组甲状腺出现滤泡扩张、胶质潴留及明显的淋巴细胞浸润伴灶性纤维化.Balb/c鼠川组甲状腺相对质量[(155.8±20.8)mg/kg]高于对照组[(105.1±22.0)mg/kg],血清TT4水平[(19.75±3.32)mmol/L]低于对照组[(23.46±6.21)mmol/L],TSH水平[(4.14±1.71)μg/L]高于对照组[(3.55±1.41)μg/L],组间比较差异均有统计学意义(t值分别为7.554、-7.239、3.140,P均<0.05);HI组甲状腺仅有甲状腺滤泡扩张,胶质潴留,而未见明显的淋巴细胞浸润.HI组NOD鼠和Balb/c鼠甲状腺滤泡上皮细胞的凋亡指数(3.97±0.91、1.05±0.45)分别高于对照组(0.21±0.15、0.10±0.03),组间比较差异均有统计学意义(t值分别为-7.167、-17.772,P均<0.05),Balb/c鼠HI组的甲状腺滤泡上皮细胞的凋亡指数低于NOD鼠HI组,组间比较差异有统计学意义(t=-7.625,P<0.05).NOD鼠HI组TRAIL mRNA表达水平(0.018 88±0.005 77)高于对照组(0.00961±0.005 91),组间比较差异有统计学意义(t=-2.710,P<0.05);Balb/c鼠HI组TRAIL表达水平(0.001 24±0.000 46)与对照组(0.000 59±0.000 39)比较,差异无统计学意义(t=-1.940,P>0.05);NOD鼠和Balb/c鼠HI组的TRAIL-sR1 mRNA表达水平(0.000 53±0.000 15、0.000 42±0.000 09)均高于对照组(0.000 28±0.000 05、0.000 17±0.000 06),组间比较差异有统计学意义(t值分别为3.050,3.990,P均<0.05),Balb/c鼠HI组的TRAIL和TRAIL-sR1的mRNA表达水平均低于NOD鼠HI组,组间比较差异均有统计学意义(t值分别为-3.370、-4.760,P均<0.05).结论 碘过量可使NOD和Balb/c鼠发生胶质潴留性甲状腺肿,并可造成NOD鼠甲状腺发生明显的炎症反应.TRAIL和TRAIL-sR1表达水平升高是碘过量导致甲状腺滤泡上皮凋亡和炎症发生的分子基础之一.遗传在甲状腺炎的发病过程中起到至关重要的作用.     

胰岛素样生长因子Ⅰ在碘缺乏和碘过量小鼠甲状腺形态变化中的作用

目的 观察碘缺乏和碘过量小鼠甲状腺胰岛素样生长因子Ⅰ(IGF-Ⅰ)的水平及在甲状腺形态变化中的作用.方法 选用Balb/c小鼠48只,体质量约16 g,雌雄各半.按体质量、性别将小鼠随机分为3组:碘缺乏组(LI,饲料中含碘量为50μg/kg,饮去离子水);适碘组(对照,NI,饲料中含碘量为300μg/kg,饮去离子水)、碘过量组(HI,饲料中含碘量为300μg/kg,饮水中含碘量14 700μg/kg);每组16只.喂养12周后处死,取小鼠甲状腺,测量甲状腺的绝对及相对质量,HE染色,光镜下观察小鼠甲状腺的形态学变化;RT-PCR法检测IGF-Ⅰ mRNA表达:免疫组化法检测甲状腺IGF-Ⅰ蛋白质表达.结果 小鼠甲状腺的绝对质量和相对质量,组间比较差异有统计学意义(F值分别为315.881、405.921,P均<0.01);其中LI组[(10.71±4.03)mg,(44.98±15.39)mg/100 g体质量]和HI组[(3.42±1.17)mg,(13.50±3.89)mg/100 g体质量]高于NI组[(2.11±0.53)mg,(8.35±1.98)mg/100 g体质量,P均<0.01].光镜下,LI组小鼠滤泡体积变小,数量增多,上皮细胞呈柱状或高柱状,增生呈复层,滤泡腔内胶质减少或缺如;而HI组小鼠发生了胶质蓄积,滤泡增大,未见滤泡增生.甲状腺IGF-Ⅰ mRNA表达,LI组(1.03±0.32)明显高于NI组(0.65±0.19),组间比较差异有统计学意义(F=7.518,P<0.01),HI组与NI组比较有下降趋势,但差异无统计学意义(P>0.05).甲状腺IGF-Ⅰ蛋白质表达,LI组小鼠甲状腺滤泡上皮细胞内棕黄色颗粒明显多于NI组和HI组,而HI组却少于NI组.结论 碘缺乏和碘过量小鼠发生甲状腺肿,甲状腺IGF-Ⅰ mRNA和蛋白表达的改变,可能参与碘缺乏和碘过量导致甲状腺形态改变的过程,甲状腺白分泌的IGF-Ⅰ在缺碘性和高碘性甲状腺肿形成过程中可能起重要调节作用.     

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...