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目的检测甲状腺毒症妊娠大鼠胰腺中葡萄糖转运蛋白2(GLUT2)和蛋白酪氨酸磷酸酶-1B(PTP-1B)的表达,探讨其影响糖代谢的可能机制。方法雌性SD大鼠分为非妊娠组和待妊娠组,待妊娠组按雌雄比例2∶1合笼受孕后进一步分为单纯妊娠(R)组、妊娠期左甲状腺素钠低剂量(RA)组、妊娠期左甲状腺素钠中剂量(RB)组和妊娠期左甲状腺素钠高剂量(RC)组,非妊娠组进一步分为正常对照(N)组、左甲状腺素钠低剂量(A)组、左甲状腺素钠中剂量(B)组和左甲状腺素钠高剂量(C)组。予A、RA组(左甲状腺素钠50μg/100g)、B、RB组(左甲状腺素钠100μg/100g)、C、RC组(左甲状腺素钠150μg/100g)灌胃制造甲状腺毒症模型,N、R组予等量生理盐水。检测各组雌鼠甲状腺功能、FPG和FIns,Western blot检测胰腺中GLUT2和PTP-1B的表达。结果随着左甲状腺素钠剂量增加,N、A、B、C组和R、RA、RB、RC组游离三碘甲状腺原氨酸(FT3)[(2.65±0.07)vs(4.05±0.10)vs(4.87±0.63)vs(5.62±0.73)pmol/L;(2.67±0.10)vs(4.07±0.09)vs(4.84±0.11)vs(5.65±0.18)pmol/L,P<0.01]、游离甲状腺素(FT4)[(10.54±0.58)vs(13.46±0.78)vs(25.77±0.85)vs(36.58±0.91)pmol/L;(10.61±0.79)vs(13.53±0.66)vs(25.90±1.12)vs(36.65±0.62)pmol/L,P<0.01]升高,促甲状腺激素(TSH)[(0.086±0.009)vs(0.029±0.002)vs(0.024±0.001)vs(0.018±0.002)μU/ml;(0.070±0.009)vs(0.027±0.002)vs(0.021±0.001)vs(0.015±0.002)μU/ml,P<0.01]降低。甲状腺毒症各组(A、B、C组和RA、RB、RC组)FPG较对照组(N组和R组)升高[(5.43±0.32)、(5.74±0.21)、(6.34±0.46)vs(4.98±0.25)mmol/L;(5.37±0.48)、(5.78±0.39)、(6.45±0.44)vs(4.88±0.38)mmol/L,P<0.01],C组FIns较N组升高[(10.40±1.52)vs(8.25±0.80)μU/ml,P<0.01],妊娠各组(R、RA、RB、RC组)FIns较非妊娠各组(N、A、B、C组)升高[(9.16±1.28)vs(8.25±0.80)μU/ml;(10.40±1.31)vs(9.20±1.32)μU/ml;(10.41±1.43)vs(9.75±1.24)μU/ml;(11.09±1.17)vs(10.40±1.52)μU/ml,P<0.01]。Western blot结果显示,甲状腺毒症各组GLUT2表达较N、R组降低,PTP-1B表达升高(P<0.05)。结论 GLUT2及PTP-1B可能与妊娠期合并甲状腺毒症雌鼠出现糖代谢异常相关。
Objective To investigate the expression of glucose transporter 2 (GLUT2) and protein tyrosine phosphatase-1B (PTP-1B) in the pancreas of thyrotoxicosis pregnant rats and to explore the possible mechanism of glucose transport. Methods Female Sprague-Dawley rats were randomly divided into non-pregnancy group and pregnancy-waiting group. The pregnant women were divided into simple pregnancy (R) group, pregnancy low-dose of levothyroxine (RA) (RB) group and high dose of levothyroxine (RC) group during gestation. The non-pregnant group was further divided into normal control (N) group, levothyroxine sodium low dose (A) group , Levothyroxine sodium (B) and levothyroxine sodium (C) groups. Thyrotoxicosis models were induced by intragastric administration of levothyroxine sodium (50μg / 100g), group B and RB (100μg / 100g of levothyroxine) and group C and RC (levothyroxine sodium 150μg / 100g) N, R group to give the same amount of saline. Thyroid function, FPG and FIns were detected in each group, and the expression of GLUT2 and PTP-1B in pancreas was detected by Western blot. Results With the increase of the dose of levothyroxine, the free triiodothyronine (FT3) in groups N, A, B and C and in groups R, RA, RB and RC [(2.65 ± 0.07) vs (4.87 ± 0.63) vs (5.62 ± 0.73) pmol / L; (2.67 ± 0.10) vs (4.07 ± 0.09 vs 4.84 ± 0.11 vs 5.65 ± 0.18 pmol / L, P <0.01] (FT4) vs (13.54 ± 0.58) vs (13.46 ± 0.78 vs 25.77 ± 0.85 vs 36.58 ± 0.91 pmol / L vs (10.61 ± 0.79 vs 13.53 ± 0.66 vs 25.90 ± 1.12 vs (0.086 ± 0.002) vs (0.024 ± 0.001) vs (0.018 ± 0.002) μU / ml, respectively; (3) The levels of thyroid stimulating hormone (TSH) 0.070 ± 0.009 vs 0.027 ± 0.002 vs 0.021 ± 0.001 vs 0.015 ± 0.002 μU / ml, P <0.01]. Compared with the control group (N group and R group), FPG in each group (group A, B, C and RA, RB and RC) of thyrotoxicosis increased (5.43 ± 0.32), (5.74 ± 0.21) and (6.34 ± 0.46 (5.37 ± 0.48), (5.78 ± 0.39) and (6.45 ± 0.44) vs (4.88 ± 0.38) mmol / L respectively, P <0.01]. The FIns in group C were significantly higher than those in group N FIns in each group (R, RA, RB, RC) were significantly higher than those in non-pregnant groups (N, A, B and C) ; (10.41 ± 1.43) vs (9.75 ± 1.24) μU / ml; ((9.16 ± 1.28) vs (8.25 ± 0.80) μU / ml; 11.09 ± 1.17 vs vs 10.40 ± 1.52 μU / ml, P <0.01]. Western blot results showed that GLUT2 expression in each group of thyrotoxicosis was lower than that of N and R groups, and PTP-1B expression was increased (P <0.05). Conclusion GLUT2 and PTP-1B may be associated with abnormal glucose metabolism in pregnant women with thyrotoxicosis.