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Well-preserved ventricular myocyte shortening in Goto–Kakizaki type 2 diabetic rats

EM Gaber, P Jayaprakash, MA Qureshi, M Oz, Frank Christopher Howarth
Published in : HAMDAN MEDICAL JOURNAL ; Vol 7, No 2 (2014)
DOI : 10.7707/hmj.v7i2.311

Abstract


The global prevalence of type 2 diabetes mellitus (T2DM) is rising at a spectacular rate and the prevalence of T2DM in the United Arab Emirates is among the highest in the world. Risk factors for diabetes mellitus include obesity, sedentary lifestyle, unhealthy eating habits, family history of diabetes mellitus, genetics, increasing age, high blood pressure and high cholesterol. A variety of diastolic and systolic dysfunctions have been reported in the hearts of type 2 diabetic patients and the severity of abnormalities is partly dependent on the patients age and the duration of diabetes mellitus. The GotoKakizaki (GK) rat is a genetic model of T2DM and its general characteristics include fasting hyperglycaemia, impaired insulin secretion and insulin resistance. In the GK rat heart, there are a variety of dysfunctions including decreased heart rate, decreased ejection fraction (mainly due to loss of left ventricular longitudinal contraction) and prolonged shortening and/or relaxation in ventricular myocytes. Widespread consumption of sugar-sweetened beverages has been linked to higher incidence of obesity and T2DM. Ventricular myocyte shortening and Ca2+ transport in GK type 2 diabetic rats that were fed a sucrose-enriched diet have been investigated. GK and control rats received either water or water enriched with increasing concentrations of sucrose (100400mmol/l) for a period of 6 months. Ventricular myocyte shortening and intracellular Ca2+ were measured by video edge detection and fluorescence photometry, respectively. Resting cell length, time to peak (TPK) shortening, time to half-relaxation of shortening and amplitude of shortening were not significantly altered in ventricular myocytes from GK/sucrose compared with GK rats and control/sucrose compared with control rats. TPK Ca2+ transient was prolonged in myocytes from GK/sucrose compared with GK and control/sucrose rats and amplitude of the Ca2+ transient was increased in myocytes from GK/sucrose compared with control rats. Myofilament sensitivity to Ca2+ was unaltered in myocytes from GK/sucrose and control/sucrose compared with GK and control rats. In conclusion, ventricular myocyte shortening was well preserved despite some alterations in Ca2+ transport in GK rats receiving a sucrose-enriched diet.


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