Monocarboxylic Acid Transporters

Morris, Marilyn E.; Kwatra, Nisha V.

doi:10.1002/9781119739883.ch7

Cited by 1 publication

(1 citation statement)

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“…In the kidney, acetate is actively metabolized to bicarbonate, as shown by the usage of sodium acetate in dialysis, which leads to urine alkalinization instead of acidosis through the excretion of bicarbonate from acetate metabolism into urine due to compromised bicarbonate reabsorption function in the patients of renal diseases [ 42 , 44 ]. In addition, monocarboxylic acid transporters capable of acetate uptake are highly abundant in the renal proximal tubule, which may further prevent unnecessary leakage of acetate into urine [ 45 , 46 ]. However, when this mechanism of metabolism and reabsorption was either overwhelmed by acetate dosing or compromised by renal injury, the elevations of urinary acetate were also observed [ 47 , 48 ], leading to the usage of urinary acetate in the diagnosis of urinary tract infection [ 49 ] and ischemia-reperfusion injury after kidney transplantation [ 48 ].…”

Section: Discussionmentioning

confidence: 99%

Characterization of Urinary N-Acetyltaurine as a Biomarker of Hyperacetatemia in Mice

Mao,

Shi,

et al. 2024

Metabolites

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Acetate is an important metabolite in metabolic fluxes. Its presence in biological entities originates from both exogenous inputs and endogenous metabolism. Because the change in blood acetate level has been associated with both beneficial and adverse health outcomes, blood acetate analysis has been used to monitor the systemic status of acetate turnover. The present study examined the use of urinary N-acetyltaurine (NAT) as a marker to reflect the hyperacetatemic status of mice from exogenous inputs and endogenous metabolism, including triacetin dosing, ethanol dosing, and streptozotocin-induced diabetes. The results showed that triacetin dosing increased serum acetate and urinary NAT but not other N-acetylated amino acids in urine. The co-occurrences of increased serum acetate and elevated urinary NAT were also observed in both ethanol dosing and streptozotocin-induced diabetes. Furthermore, the renal cortex was determined as an active site for NAT synthesis. Overall, urinary NAT behaved as an effective marker of hyperacetatemia in three experimental mouse models, warranting further investigation into its application in humans.

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