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Na(+)-dependent biotin transport into brush-border membrane vesicles from human kidney cortex
1University Children's Hospital, Metabolic Unit, Basel, Switzerland.
Pflugers Archiv : European Journal of Physiology
|February 1, 1993
Summary
Human kidney reabsorbs biotin via a sodium-dependent, saturable, and electroneutral transport system. This secondary active transport mechanism is specific and crucial for biotin homeostasis.
Area of Science:
- Nephrology
- Biochemistry
- Molecular Biology
Background:
- Biotin is an essential vitamin crucial for various metabolic processes.
- Understanding renal biotin reabsorption is vital for maintaining biotin homeostasis and preventing deficiency.
Purpose of the Study:
- To investigate the mechanism of biotin reabsorption in the human kidney.
- To characterize the transport system involved in renal biotin uptake.
Main Methods:
- Isolated brush-border membrane vesicle technique.
- Sodium-gradient and K+/valinomycin voltage-clamp experiments.
- Kinetic analysis of biotin uptake at varying concentrations.
Main Results:
- Biotin uptake is sodium-dependent and saturable, with a stoichiometry of 1:1 for Na(+)-biotin cotransport.
- The transport system exhibits Michaelis-Menten kinetics with specific kinetic parameters.
- Uptake is electroneutral and inhibited by dethiobiotin, bisnorbiotin, thioctic acid, and probenecid, but not by biocytin.
Conclusions:
- Renal biotin reabsorption in humans is a secondary active, carrier-mediated process.
- The transport system is specifically sodium-dependent, saturable, and electroneutral.
- Biocytin is not identified as an inhibitor of renal biotin reabsorption.