Question

Question: Why do you think that infusion of pure sodium-free β-hydroxybutyric acid prepared resulted in a 50% decrease in renal ammoniogenesis in spite of the fact that both urinary pH and plasma bicarbonate fell significantlyWhy do you think that infusion of pure sodium-free β-hydroxybutyric acid prepared resulted in a 50% decrease in renal ammoniogenesis in spite of the fact that both urinary pH and plasma bicarbonate fell significantly

Article: (based off of this little exerpt)  During all experiments where ketones were infused, the renal extraction of glutamine became negligible as the renal glutamine arteriovenous difference was abolished. Renal hemodynamics did not vary significantly. Infusion of β-hydroxybutyrate into the left renal artery resulted in a rapid decrease in ammoniogenesis by the perfused kidney.

Answer 1

Beta hydroxybutyric acid:

In humans, the beta-hydroxybutyrate can be formed in the liver by the breakdown of the fatty acid.

During the fasting state, the ketogenic amino acids and β-hydroxy β-methyl butyrate undergoes a sequence of reactions and form the acetoacetate. It is the first ketone body. Then acetoacetate forms the β-hydroxybutyrate with the help of an enzyme (β-hydroxybutyrate dehydrogenase). Probably, these ketone bodies can considerably depress renal ammoniogenesis.

However, Beta hydroxybutyric acid does not affect the formation of ammonia via the extrarenal mechanism. Beta hydroxybutyric molecules could lead to a reduction in NAD/NADH ratio. It occurs because of the raised the conversion of alpha-ketoglutarate to the glutamate. It will then cause a decrease in ammonia production.

The reason is:

Research also shows that the ketone bodies possess an inhibitory influence on the renal tubular cell. Since their effect is not influenced by the systemic acid-base or urinary variations. Ketone body prohibits the activity of glutamine I or II. It thus decreases the renal extraction of glutamine and affects renal ammoniogenesis.