Original Articles

Endocrine

, Volume 29, Issue 1, pp 135-141

First online:

Effects of gender difference on cardiac myocyte dysfunction in streptozotocin-induced diabetic rats

  • Yanfeng DingAffiliated withDepartment of Anatomy, Physiology and Pharmacology, College of Veterinary Medicine, Auburn University
  • , Ruijiao ZouAffiliated withDepartment of Anatomy, Physiology and Pharmacology, College of Veterinary Medicine, Auburn University
  • , Robert L. JuddAffiliated withDepartment of Anatomy, Physiology and Pharmacology, College of Veterinary Medicine, Auburn University
  • , Juming ZhongAffiliated withDepartment of Anatomy, Physiology and Pharmacology, College of Veterinary Medicine, Auburn University Email author 

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Abstract

The main characteristics of type 1 diabetic cardiomyopathy include depressed contractility and altered electrophysiological properties in ventricular myocytes. The goal of the present study was to determine the potential influence of gender in the diabetes-induced pathogenesis of ventricular myocyte function. Diabetes in both male and female rats was induced by a single intravenous injection of streptozotocin (STZ). Diabetic rats exhibited hyperglycemia and reduced body weight gain in both male and female groups. Neither contractile profiles nor activity of three types of K+ channels of ventricular myocytes was significantly different between nondiabetic male and female rats. Ventricular myocytes isolated from diabetic rats exhibited significant depresion in cell contraction and relaxation, which was associated with depression of intracellular Ca2+ ([Ca2+]i) transient. The degrees of contractile depression were comparable in ventricular myocytes obtained from both male and female diabetic rats. Similarly, diabetes depressed three types of outward K+ currents (Ito, Ik, and iss) to the same extent in both gender myocytes. These data demonstrate that in this animal model of diabetes, gender difference in cardiac myocyte functions was eliminated.

Key Words

Diabetes gender cardiac myocyte cell shortening Ca2+ transient potassium channels