Among the ketone bodies, acetoacetate, a salt of acetoacetic acid, should also be identified. Acetoacetate is not a stable molecule and, as a result, is easily converted to other ketone bodies, whether acetone or beta-hydroxybutyric acid. In this sense, acetoacetate should be considered the most crucial precursor of ketogenesis in the body, which in turn is formed from acetyl-KoA.
Acetoacetate itself, however, does not necessarily have to be converted into the other two ketone body variants, but it can be used as a strategic source of energy, especially during carbohydrate deficiency or starvation. As in the previous case, the addition of the ketone body, for some reason, led to a suppression of ammonia genesis in the kidneys, which was detected as a decrease in the concentration of ammonia in the urine. A possible reason for this effect is the comparatively simple reduction of acetoacetate to beta-hydroxybutyric acid salts in liver cells by the following formula:
Consequently, acetoacetate converting to beta-hydroxybutyrate also could not intensify ammonia genesis by possibly inhibiting blood glutamate conversion. On the other hand, beta-hydroxybutyrate also converts unimpeded to acetoacetate by the formula:
A related explanation may be changed in the mitochondrial reduction potential, which disrupts the NADH/NAD+ balance and negatively affects the ammonia genesis capabilities. Thus, as in the case of beta-hydroxybutyrate, acetoacetate as a ketone body unexpectedly suppressed ammonia production through mechanisms not yet fully understood.