Biophysical investigation on left ventricular myocytes in rats with experimentally induced diabetes

• Published in: Physiological research Vol. 59 Suppl 1; pp. S9 - S17
• Main Authors: Waczulíková, I, Cagalinec, M, Uličná, O, Slezák, P, Ziegelhöffer, A
• Format: Journal Article
• Language: English
• Published: Czech Republic Institute of Physiology 2010
• Subjects: Animals; Anisotropy; Aqueous solutions; Calcium Signaling; Cell Size; Cells; Diabetes; Diabetes Mellitus, Experimental - complications; Diabetes Mellitus, Experimental - metabolism; Diabetes Mellitus, Experimental - physiopathology; Energy Metabolism; Free radicals; Heart Ventricles - metabolism; Heart Ventricles - physiopathology; Membrane Fluidity; Membrane Potentials; Methods; Mitochondria; Mitochondria, Heart - metabolism; Mitochondrial Membranes - metabolism; Models, Biological; Myocytes, Cardiac - metabolism; Proteins; Rats; Sarcolemma - metabolism
• ISSN: 0862-8408; 1802-9973
• DOI: 10.33549/physiolres.932011

Diabetes is a recognized risk factor of heart disease. The abnormalities related to a decreased heart performance probably arise at cellular and molecular levels already in the asymptomatic phase of diabetes. However, the early alterations initiating a sequence of events that culminates in the clinical signs have not been fully elucidated yet. This review deals with some biophysical methods applied to investigation of left ventricular myocytes in rats with streptozotocin diabetes, as well as our most important findings concerning diabetes-induced cell changes which cannot be captured by other techniques. The observed decrease in sarcolemmal membrane fluidity is causatively associated with increased glycation and glycoxidation. On the other hand, an increase in the mitochondrial membrane fluidity may be attributed to augmented energy transduction through the membranes. We reported for the first time concurrent measurements of membrane potential and dynamics, and respiratory chain activities in rat heart mitochondria, as well as calcium transients in the myocytes from diabetic hearts together with the assessed quantitative relationships among these variables. We were able to detect some significant alterations that may underlie myocyte dysfunction and subsequent remodeling of the heart. We suppose that not all these changes reflect mechanisms leading to pathology; some may represent adaptive and compensatory responses to diabetes.