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作 者:刘玉珍[1] 张捷[1] 高妍[1] 高燕明[1] 杨大木[1]
机构地区:[1]北京医科大学第一医院内分泌科
出 处:《中华内分泌代谢杂志》1997年第3期154-157,共4页Chinese Journal of Endocrinology and Metabolism
摘 要:为了探讨T3受体亚型在低T3综合征发病机制中的可能作用,我们分别从人c_erbAα1、α2及βmRNA的cDNA片段为探针,应用分子杂交技术测定了8例糖尿病T3正常患者、5例糖尿病及7例其他慢性非甲状腺疾病伴低T3综合征患者外周血淋巴细胞T3受体亚型mRNA含量,并分别与正常对照进行比较。结果:糖尿病及其他疾病伴低T3综合征患者外周血淋巴细胞c_erbAα1、α2及βmRNA含量均增高,以c_erbAα1mRNA增高最明显,但是在两组疾病中3种c_erbAmRNA含量增加比率不一致,与对照组比较,糖尿病T3正常组变化不明显。提示低T3综合征患者外周血淋巴细胞T3受体3种亚型mRNA表达水平呈上调趋势。To investigate the changes of T3 receptor genes in the “sick euthyroid” syndrome, c_erbA α1, α2 and β mRNA had been isolated from peripheral lymphocytes in 5 NIDDM patients and 7 other chronic non_thyroidal disease patients with sick euthyroid syndrome and compared with 8 NIDDM patients with normal thyroid hormone level and 8 normal controls. mRNAs were examined using Northern blot and Slot blot hybridization. The study showed that the levels of c_erbA α1, α2 and β mRNA were all increased in NIDDM and other disease patients with “sick euthyroid” syndrome, and the level of c_erbA α1 mRNA was higher than those of c_erbA α2 and β mRNA. But the ratios of increase in 3 c_erbA mRNA contents between the two disease groups of patients were not uniform. As compared with the controls, there was no obvious change in NIDDM patients with normal thyroid hormone level.The results suggest that, when circulatory T3 level decreases in sick euthyroid syndrome, the body enhances the expression of these mRNAs to maintain normal metabolism. This may be a kind of compensatory mechanism in “sick euthyroid” syndrome.
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