Slc30a10, a manganese (Mn) efflux transporter, is crucial for maintaining Mn homeostasis. It exports Mn from hepatocytes into bile and from enterocytes into the lumen of the gastrointestinal tract, thus playing a key role in physiological Mn excretion [1,3,4]. Mn is an essential metal, but excess can lead to toxicity, and Slc30a10 is vital in preventing such toxicity. Genetic models, like knockout (KO) mice, have been instrumental in studying its function.

Whole-body Slc30a10-deficient mice develop severe Mn excess and impaired systemic and biliary Mn excretion, highlighting the gene's essential role in Mn excretion by hepatocytes and enterocytes [1]. Mice with liver-specific or small-intestine-specific Slc30a10 deficiency develop less severe Mn excess, suggesting additional sites of Slc30a10 expression contribute to Mn homeostasis [1]. Pan-neuronal/glial Slc30a10 knockout mice show elevated Mn levels in specific brain regions during early postnatal development and neuromotor deficits in adolescence or adulthood, indicating its role in regulating brain Mn levels and protecting against neuromotor and dopaminergic neurotransmission deficits [2].

In conclusion, Slc30a10 is essential for Mn excretion in hepatocytes and enterocytes and for regulating Mn levels in the brain, especially during early postnatal development. The study of Slc30a10 using KO mouse models has enhanced our understanding of Mn-related diseases such as hereditary Mn-induced neuromotor disease, highlighting its potential as a target for treating Mn toxicity [1,2].