The objective of the present study was to investigate the effects of oral
selenate application in comparison to
selenium deficiency and
selenite treatment on the development of the diabetic status (
glucose tolerance,
insulin resistance and activities of glycolytic and gluconeogenic marker
enzymes) in dbdb mice, representing a type II diabetic animal model. Therefore 21 adult male dbdb mice were assigned to 3 experimental groups of 7 animals each and put on a
selenium deficient diet (< 0.03 mg/kg diet) based on torula yeast. Group 0Se was kept on
selenium deficiency for 10 weeks while the mice of the groups SeIV and SeVI were supplemented daily with 15% of their individual LD(50) of
sodium selenite or
sodium selenate in addition to the diet. After 10 weeks a distinct melioration of the diabetic status indicated by a corrected
glucose tolerance and a lowered
insulin resistance was measured in
selenate treated mice (group SeVI) in comparison to their
selenium deficient and
selenite treated companions and to their initial status. Activities of the glycolytic marker
enzymes hexokinase,
phosphofructokinase and
pyruvate kinase were increased 1.7 to 3-fold in liver and/or adipose tissue by
selenate treatment as compared to mice on
selenium deficiency and mice with
selenite administration. In contrast
selenate treatment (SeVI) repressed the activity of liver
pyruvate carboxylase the first
enzyme in gluconeogenesis by about 33% in comparison to the
selenium deficient (0Se) and
selenite treated mice (SeIV). However the current study revealed an insulinomimetic role for
selenate (
selenium VI) also in type II diabetic animals due to a melioration of
insulin resistance. In contrast
selenium deficiency and especially
selenite (
selenium IV) impaired the diabetic status of dbdb mice, demonstrating the need for investigations on the insulinomimetic action of
selenium due to the metabolism of different
selenium compounds.