首页> 外文期刊>Endocrine journal >Effect of Triiodothyronine Administration on Reduced Expression of Type 1 lodothyronine Deiodinase Messenger Ribonucleic Acid in Streptozotocin-induced Diabetic Rats
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Effect of Triiodothyronine Administration on Reduced Expression of Type 1 lodothyronine Deiodinase Messenger Ribonucleic Acid in Streptozotocin-induced Diabetic Rats

机译:给予三碘甲状腺素对链脲佐菌素诱导的糖尿病大鼠1型碘甲状腺素脱碘酶信使核糖核酸表达降低的影响

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References(29) Cited-By(2) To examine the mechanism behind a decrease in type 1 iodothyronine deiodinase (D1) gene expression in diabetes mellitus, we evaluated the effect of administering T3 and/or insulin on D1 activity and the mRNA levels in the liver of streptozotocin (STZ)-induced diabetic rats. STZ (100mg/kg BW) was administered to male Wistar rats, and the rats were divided into four groups as follows: (1) STZ alone, (2) STZ and T3 (5μg/100g BW daily for 7 days), (3) STZ and insulin (intermediate-acting insulin, 4units/100g BW daily for 7 days), and (4) STZ, T3, and insulin. Blood glucose levels increased in Group 1, but were normalized in Group 3. Serum T3 levels were markedly decreased in Group 1. They were within normal limits 24hours after the last administration of T3 in Group 2 and after the administration of insulin in Group 3. T3 levels were supranormal in Group 4. TSH levels were normal in Groups 1 and 3, but were suppressed in Groups 2 and 4, suggesting that rats in Groups 2 and 4 were actually in a hyperthyroid state after injecting a large amount of T3. D1 activity in Group 1 was reduced significantly, but it was normal in Groups 2 and 3, and increased in Group 4. D1 mRNA levels in the liver in Group 1 decreased significantly, but they were increased to within normal limits by adding insulin in Group 3. They were also normal in Group 2 where hyperglycemia was evident and rats were hyperthyroid after administering T3. D1 mRNA in Group 4 increased significantly where glucose levels were normal and T3 levels were increased. We suggest that the decrease in hepatic D1 mRNA in STZ-induced diabetic rats is due to metabolic derangement caused by insulin deficiency in addition to a possible decrease in tissue T3 availability.
机译:参考文献(29)被引用人(2)为了研究糖尿病中1型碘甲状腺素脱碘酶(D1)基因表达下降的背后机制,我们评估了施用T3和/或胰岛素对D1活性和mRNA表达的影响。链脲佐菌素(STZ)诱导的糖尿病大鼠的肝脏。将雄性Wistar大鼠以STZ(100mg / kg体重)分为四组:(1)单独使用STZ;(2)STZ和T3(每天5μg/ 100g BW,连续7天),(3 )STZ和胰岛素(中效胰岛素,每天4单位/ 100 g BW,连续7天),以及(4)STZ,T3和胰岛素。第1组的血糖水平升高,但在第3组恢复正常。第1组的血清T3水平明显降低。在第2组中最后一次服用T3和第3组中注射胰岛素后的24小时内,它们处于正常范围内。在第4组中,T3水平超正常。在第1和第3组中,TSH水平正常,但在第2和第4组中被抑制,这表明第2和第4组中的大鼠在注射大量T3后实际上处于甲亢状态。第1组中的D1活性显着降低,但在第2和第3组中是正常的,而在第4组中升高。第1组中肝脏中D1 mRNA的水平显着降低,但通过在第2组中添加胰岛素使D1 mRNA水平升高至正常范围3.在第2组中它们也是正常的,在第2组中,高血糖很明显,并且在服用T3后大鼠甲状腺功能亢进。在葡萄糖水平正常且T3水平升高的情况下,第4组的D1 mRNA显着增加。我们建议在STZ诱导的糖尿病大鼠中肝D1 mRNA的降低是由于胰岛素缺乏引起的代谢紊乱,以及组织T3利用率可能降低。

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