title: Profiling of cardiac β-adrenoceptor subtypes in the cardiac left ventricle of rats with metabolic syndrome: Comparison with streptozotocin-induced diabetic rats.
abstract: Little is known about metabolic syndrome (MetS)-associated cardiomyopathy, especially in relation to the role and contribution of beta-adrenoceptor (β-AR) subtypes. Therefore, we examined the roles of β-AR subtypes in the cardiac function of rats with MetS (MetS group) and compared it with that of rats with streptozotocin (STZ)-induced diabetes (STZ group). Compared with the normal control rats, the protein levels of cardiac β1- and β2-AR in the MetS group were significantly decreased and with no changes in their mRNA levels, whereas the protein levels of β3-AR were similar to those of the controls. However, as shown previously, the protein levels of cardiac β1- and β2-AR in the STZ group were decreased, whereas the β3-AR levels were significantly increased by comparison with the controls. Additionally, the mRNA levels of β2- and β3-AR were increased, but β1-AR mRNA was decreased in the STZ group. Furthermore, left ventricular developed pressure responses to β3-AR agonist BRL37344 were increased in the STZ group but not in the MetS group, whereas for both groups, the responses to noradrenaline were not different from those of the controls. However, the response to stimulation with high concentrations of fenoterol was depressed in the MetS group, compared with the controls, but not in the STZ group. Consequently, our data suggest that the contribution of the β-AR system to cardiac dysfunction in the rats with MetS is not the same as that in the STZ group, although they have similar cardiac dysfunction with similar ultrastructural changes to the myocardium.
authors.affiliation: Department of Biophysics, Ankara University, Faculty of Medicine, 06100 Ankara, Turkey.|Department of Biophysics, Ankara University, Faculty of Medicine, 06100 Ankara, Turkey.
authors.forename: Esma N
authors.initials: EN
authors.lastname: Okatan
authors.affiliation: Department of Biophysics, Ankara University, Faculty of Medicine, 06100 Ankara, Turkey.|Department of Biophysics, Ankara University, Faculty of Medicine, 06100 Ankara, Turkey.
authors.forename: Erkan
authors.initials: E
authors.lastname: Tuncay
authors.affiliation: Department of Biophysics, Ankara University, Faculty of Medicine, 06100 Ankara, Turkey.|Department of Biophysics, Ankara University, Faculty of Medicine, 06100 Ankara, Turkey.
authors.forename: Gaye
authors.initials: G
authors.lastname: Hafez
authors.affiliation: Department of Biophysics, Ankara University, Faculty of Medicine, 06100 Ankara, Turkey.|Department of Biophysics, Ankara University, Faculty of Medicine, 06100 Ankara, Turkey.
authors.forename: Belma
authors.initials: B
authors.lastname: Turan
mesh_terms: D000818:Animals; D002118:Calcium / Q000378:metabolism; D003921:Diabetes Mellitus, Experimental / Q000378:metabolism* / Q000473:pathology; D058065:Diabetic Cardiomyopathies / Q000378:metabolism* / Q000473:pathology; D015870:Gene Expression; D006352:Heart Ventricles / Q000378:metabolism* / Q000648:ultrastructure; D006439:Hemodynamics / Q000502:physiology; D008297:Male; D024821:Metabolic Syndrome / Q000378:metabolism* / Q000473:pathology; D046529:Microscopy, Electron, Transmission; D032383:Myocytes, Cardiac / Q000378:metabolism / Q000648:ultrastructure; D017208:Rats, Wistar; D011943:Receptors, Adrenergic, beta / Q000235:genetics / Q000378:metabolism*; D013311:Streptozocin / Q000494:pharmacology; D018487:Ventricular Dysfunction, Left / Q000378:metabolism* / Q000473:pathology
chemical_list: D011943:Receptors, Adrenergic, beta; D013311:Streptozocin; D002118:Calcium
keywords: cardiac dysfunction; diabète de type 1; dysfonction cardiaque; high-sucrose diet; homéostasie du calcium intracellulaire; intracellular calcium homeostasis; régime à teneur élevée en glucose; stimulation sympathique; sympathetic stimulation; type 1 diabetes