Endocrine Abstracts

Thyroid hormone plays an important role on carbohydrate and lipid metabolism. In hypothyroidism is observed reduction of glucose transporter-4 expression and insulin sensitivity and in hyperthyroid states the key enzymes of gluconeogenesis and glycogenolysis are induced, and both conditions lead to glucose intolerance. It has been reported an increased prevalence of thyroid dysfunction in obese and diabetic patients. Recently we have demonstrated a hypothyroid state in alloxan-induced diabetic rats, in which the treatment with triiodothyronine (T3) improved glycemia control and insulin sensitivity. These alterations were accompanied by reduction of inflammatory cytokines in white adipose tissue and skeletal muscle. The present study aimed at evaluating the thyroid function of cafeteria diet-induced obese rats and the effects of thyroid hormone treatment on their glycemia control, insulin sensitivity and subclinical inflammation.

Methods: Obesity was induced in male Wistar rats by cafeteria diet. A subset of the obese rats was treated with T3 (1.5 μg per 100 g body weight) for a 28-day period (DT₃). Thyroid function was evaluated by molecular (TG, NIS, TSHR and TPO expression in thyroid gland) and biochemical parameters (serum TSH, T4 and T3 concentrations). Cytokines concentration was measured in mesenteric white adipose tissue (MWAT) (MILIplex assay kit).

Results: Obese rats exhibited decreased insulin sensitivity, thyroid function and serum TSH concentration, and increased MWAT inflammatory cytokines, NIS and TSHR expression in thyroid gland. Thyroid hormone treatment improved insulin sensitivity, glucose tolerance and reduced MWAT inflammatory cytokines content, which are known to induce insulin resistance.

Conclusions: The present data provide evidence that thyroid function is reduced in obese rats and reinforce the role of T3 treatment on improvement of insulin sensitivity by its negative modulation of inflammatory cytokine expression in metabolic disorders as obesity or diabetes mellitus.