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Bile salt-activated lipase (BAL), also known as bile salt-dependent lipase, carboxyl ester lipase (CEL), or, in the milk context, bile salt-stimulated lipase (BSSL), is a broad-specificity pancreatic enzyme crucial for lipid digestion in the small intestine[2][3][5][10]. Unlike other lipases, BAL requires bile salts for optimal hydrolytic activity, especially on substrates with long acyl chains or bulky alcoholic groups[2][3][5]. BAL catalyzes the hydrolysis of dietary cholesteryl esters, phospholipids, lysophospholipids, triglycerides, and fat-soluble vitamin esters, facilitating efficient absorption of fats and related nutrients[5][10]. Structurally, BAL belongs to the alpha/beta hydrolase family, and its activity is regulated by conformational changes induced by the binding of bile salts[1][2][4]. In adults, BAL is produced primarily by the pancreas, whereas in neonates, especially those relying on breast milk, a similar enzyme in milk compensates for lower pancreatic production, emphasizing its importance in early life nutrition[5][7]. Dysfunction or inhibition of BAL impairs intestinal fat absorption and can contribute to malabsorption syndromes[5][10].
Competitive inhibition of lipolytic activity (e.g., by lipase inhibitors such as orlistat, though specificity for BAL is not strong)
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