Insulin resistance is defined as a glucose homeostasis disorder involving a decreased sensitivity of muscles, adipose tissue, liver and other body tissues to insulin, despite its normal or increased concentration in blood. Insulin resistance may be asymptomatic or occur presenting a variety of disorders, such as: glucose tolerance impairment, type 2 diabetes, as well as hypercholesterolaemia, hypertriglyceridaemia, obesity, and arterial hypertension. Insulin acts via specific receptors present on the surface of most cells of the body. The greatest number of these receptors is found on adipocytes, hepatocytes and striated muscle cells. There are three mechanisms of insulin resistance: pre-receptor, receptor and post-receptor. Multiple methods of assessing insulin resistance are based on the concurrent measurements of glucose and insulin levels in blood serum. The glucose and insulin measurements are conducted in baseline conditions or after intravenous administration of a specific quantity of glucose or insulin. The methods of assessing insulin resistance are divided into direct and indirect. The current 'gold standard' in the assessment of insulin sensitivity is the determination of tissue glucose utilisation using the metabolic clamp technique. The presence of disorders of carbohydrate metabolism has been demonstrated in thyroid disease involving either overt hyperthyroidism or overt hypothyroidism. The severity of the disease is proportional to the severity of these disorders. The possible influence of subclinical forms of both hyperthyroidism and hypothyroidism on carbohydrate disorders is still under discussion. Thyroid hormones have a significant effect on glucose metabolism and the development of insulin resistance. In hyperthyroidism, impaired glucose tolerance may be the result of mainly hepatic insulin resistance, whereas in hypothyroidism the available data suggests that the insulin resistance of peripheral tissues prevails.