Slc10a2, also known as the apical sodium-dependent bile acid transporter (ASBT), is a crucial transporter protein in the solute carrier family (SLC). It is mainly expressed in the small intestine and is responsible for the reabsorption of ileal bile acids. This function is key in regulating the enterohepatic circulation of bile acids and cholesterol homeostasis, which is essential for fat digestion and maintaining the balance of bile acids and cholesterol in the body [1,2,3].

In Slc10a2-null mice, fecal bile acid excretion is augmented more than 10-fold. These mice show a 54% increase in aberrant crypt foci, and 70% and 59% increases in colon tumor number and size respectively, along with a 2-fold increase in the number of colon adenocarcinomas. This indicates that endogenous fecal bile acids promoted by Slc10a2 deficiency play a role in colon carcinogenesis [5]. Also, in rats with pelvic radiation-induced diarrhea, the mRNA and protein expression of Asbt (Slc10a2) in the ileum gradually decreased, suggesting that bile acid malabsorption due to Slc10a2 down-regulation is partially responsible for the diarrhea [4].

In conclusion, Slc10a2 is essential for maintaining bile acid and cholesterol homeostasis through its role in the enterohepatic circulation. Studies using gene-knockout mouse models have revealed its significance in diseases such as colon cancer and radiation-induced diarrhea, enhancing our understanding of these disease mechanisms and potentially providing new targets for treatment.