![](https://d3ilqtpdwi981i.cloudfront.net/rdwiOIQYmSUjCicMs8AaY3sai5c=/425x550/smart/https://bepress-attached-resources.s3.amazonaws.com/uploads/78/3e/dd/783edd7a-ecc9-47e4-943b-c53134405e0c/thumbnail_c913a24a-fbb0-4f7e-bbf4-32c413caee67.jpg)
© 2018 L. Al Kury et al. The association between diabetes mellitus (DM) and high mortality linked to cardiovascular disease (CVD) is a major concern worldwide. Clinical and preclinical studies have demonstrated a variety of diastolic and systolic dysfunctions in patients with type 2 diabetes mellitus (T2DM) with the severity of abnormalities depending on the patients' age and duration of diabetes. The cellular basis of hemodynamic dysfunction in a type 2 diabetic heart is still not well understood. The aim of this review is to evaluate our current understanding of contractile dysfunction and disturbances of Ca2+ transport in the Goto-Kakizaki (GK) diabetic rat heart. The GK rat is a widely used nonobese, nonhypertensive genetic model of T2DM which is characterized by insulin resistance, elevated blood glucose, alterations in blood lipid profile, and cardiac dysfunction.
- animal,
- calcium signaling,
- cardiac muscle,
- cardiac muscle cell,
- disease model,
- glucose blood level,
- heart ventricle,
- metabolism,
- non insulin dependent diabetes mellitus,
- physiology,
- rat,
- Animals,
- Blood Glucose,
- Calcium Signaling,
- Diabetes Mellitus,
- Type 2,
- Disease Models,
- Animal,
- Heart Ventricles,
- Myocardium,
- Myocytes,
- Cardiac,
- Rats
Available at: http://works.bepress.com/lina-alkury/42/