THs & Diabetes

What is it about?

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

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Why is it important?

In this review we have summarized recent reports concerning the relationship between of thyroid hormones, hypoand hypothyroidism, and insulin resistance. Taken together these observations suggest a strong association between thyroid hormone-induced effects on glucose metabolism, immune cells functions, and the oxidative status in the development of insulin resistance and diabetes. Thyroid hormones have a large impact on glucose metabolism and can act as insulin agonist or antagonist, depending on the tissues and cells studied; this suggests the existence of one or more complex signaling pathways shared by insulin and thyroid hormones (Fig. 1). The relationship between thyroid hormones and insulin appears very complex with respect to the role of immune system cells, and also for the importance of oxidative stress in the induction of insulin resistance. The ability of thyroid hormones to modulate several macrophage activities can be considered an important target in order to define a new strategy to modulate the crosstalk between thyroid hormones and skeletal muscle during insulin resistance. In this context the activation of several antinflammatory mechanisms [72] represents another step where thyroid hormones and insulin seem to interact, but neither the mechanisms involved nor their specific function to counteract peripheral insulin resistance are well understood.

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