Effects of starvation on the urinary contents of primary thromboxane and prostacyclin metabolites and a possible selenium-dependent role of prostacyclin in the renal handling of ketone bodies

Abstract

The aim of this study was to investigate whether urinary prostanoids, as an index of renal synthesis of these compounds, are affected in selenium (Se) deficiency and, if so, whether such changes could add to our understanding of the high excretion of ketone bodies in Se-deficient rats (p < 0.005 vs Se-adequate rats). Male rats were fed a Se-deficient diet with less than 0.01 mg Se/kg or the same diet supplemented with 0.2 mg Se/kg. The urinary contents of prostaglandin E 2 (PGE 2), PGF 2α and 6-keto PGF 1α were not significantly affected by the Se status. However, there was a positive correlation between the urinary contents of ketone bodies and 6-keto PGF 1α in Se deficiency (with p < 0.02 for acetaoacetate and p < 0.05 for 3-hydroxybutyrate). In contrast, only negative (nonsignificant) relationships were observed between these same parameters in Se-adequate rats. No correlations between urinary contents of ketone bodies and PGE 2, PGF 2α or thromboxane B 2 (TXB 2) were obtained. Compared to fed rats, starvation caused a 4-fold increase in the urinary TXB 2 content in Se-adequate, as well as in Se-deficient rats (p < 0.001). Starvation had an opposite effect on the content of 6-keto PGF 1α, which decreased (to 64% that of fed animals p < 0.001) in Se-adequate rats and, nonsignificantly (to 93% that of fed animals) in the Se-deficient group. It is concluded that starvation profoundly affects the urinary contents (and thus, probably renal synthesis) of TX and prostacycline (PGI 2). The lack of significant decrease in the urinary level of 6-keto PGF 1α during starvation and the positive correlation between the urinary contents of ketone bodies and 6-keto PGF 1α in the Se-deficient rat indicate that renal PGI 2 plays a role in the increased ketonuria of these rats.