Bile acid transporters

The regulation of blood cholesterol level via bile acid binding and excretion is not a single molecular target but rather a physiological process involving multiple **bile acid transporters**. These include canalicular membrane proteins such as the **bile salt export pump** (BSEP/ABCB11), **multidrug resistance-associated protein 2** (MRP2/ABCC2), **ATP-binding cassette subfamily G members 5 and 8** (ABCG5/G8), as well as uptake systems like the **sodium/taurocholate cotransporting polypeptide** (**NTCP/SLC10A1**) in hepatocytes. These transporters mediate the movement of bile acids from hepatocytes into the biliary tract, facilitating their eventual excretion in feces—a major route for eliminating excess cholesterol from the body since most hepatic cholesterol is converted into bile acids before being secreted. Pharmacologically, drugs such as **bile acid sequestrants** act by binding intestinal bile acids, preventing their reabsorption, which forces increased hepatic conversion of plasma cholesterol into new bile acids—thereby lowering circulating LDL-cholesterol. The process is tightly regulated at both transcriptional and post-translational levels by nuclear receptors including FXR, LXR, PPARs, which sense intracellular sterol/bile acid concentrations and adjust gene expression accordingly[1][3][7]. Because "blood cholesterol level regulation via bile acid binding/excretion" describes a pathway rather than a discrete molecule or receptor, it does not fit standard definitions for canonical molecular targets; instead it encompasses several key transporter proteins that are valid therapeutic targets individually. > “In hepatocytes, bile excretion occurs mainly at the canalicular membrane predominantly via ABC transporters... Cooperation among transporters is critical to maintaining bile homeostasis” [2]. > “Bile acids are amphipathic molecules synthesized from cholesterol in the liver... Recent studies suggest that agonists of peroxisome proliferator–activated receptors regulate lipoprotein metabolism... activation alters both synthesis and secretion pathways” [1]. Thus, *the entry "Blood cholesterol level regulation via bile acid binding/excretion"* should be mapped more specifically to individual *bile acid transporter* proteins or nuclear receptors involved in this pathway for structured data purposes.

Other names

Bile salt transportersABC transporters (specific members)Sodium/taurocholate cotransporting polypeptide (NTCP)Bile salt export pump (BSEP)Multidrug resistance-associated protein 2 (MRP2)ATP-binding cassette subfamily G member 5/8 (ABCG5/G8)

Inhibition or modulation of bile acid reabsorption/excretion to lower blood cholesterol by increasing conversion of cholesterol into bile acids and promoting their fecal elimination[1][3]