15 exons, spanning 54023 bp.

3286 bases, open reading frame: 1833 bp. No alternative splicing variants have been reported. SLC5A8 transcription is regulated by hypermethylation of CpG-rich islands in the promoter region.

No pseudogenes identified.

610 amino acids; 66,560 Da; 13 transmembrane domains, extracellular N-terminal, cytosolic C-terminal.

Gastrointestinal tract (stomach, colon, ileum), kidney, thyroid, brain, retina, breast, prostate, salivary gland ducts.

Cell membrane; apical membrane in thyrocytes and colonocytes.

Sodium coupled transport of short-chain monocarboxylates, including lactate, butyrate, pyruvate, acetate, proprionate, ketone bodies and nicotinate. The sodium/substrate stoichiometry depends on the transported substrate. SLC5A8 is considered a tumor suppressor, and its expression is downregulated in several kinds of tumor. Its tumor suppressor activity may be due to its ability to transport and accumulate histone deacetylase inhibitors such as butyrate and pyruvate.
- Gastrointestinal tract: colonocyte absorption and accumulation of short chain fatty acids produced by bacteria in the intestinal lumen. In particular, butyrate and pyruvate are inhibitors of histone deacetylases and are known to promote differentiation in normal colon epithelial cells but selectively induce apoptosis in tumor cells.
- Kidney: lactate transport; reabsorption of lactate from urine to blood.
- Thyroid: unknown function. When first identified, SLC5A8 was shown to localize on the apical membrane of thyrocytes and to transport iodide by a passive mechanism. Lately, this evidence has been rejected by different groups that showed that iodide is not a SLC5A8 substrate.
- Brain: transport of lactate and ketone bodies; role in energy maintenance in neurons.

Belongs to the SLC superfamily of solute carriers; the SLC5 family has 12 members to date (SLC5A1-SLC5A12) and includes Na⁺-coupled cotransporters that rely on the Na⁺ electrochemical gradient to drive solute transport into cells. 53% identity with SLC5A12, a sodium/monocarboxylate transporter; 46% identity with SLC5A5, the Sodium-Iodide Symporter.

No germinal mutations implicated in human disease to date.
SLC5A8 knockout mouse (deletion of exons 4 and 5) is viable and fertile, with no evident malformation; affected by lactaturia and loss of sodium-dependent lactate uptake in the colon.

No somatic mutations implicated in human disease to date.