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Thyroid hormone treatment decreases hepatic glucose production and renal reabsorption of glucose in alloxan‐induced diabetic Wistar rats

机译:甲状腺激素治疗降低了四氧嘧啶致糖尿病的Wistar大鼠的肝葡萄糖生成和肾脏对葡萄糖的重吸收

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摘要

The thyroid hormone (TH) plays an important role in glucose metabolism. Recently, we showed that the TH improves glycemia control by decreasing cytokines expression in the adipose tissue and skeletal muscle of alloxan‐induced diabetic rats, which were also shown to present primary hypothyroidism. In this context, this study aims to investigate whether the chronic treatment of diabetic rats with T3 could affect other tissues that are involved in the control of glucose homeostasis, as the liver and kidney. Adult Male Wistar rats were divided into nondiabetic, diabetic, and diabetic treated with T3 (1.5 μg/100 g BW for 4 weeks). Diabetes was induced by alloxan monohydrate (150 mg/kg, BW, i.p.). Animals showing fasting blood glucose levels greater than 250 mg/dL were selected for the study. After treatment, we measured the blood glucose, serum T3, T4, TSH, and insulin concentration, hepatic glucose production by liver perfusion, liver PEPCK, GAPDH, and pAKT expression, as well as urine glucose concentration and renal expression of SGLT2 and GLUT2. T3 reduced blood glucose, hepatic glucose production, liver PEPCK, GAPDH, and pAKT content and the renal expression of SGLT2 and increased glycosuria. Results suggest that the decreased hepatic glucose output and increased glucose excretion induced by T3 treatment are important mechanisms that contribute to reduce serum concentration of glucose, accounting for the improvement of glucose homeostasis control in diabetic rats.
机译:甲状腺激素(TH)在葡萄糖代谢中起重要作用。最近,我们发现TH可以通过降低四氧嘧啶诱发的糖尿病大鼠脂肪组织和骨骼肌中细胞因子的表达来改善血糖控制,这也表明原发性甲状腺功能减退症。在此背景下,本研究旨在研究用T3对糖尿病大鼠的慢性治疗是否会影响其他参与控制葡萄糖稳态的组织,例如肝脏和肾脏。将成年雄性Wistar大鼠分为非糖尿病,糖尿病和接受T3(1.5μg/ 100 g BW连续4周)治疗的糖尿病。尿嘧啶一水合物(150 mg / kg,BW,i.p.)诱发糖尿病。选择空腹血糖水平高于250 mg / dL的动物进行研究。治疗后,我们测量了血糖,血清T3,T4,TSH和胰岛素浓度,肝脏灌注产生的肝葡萄糖,肝脏PEPCK,GAPDH和pAKT的表达,以及尿葡萄糖浓度和SGLT2和GLUT2的肾脏表达。 T3降低血糖,肝葡萄糖生成,肝脏PEPCK,GAPDH和pAKT含量以及SGLT2的肾脏表达并增加糖尿。结果表明,T3处理引起的肝葡萄糖输出减少和葡萄糖排泄增加是导致降低血清葡萄糖浓度的重要机制,这说明了糖尿病大鼠体内葡萄糖稳态控制的改善。

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