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甲状腺功能减退症及三碘甲状腺原氨酸治疗大鼠肝脏和心脏某些酶的活性和动力学变化。

Changes of activity and kinetics of certain liver and heart enzymes of hypothyroid and T(3)-treated rats.

机构信息

Department of Cytobiochemistry, Institute of Biology, University of Bialystok, ul. Swierkowa 20B, 15-950 Bialystok, Poland.

出版信息

J Physiol Biochem. 2012 Sep;68(3):345-51. doi: 10.1007/s13105-012-0146-2. Epub 2012 Jan 25.

Abstract

Thyroid diseases are one of the most common metabolic disorders in the human population. In this work, we present data concerning changes in the activity and kinetic parameters of several enzymes associated with both anabolic (glucose-6-phosphate dehydrogenase-G6PDH, EC 1.1.1.49; 6-phosphogluconate dehydrogenase-6PGDH, EC 1.1.1.44; malic enzyme-ME, EC 1.1.1.40; and isocitrate dehydrogenase-IDH, EC 1.1.1.42) and catabolic (NAD-dependent malate dehydrogenase-NAD-MDH, EC 1.1.1.37; and lactate dehydrogenase-LDH, EC 1.1.1.27) processes under conditions of hypothyroidism and T(3) treatment. Hypothyroidism was induced in rats by the surgical removal of the thyroid gland. T(3)-treated rats were injected by T(3) (0.5 mg T(3)/kg body weight daily during 10 days). We have found that T(3) treatment caused an increase of NAD-MDH activity as well as heart hypertrophy whereas the activity of LDH increased in the direction of pyruvate reduction. Moreover, we observed increased activity of both enzymes in the liver. These results confirm earlier observation concerning the relevance of oxidative metabolism in the heart under T(3) treatment. Hypothyroidism resulted in changes in the LDH activity in the heart whereas NAD-MDH activity did not change. Moreover, our data show that T(3) treatment caused an increase of G6PDH, 6PGDH, and ME activities in the liver. We also observed a decrease of IDH activity in both organs, whereas hypothyroidism caused the opposite effect. This data indicate that either deficiency or excess of thyroid hormones can prove to be particularly dangerous for the physiology of the heart muscle by disturbing bioenergetic and anabolic processes.

摘要

甲状腺疾病是人类最常见的代谢紊乱之一。在这项工作中,我们提供了有关甲状腺功能减退症和 T3 治疗条件下与合成代谢(葡萄糖-6-磷酸脱氢酶-G6PDH,EC 1.1.1.49;6-磷酸葡萄糖酸脱氢酶-6PGDH,EC 1.1.1.44;苹果酸酶-ME,EC 1.1.1.40;异柠檬酸脱氢酶-IDH,EC 1.1.1.42)和分解代谢(NAD 依赖性苹果酸脱氢酶-NAD-MDH,EC 1.1.1.37;乳酸脱氢酶-LDH,EC 1.1.1.27)过程中几种酶的活性和动力学参数变化的数据。通过手术切除甲状腺来诱导大鼠甲状腺功能减退症。T3 处理的大鼠每天注射 0.5mg T3/kg 体重的 T3(持续 10 天)。我们发现 T3 处理导致 NAD-MDH 活性增加和心脏肥大,而 LDH 活性朝着丙酮酸还原的方向增加。此外,我们观察到肝脏中两种酶的活性均增加。这些结果证实了早期关于 T3 处理下心脏氧化代谢相关性的观察结果。甲状腺功能减退症导致心脏 LDH 活性发生变化,而 NAD-MDH 活性没有变化。此外,我们的数据表明 T3 处理导致肝脏中 G6PDH、6PGDH 和 ME 活性增加。我们还观察到两种器官中 IDH 活性降低,而甲状腺功能减退症则产生相反的效果。这些数据表明,甲状腺激素缺乏或过多都会通过干扰生物能量和合成代谢过程,对心肌生理学造成特别危险。

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