One of the central features of the metabolic syndrome is insulin resistance which is described as the inability of insulin to stimulate glucose uptake. This disorder has been intensively investigated in adipocytes and skeletal muscles. Insulin resistance also affects the myocardium however the involved mechanisms remain elusive. Therefore, we aimed to investigate the cellular mechanisms contributing to impaired glucose metabolism in cultured adult rat cardiomyocytes (ARC). Firstly, we demonstrated that ERK1/2 activation prevents the formation of the microtubule organizing center and disrupts microtubule architecture leading to altered stimulated-glucose transport in ARC. Secondly, we found that exposure of cardiomyocytes to fatty acids and peroxisome proliferator activated receptors agonist was accompanied by impaired stimulated glucose transport. Thirdly, we showed that cardiotrophin-1 is involved in regulation of myocardial glucose metabolism in a dose dependant manner. In summary, this thesis provides new insights into the mechanisms regulating glucose metabolism in cardiomyocytes.