Abstract
Phosphoinositide (PI) synthesis and hydrolysis were investigated in pancreatic islet homogenates from neonatal streptozotocin diabetic (n-STZ) and control rats. In the diabetics, ATP, in absence of Ca2+, failed to increase the amount of phosphatidylinositol 4-phosphate (PtdInsP) and phosphatidyl inositol 4,5-bisphosphate (PtdInsP2) at variance with the pattern in controls. Also, the Ca2+-stimulated generation of inositol phosphates (InsP) was dramaticaly decreased, whether in the absence or presence of ATP. Moreover, phosphatidylinositol (PtdIns) kinase activity was reduced while PtdInsP kinase activity was not impaired. These data suggest that the suppressed formation of PtdInsP and subsequent PtdInsP2synthesis, concomitantly with a decreased Ca2+-stimulated phospholipase C activity, may participate to the alteration of the PI pathway, the limitation of the InsP production, and finally the impairment of the insulin release in the n-STZ model of non-insulin-dependent diabetes.
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