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Pharmacology: Ketobest allows the intake of essential amino acids while minimizing the amino-nitrogen intake. Following ingestion, the ketoanalogues are transaminated by taking nitrogen from non-essential amino acids, thereby decreasing the formation of urea by re-using the amino group. The levels of accumulating uremic toxins are decreased. Keto- and/or hydroxy-acids do not elicit hyperfiltration of residual nephrons. Ketoacid-containing supplements have a positive influence on the renal hyperphosphatemia and secondary hyperparathyroidism and can improve renal osteodystrophy. The use of Ketobest in association with a very low protein diet allows a reduced intake of nitrogen while avoiding the deleterious consequences of inadequate dietary protein intake and malnourishment.
Pharmacokinetics: In normal individuals, there is an increase in the plasma level of ketoanalogues, 10 min after oral ingestion. These levels reach values that are approximately 5 times higher than the initial level. Peak levels are reached within 20-60 min, and normal levels are reached again after 90 min. Gastrointestinal absorption is thus very rapid. In the plasma, a simultaneous increase in levels of the ketoanalogue and the corresponding amino acid show that transamination of the ketoanalogues is very rapid. Due to the natural pathways of disposal of α-ketonic acids in the organism, it is probable that exogenous intakes are very rapidly integrated into metabolic cycles. Ketoacids follow the same catabolic pathways as the classical amino acids.
Toxicology: Toxicological studies indicate that Ketobest has a low toxicity. Chronic toxicity study showed that minimum toxic dose (MIT) was 1200 mg/day (dog) and 2700 mg/day (rat), respectively. The minimum toxic dose of human being (70 kg) after dose conversion was 84 g/day (according to dog) and 189 g/day (according to rat), respectively.
Ketobest was found to show no fetal toxicity.
