Solute carrier family 13 member 5 (sodium-dependent citrate transporter) (SLC13A5 (also NaCT))

Solute carrier family 13 member 5 (SLC13A5), also known as the sodium-dependent citrate transporter (NaCT), is a plasma membrane transporter highly expressed in the liver, brain, and other tissues. It facilitates the import of extracellular citrate into cells using a sodium gradient, playing a critical role in cellular energy metabolism and metabolic sensing. Genetic mutations in SLC13A5 cause a rare autosomal recessive neurological disorder, early infantile epileptic encephalopathy (EIEE25), manifesting as epilepsy, developmental delay, abnormal movement, and dental enamel defects. SLC13A5 is also implicated in metabolic diseases such as non-alcoholic fatty liver disease, obesity, and type 2 diabetes. Therapeutic interest centers on developing liver-selective inhibitors to harness metabolic benefits while avoiding neurological toxicity. SLC13A5’s function is tightly linked to the regulation of key metabolic pathways, making it a promising but challenging therapeutic target.

Other names

Na+/citrate cotransporterNaCTmIndy

Inhibition or modulation of citrate uptake into cells by blocking sodium-dependent transport at SLC13A5. Altered metabolic flux, fatty acid synthesis, and energy homeostasis. Potential selective inhibition in the liver to avoid neurological side effects.