The association between type 2 diabetes and obesity is very strong, and cardiovascular complications are the major cause of morbidity and mortality in diabetic patients. The aim of this study was to investigate early changes in the pattern of genes encoding cardiac muscle regulatory proteins and associated changes in ventricular myocyte contraction and Ca 2+ transport in young (9-to 13-week-old) type 2 Zucker diabetic fatty (ZDF) rats. The amplitude of myocyte shortening was unaltered; however, time-to-peak shortening and time to half-relaxation of shortening were prolonged in ZDF myocytes (163 ± 5 and 127 ± 7 ms, respectively) compared with age-matched control rats (136 ± 5 and 103 ± 4 ms, respectively). The amplitude of the Ca 2+ transient was unaltered; however, time-to-peak Ca 2+ transient was prolonged in ZDF myocytes (66.9 ± 2.6 ms) compared with control myocytes (57.6 ± 2.3 ms). The L-type Ca 2+ current was reduced, and inactivation was prolonged over a range of test potentials in ZDF myocytes. At 0 mV, the density of L-type Ca 2+ current was 1.19 ± 0.28 pA pF −1 in ZDF myocytes compared with 2.42 ± 0.40 pA pF −1 in control myocytes. Sarcoplasmic reticulum Ca 2+ content, release and uptake and myofilament sensitivity to Ca 2+ were unaltered in ZDF myocytes compared with control myocytes. Expression of genes encoding various L-type Ca 2+ channel proteins (Cacna1c, Cacna1g , Cacna1h and Cacna2d1) and cardiac muscle proteins (Myh7) were upregulated, and genes encoding intracellular Ca 2+ transport regulatory proteins (Atp2a2 and Calm1) and some cardiac muscle proteins (Myh6, Myl2, Actc1, Tnni3, Tnn2, and Tnnc1) were downregulated in ZDF heart compared with control heart. A change in the expression of genes encoding myosin heavy chain and L-type Ca 2+ channel proteins might partly underlie alterations in the time course of contraction and Ca 2+ transients in ventricular myocytes from ZDF rats. There has been a spectacular rise in the global prevalence of type 2 diabetes mellitus, and the number of cases of diabetes mellitus has reached pandemic proportions and will continue to escalate. The association between type 2 diabetes and obesity is very strong, and cardiovascular disease is the major cause of morbidity and mortality in diabetic patients (Julien, 1997;Zimmet & Alberti, 2006). Clinical and preclinical studies using Doppler imaging, echocardiography, radionuclide angiography and other techniques have demonstrated a variety of diastolic and systolic dysfunctions in type 2 diabetic patients. These haemodynamic abnormalities include reduced left ventricular ejection fraction, impaired myocardial velocity at early diastole, abnormal relaxation during the early filling phase, prolonged isovolumetric relaxation, lower peak systolic and early diastolic velocity, impaired diastolic relaxation and filling and reduced peak filling rate, with the severity of the abnormalities depending on the patients'