Panveloski-Costa A C, Silva Teixeira S, Ribeiro I M R, Serrano-Nascimento C, das Neves R X, Favaro R R, Seelaender M, Antunes V R, Nunes M T
Department of Physiology and Biophysics, Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil.
Department of Cell and Developmental Biology, Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil.
Acta Physiol (Oxf). 2016 Jun;217(2):130-40. doi: 10.1111/apha.12647. Epub 2016 Jan 30.
This study aimed at evaluating whether thyroid hormone treatment could improve glycaemia and insulin response in alloxan-induced diabetic rats by altering cytokine expression in the skeletal muscle and epididymal white adipose tissue (eWAT) as well as altering inflammatory cell infiltration in eWAT.
Diabetes mellitus (DM) was induced in male Wistar rats by alloxan injection, and a subset of the diabetic rats was treated with T3 (1.5 μg per 100 g body weight) for a 28-day period (DT3 ). Cytokines were measured in serum (MILIplex assay kit) as well as in soleus and EDL skeletal muscles and eWAT by Western blotting. Thyroid function was evaluated by morphological, molecular and biochemical parameters. Cardiac function was assessed by measuring heart rate, blood pressure, maximal rate of pressure development (dp/dtmax ) and decline (dp/dtmin ) as well as the contractility index (CI). Sixty rats were used in the study.
Diabetic rats exhibited decreased thyroid function and increased inflammatory cytokines in serum, soleus muscle and eWAT. T3 treatment decreased glycaemia and improved insulin sensitivity in diabetic animals. These alterations were accompanied by decreased TNF-alpha and IL-6 content in soleus muscle and eWAT, and inflammatory cell infiltration in eWAT. T3 treatment did not affect cardiac function of diabetic rats.
The present data provide evidence that T3 treatment reduces glycaemia and improves insulin sensitivity in diabetic rats, and that at least part of this effect could result from its negative modulation of inflammatory cytokine expression.
本研究旨在评估甲状腺激素治疗是否可通过改变骨骼肌和附睾白色脂肪组织（eWAT）中的细胞因子表达以及改变eWAT中的炎性细胞浸润，来改善四氧嘧啶诱导的糖尿病大鼠的血糖和胰岛素反应。
通过注射四氧嘧啶诱导雄性Wistar大鼠患糖尿病，一部分糖尿病大鼠接受T3（每100克体重1.5微克）治疗28天（DT3组）。通过蛋白质免疫印迹法检测血清（MILIplex检测试剂盒）、比目鱼肌和趾长伸肌骨骼肌以及eWAT中的细胞因子。通过形态学、分子和生化参数评估甲状腺功能。通过测量心率、血压、压力最大上升速率（dp/dtmax）和下降速率（dp/dtmin）以及收缩力指数（CI）来评估心脏功能。本研究共使用了60只大鼠。
糖尿病大鼠的甲状腺功能降低，血清、比目鱼肌和eWAT中的炎性细胞因子增加。T3治疗可降低糖尿病动物的血糖并改善胰岛素敏感性。这些改变伴随着比目鱼肌和eWAT中肿瘤坏死因子-α和白细胞介素-6含量的降低以及eWAT中炎性细胞浸润的减少。T3治疗对糖尿病大鼠的心脏功能没有影响。
目前的数据表明，T3治疗可降低糖尿病大鼠的血糖并改善胰岛素敏感性，并且这种作用至少部分可能源于其对炎性细胞因子表达的负向调节。
