The effects of 4 weeks of streptozotocin-induced diabetes in the rat on sciatic nerve homogenate protein kinase activities were studied. There was a 47 +/- 7% inhibition of Ca+2-dependent protein kinase activity in nerves from the diabetic rats compared to that in their paired normal controls. This Ca+2-dependent activity did not require the addition of phospholipid and was only minimally affected by Sephadex G-50 gel filtration, suggesting that endogenous phospholipid activation was not responsible for this activity. The addition of phospholipid in the presence of Ca+2 revealed an additional activity in these homogenates which probably represents the Ca+2-phospholipid-dependent protein kinase (protein kinase-C). The diabetic state did not appear to alter that activity. The Ca+2-dependent protein kinase was sensitive to agents known to inhibit calmodulin-dependent protein kinase or protein kinase-C. The IC50 values of the inhibitors for the Ca+2-dependent protein kinase, however, differed from those reported for the other two kinases.
No takes yet. Share an insight, caveat, or question.
Gabbay et al. (1990) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: