In view of the depressed sarcoplasmic reticulum (SR) Ca
2؉-pump and Ca 2؉ -release activities in the diabetic heart and the critical role of phosphorylation in regulating the SR function, we examined the status of Ca -pump ATPase, and phospholamban. On the other hand, the CaMK-and PKA-mediated phosphorylations of these Ca 2؉ -cycling proteins, the endogenous SR CaMK and PKA activities, and the endogenous SR and cytosolic phosphatase activities were increased in the diabetic heart. Treatment of 3-week diabetic animals with insulin partially or fully prevented the diabetesinduced changes in cardiac performance, SR Ca 2؉ -uptake and -release activites, and SR protein content, whereas the diabetes-induced changes in SR CaMK-and PKA-mediated phosphorylations and activities, as well as phosphatase activities, were not significantly affected. These results suggest that the reduced content of the Ca 2؉ -cycling proteins, unlike alterations in PKA and phosphatase activities, appear to be the major defect underlying SR dysfunction in the diabetic heart.
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