Selenium-Deficiency and the Metabolism of Ketone Bodies

Abstract

It was previously reported that selenium (Se) deficiency caused a significant increase of urinary acetoacetate excretion in fed rats, and 24 or 48 h of starvation enhanced this effect (Olsson 1985). Further, control rats fed the Se-deficient torula yeast-based diet but supplemented with 0.2 ppm selenium in the drinking water were quite comparable to rats fed a standard diet, thus indicating that the torula diet as such did not affect the metabolism or excretion of ketone bodies. No Se-dependent effect was found for the liver or blood content of glucose or the two ketone bodies, i.e., acetoacetate (AcAc) and 3-hydroxybutyrate (3-OHBA), while indications for a higher renal content of ketone bodies (AcAc plus 3-OHBA) was noted in the Se-deficient rat. Two days of Se supplementation to Se-deficient rats reduced the amount of urinary AcAc and 3-OHBA to 50% of the deficiency value, indicating an enzymatic role for selenium regarding ketone bodies (Olsson 1985). This role might be unrelated to the activity of GSH-Px as only a very small increase of this enzyme activity was noted after 2 days of Se supplementation (unpublished results).

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