Changes in the Functioning of Ca2+-ATPases of Rat Exocrine Cells in Experimental Diabetes Mellitus

It is obvious that disruption of functions of the nervous system in diabetes mellitus is to a great extent related to the changes of synthesis or exocytosis of neurotransmitters. Since the mechanisms underlying exocytosis are similar in cells of different types, it may be assumed that studying these mechanisms in secretory cells will allow experimenters to obtain information on ways to control this process in neurons. Based on the supposition that changes in the activity of Ca2+-controlling systems in exocrine cells play an important role in functional disorders in the salivary glands in diabetes mellitus, we demonstrated, using the fura-2/AM dye, that the intracellular calcium concentration ([Ca2+]i) in secretory cells of the above glands in rats with streptozotocin-induced diabetes mellitus (being in the resting state) is significantly increased (on average, by 65%). In our study, we showed that Ca2+-ATPases play an important role in the control of calcium homeostasis in secretory cells of salivary glands in diabetes mellitus. In particular, we demonstrated that the kinetic parameters of microsomal Ca2+-ATPases decreased: V0, by 50 ± 7, and Pmax, by 52 ± 6%, on average. In diabetes mellitus, Vmax of Ca2+-ATPases also dropped significantly, by 47 ± 8 and 79 ± 9%, on average, for PMCA and SERCA, respectively. The decrease in KATP was 71 ± 11% for SERCA and that in KCa was 92 ± 3% for PMCA. We concluded that the activity of Ca2+-ATPases of secretory cells in diabetes mellitus is suppressed because of a decrease in the turnover and/or in the specific number of active molecules of the enzyme.