Abstract
Though non-insulin-dependent (type 2) diabetes which accounts for over 90% of all diabetic patients leads to congestive heart failure, contractile property of cardiac muscle in type 2 diabetes has not been well characterized. We studied the contractile property of left ventricular papillary muscle of model mouse of the type 2 diabetes, db/db mouse, and effect of insulin and palmitate on it at 20 °C. There was no difference in the time course of twitch between db/db mouse and the control except its magnitude; the rested-state twitch force (Fmax) in the Krebs solution (10 mM glucose) was 21.2 mg/mm2 (n=6) in the db/bd mouse and 190.3 mg/mm2 (n=6) in the control. Application of either insulin (80 i.u./l) or palmitate (0.4 mM) increased Fmax in both the db/db mouse and the control. Steady-state force decreased with increasing stimulus frequency. Insulin and palmitate increased the steady-state force at a frequency > 1 Hz in the bd/bd mouse and the control except that palmitate decreased it at a frequency > 1 Hz in the db/db mouse. The rate of short-term mechanical restitution (SMR) decreased with increasing magnitude of the preceding twitch. Palmitate delayed the SMR, while insulin had variable effect on it. There was no apparent difference in the characteristics of the SMR between the db/db mouse and the control. We characterized Ca2+ release/content in the cardiac sarcoplasmic reticulum from the SMR with or without insulin and palmitate in the db/db mouse and the control according to the rationale described previously (Tameyasu et al, 2004). [J Physiol Sci. 2006;56 Suppl:S130]
