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Bile salt hydrolase (BSH) from Lactobacillus plantarum TCI378 is a microbial enzyme that plays a pivotal role in the metabolism of bile acids within the mammalian gastrointestinal tract. It specifically targets conjugated bile acids at its active site, catalyzing the cleavage of the amide bond to produce free bile acids and amino acids [1][3]. This enzymatic activity is a primary mechanism by which probiotic strains like TCI378 exert cholesterol-lowering effects; by deconjugating bile salts, the enzyme reduces their solubility and reabsorption, prompting the liver to convert more systemic cholesterol into new bile acids [2][5]. Beyond lipid digestion, the BSH-mediated alteration of the bile acid pool significantly impacts host metabolic signaling. The resulting free bile acids serve as ligands for nuclear receptors such as the farnesoid X receptor (FXR) and G protein-coupled receptors like TGR5, which regulate glucose metabolism, energy expenditure, and inflammation [4][6]. Lactobacillus plantarum TCI378 is specifically utilized in therapeutic and supplemental contexts to manage obesity and metabolic syndrome by modulating these pathways. While beneficial for weight management, the activity must be balanced to avoid the excessive accumulation of secondary bile acids, which can impact intestinal health [1][4]. Sources: [1] PubMed Central, PMC6115913: "Bile Salt Hydrolase: A Microbial Enzyme with Implications in Health and Disease." [2] TCI Co., Ltd. Technical Report: "Lactobacillus plantarum TCI378 and its role in lipid metabolism and weight management." [3] UniProt, P0C1U1: "Choloylglycine hydrolase (BSH) protein information." [4] Nature Communications, 10.1038/s41467-018-06855-z: "Microbial bile salt hydrolases mediate the gut-liver axis." [5] Journal of Dairy Science, 10.3168/jds.2012-5903: "Cholesterol-lowering properties of Lactobacillus plantarum." [6] Frontiers in Microbiology, 10.3389/fmicb.2020.00412: "Structural and functional diversity of bacterial bile salt hydrolases."
The enzyme catalyzes the hydrolysis of the C-24 amide bond in conjugated bile acids (glycine or taurine conjugates), releasing free bile acids and amino acids. This deconjugation reduces the efficiency of bile salts in emulsifying dietary lipids and alters signaling through host bile acid receptors like FXR and TGR5.
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