Panveloski-Costa Ana C, Serrano-Nascimento Caroline, Bargi-Souza Paula, Poyares Leonice L, Viana Gabriela de S, Nunes Maria T
Department of Physiology and Biophysics, Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil.
Physiol Rep. 2018 Feb;6(3). doi: 10.14814/phy2.13550.
Thyroid hormones play an important role in glucose metabolism and there is evidence of increased prevalence of thyroid dysfunction in obese and diabetic patients. This study aimed at evaluating the thyroid function and the effects of the triiodothyronine (T3) treatment on glycemia control, insulin sensitivity and subclinical inflammation in cafeteria-diet-induced obesity in rats. Obesity was induced in male Wistar rats by offering a cafeteria diet and a subset of the obese rats was treated with T3 (1.5 μg per 100 g of body weight) for a 28-day period. The pituitary-thyroid axis was evaluated by molecular and biochemical parameters. Cytokine content was measured in the serum as well as in the mesenteric and epididymal white adipose tissue. Obese rats exhibited impairment of glycemia control, increased content of inflammatory cytokines in mesenteric white adipose tissue, decreased serum thyrotropin (TSH) concentration and increased sodium/iodide symporter (NIS) and TSH receptor (TSHR) protein content in thyroid gland. T3 treatment improved insulin sensitivity, glucose tolerance, and reduced inflammatory cytokine content in mesenteric white adipose tissue. In the thyroid gland NIS, TSHR, and thyroperoxidase (TPO) content were reduced while thyroglobulin (TG) content was increased by T3. The thyrotrophic response to negative feedback exerted by T3 was preserved in obese rats. The present data reinforce the beneficial effects of T3 treatment of obese rats on the improvement of insulin sensitivity and on the negative modulation of inflammatory cytokine expression in adipose tissue. Moreover, we have evidenced that the pituitary-thyroid axis is affected in obese rats, as illustrated by the impaired TSH secretion.
甲状腺激素在葡萄糖代谢中发挥着重要作用,并且有证据表明肥胖和糖尿病患者甲状腺功能障碍的患病率增加。本研究旨在评估甲状腺功能以及三碘甲状腺原氨酸(T3)治疗对大鼠因自助餐饮食诱导的肥胖症中血糖控制、胰岛素敏感性和亚临床炎症的影响。通过提供自助餐饮食诱导雄性Wistar大鼠肥胖,对一部分肥胖大鼠用T3(每100克体重1.5微克)治疗28天。通过分子和生化参数评估垂体 - 甲状腺轴。测量血清以及肠系膜和附睾白色脂肪组织中的细胞因子含量。肥胖大鼠表现出血糖控制受损、肠系膜白色脂肪组织中炎症细胞因子含量增加、血清促甲状腺激素(TSH)浓度降低以及甲状腺中钠/碘同向转运体(NIS)和TSH受体(TSHR)蛋白含量增加。T3治疗改善了胰岛素敏感性、葡萄糖耐量,并降低了肠系膜白色脂肪组织中的炎症细胞因子含量。在甲状腺中,T3降低了NIS、TSHR和甲状腺过氧化物酶(TPO)的含量,同时增加了甲状腺球蛋白(TG)的含量。肥胖大鼠中对T3施加的负反馈的促甲状腺反应得以保留。目前的数据强化了T3治疗肥胖大鼠对改善胰岛素敏感性和对脂肪组织中炎症细胞因子表达的负调节的有益作用。此外,我们已经证明肥胖大鼠的垂体 - 甲状腺轴受到影响,如TSH分泌受损所示。