Summary
Diabetes was induced in rats by administration of streptozotocin. Diabetes occurred
within 24 h after treatment. Two forms of diabetes were studied, an acute form (4
days) and a chronic form (2 months). In a separate experiment the effect of insulin
and an aldose reductase inhibitor on acute diabetes was studied. Phosphoinositide
labelling was done in biopsies of heart with [3H] myo-inositol. It was shown that the incorporation of myo-inositol amounted to about
65% in acute diabetes and 80% in chronic diabetes compared to age-matched controls.
The incorporation both in atria and ventricles was affected in a similar way.
Muscarinic receptor-mediated phosphatidylinositol breakdown and release of myo-Ins-1
P (myo-inositol 1-phosphate) was unaffected in diabetic hearts in the chronic model.
In hearts of diabetic ketotic animals uncoupling of the muscarinic receptor from the
phosphoinositide metabolism was apparent. Calcium net influx was significantly reduced
in both acute and chronic diabetes compared to age-matched controls.
Insulin supplementation to acute diabetic animals significantly improved phosphoinositide
labelling with [3H] myo-inositol. No improvement was seen in calcium transport. An aldose reductase
inhibitor also facilitated phosphoinositide labelling without improving calcium transport.
It is suggested that phosphoinositide metabolism and calcium entry through the slow
inward current are independent of one another and the former is sensitive to insulin.
It is suggested that insulin by regulating the pool of phosphoinositides and release
of endogenous calcium may modulate cardiac function.
Key-Words
Experimental Diabetes
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Myocardium
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Phosphatidylinositol Turnover
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Calcium Influx
