Published online May 22, 2022. doi: 10.4291/wjgp.v13.i3.73
Peer-review started: August 9, 2021
First decision: October 16, 2021
Revised: October 26, 2021
Accepted: April 21, 2022
Article in press: April 21, 2022
Published online: May 22, 2022
Processing time: 281 Days and 20.1 Hours
The heart and liver are inextricably linked by virtue of blood flow and metabolism of medications. Drugs with biliary elimination, such as digoxin, decrease clearance with cholestasis.
We performed this study to better understand the effect of extrahepatic cholestasis on regulations of membrane transporters involving digoxin and its implication for digoxin clearance.
The efflux transporter, multidrug resistance 1 (MDR1), and influx transporters, organic anion transporting polypeptides (OATP)1A4 and OATP4C1 in kidney, intestine and liver were examined.
Twelve adult Sprague Dawley rats were included in this study; baseline hepatic and renal laboratory values and digoxin pharmacokinetic (PK) studies were established before evenly dividing them into two groups to undergo bile duct ligation (BDL) or a sham procedure. After 7 d repeat digoxin PK studies were completed and tissue samples were taken to determine the expressions of MDR1, OATP1A4 and OATP4C1 by quantitative western blot and real-time polymerase chain reaction.
Digoxin clearance was decreased and liver function, but not renal function, was impaired in BDL rats. BDL resulted in significant up-regulation of MDR1 expression in the liver and kidney and its down-regulation in the small intestine. OATP1A4 was up-regulated in the liver but down-regulated in intestine after BDL. OATP4C1 expression was markedly increased in the kidney following BDL.
The results suggest that cell membrane transporters of digoxin are regulated during cholestasis. These regulations are favorable for increasing digoxin excretion in kidney and decreasing its absorption from intestine in order to compensate the reduced digoxin clearance due to cholestasis.
The current study was designed as an exploratory research for providing clues for future study in this field. Previous studies on the transporters in kidney and intestine were done only by in vitro experiments. To the best of our knowledge, the current report is the first study to investigate the regulation of the digoxin transporters in kidney and intestine in animal model of cholestasis. Our results does demonstrate that the cell membrane transporters were regulated which is in favor of digoxin excretion during cholestasis. To confirm our finding, more detailed PK studies need to be done, for example, tissue distributions of digoxin and digoxin concentrations in urine and in intestine. Knock-out (KO) animal lacking the transporters, especially tissue-specific KO, will be a powerful tool in further study.