Abstract
Summary
We compared the rate of accumulation, oxidation and turnover of citrate in normal and alloxan-diabetic rats, in order to explain the elevations of citric acid reported in diabetic states. Citrate utilization was blocked by intraperitoneal injections of sodium trans-aconitate (a competitive inhibitor of the enzyme aconitase); the rate of accumulation of citrate was found significantly lower in the diabetic rats. This suggested a decreased synthesis of citrate in vivo, and correlated with earlier findings of decreased in vitro citrate synthesis by diabetic rat tissues. Normal and diabetic rats were injected intraperitoneally with 6-14C citrate, and expired 14CO2 was collected at definite time periods to determine the rate of oxidation of injected citrate. In other groups of rats, the plasma citrate specific radioactivity and turnover were calculated following intravenous injection of 6-14C citrate. No significant difference was found in the oxidation or turnover rate of plasma citrate between normal and alloxan-diabetic rats. On the basis of these studies it seems that the hypercitremia in diabetes is not solely of endogenous origin.
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