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Solute carrier family 23 member 1 (SVCT1) is a sodium-dependent symporter that plays a pivotal role in the systemic homeostasis of vitamin C (L-ascorbic acid) [1, 2]. Primarily expressed in the epithelial cells of the small intestine and the proximal tubules of the kidney, SVCT1 facilitates the absorption of dietary vitamin C and its subsequent renal reabsorption, thereby regulating circulating plasma levels [4, 5]. Unlike its isoform SVCT2, which provides vitamin C to metabolically active tissues, SVCT1 is a high-capacity, low-affinity transporter focused on whole-body maintenance [2, 9]. Recent studies have also identified SVCT1 as a physiological urate importer, suggesting it may contribute to uric acid handling and the pathogenesis of hyperuricemia and gout [6, 7]. Genetic variations in the SLC23A1 gene, such as the rs33972313 polymorphism, are linked to altered plasma vitamin C concentrations and have been associated with increased risks for gastric cancer, cataracts, and cardiovascular diseases [10, 12, 15]. In drug development, SVCT1 is being investigated as a vehicle for targeted drug delivery, where therapeutic agents are conjugated with ascorbate to enhance their oral bioavailability through this specific transport pathway [3, 8].
SVCT1 functions as a secondary active transporter that co-transports two sodium ions and one molecule of L-ascorbic acid (or urate) across the plasma membrane, driven by the sodium electrochemical gradient [2, 6, 9]. It utilizes an elevator-type mechanism where a core domain moves relative to a gate domain to translocate the substrate [16].
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