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Assessment of alternative interventions seems relevant. Based on these natural bile acids (such as chenodeoxycholic acid and ursodeoxycholic acid), synthetic or semi-synthetic substances, referred to as bile acid derivatives, have shown promising experimental results in preclinical studies and are currently under further clinical investigation. Nuclear receptors (the farnesoid X receptor, pregnane X receptor, peroxisome proliferator-activated receptor α, and vitamin D receptor) play an important role in bile acid homeostasis and are potential new interventions for people with primary biliary cholangitis.
The resulting primary bile acid chenodeoxycholic acid (CDCA) can be further hydroxylated to cholic acid (CA) by CYP8B1. Bile acids are exported across the canalicular membrane of hepatocytes into the bile duct lumen via distinct bile acid transporters, of which BSEP (ABCB11) transports the bulk of bile acids, accompanied by MRP2, the latter one transporting conjugated bilirubin and other xenobiotics. In addition, formation of primary bile requires active transport of phospholipids (via MDR3), cholesterol (via ABCG5/8), glutathione (also via MRP2), bicarbonate (via CFTR), and passive dilution by water. Along the bile ducts, bile is further modified by bicarbonate-enriching mechanisms and further bile acid uptake mechanisms within the liver. UDCA soluble in ethanol, insoluble in chloroform; soluble in glacial acetic acid, dissolved in the sodium hydroxide solution. Medicine for increasing bile acid secretion, and bile composition changes, reducing fat and cholesterol in bile cholesterol, cholesterol gallstones in favor of gradually dissolved.
Unlike chenodeoxycholic acid (CDCA), ursodeoxycholic acid (UDCA) is the only approved drug for treating chronic cholestatic disorders. Currently, the only approved drug for treating chronic cholestatic disorders is the hydrophilic bile acid ursodeoxycholic acid (UDCA). UDCA’s anti-cholestatic properties are mainly attributed to its choleretic effects by stimulating hepatocellular secretion of bile acids and organic anions post-translationally and by inducing/stabilizing a bicarbonate-rich protection “umbrella” along the biliary tree. Anti-apoptotic and anti-inflammatory actions may additionally support UDCA’s beneficial anticholestatic action. Its clinical efficacy is limited because only approximately two-thirds of patients with PBC respond to UDCA therapy and in PSC patients UDCA has no effect on transplant-free survival. NorUDCA is a side chain shortened UDCA derivative, which induces bicarbonate-rich hypercholeresis as a result of cholehepatic shunting of conjugation-resistant NorUDCA and shows additional anti-inflammatory and anti-fibrotic qualities.

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