Abstract
Several recent studies suggest that thyroid hormones role is not completely understood in insulin resistance as well as in the development of type 2 diabetes mellitus. Through the perturbation of gene expression linked to glucose metabolism both hyper- and hypothyroidism may cause impaired glucose utilization in skeletal muscle or overproduction of hepatic glucose, thus contributing to the induction of insulin resistance. The complex crosstalk between immune cells and skeletal muscle cells and adipose tissue, the ability of macrophages to release thyroid hormones, the ability of T3 to induce M2 macrophage polarization, the proinflammatory role of thyroid hormones and the antinflammatory effects of insulin all represent important events where thyroid hormone interference may lead to insulin resistance. The crosstalk between thyroid hormones and insulin in the modulation of oxidative status, and also to some extent in the antagonistic effects on several aspects of mitochondrial activities, could represent novel downstream targets for future therapeutic strategies in the treatment of insulin resistance and type 2 diabetes.
Keywords: Diabetes, hormone crosstalk, hyperthyroidism, hypothyroidism, inflammation, insulin resistance, oxidative stress, thyroid hormones.
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