Enzymatic Synthesis of .ALPHA.-Linked Galactooligosaccharide (.ALPHA.-GOS) and Its Functions
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概要
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Oligosaccharides with α-D-galactosidic linkages, especially the positional isomers of α-galactobiose (α-Gal 2), participate in such biological processes as immunity and pathogen-to-cell adhesion on the basis of molecular mechanisms for ligand-receptor interaction. α-Linked galactooligosaccharide (α-GOS) containing positional isomers of α-Gal 2 produced from galactose by the reverse reaction of α-galactosidase, is a potential food for the prevention of infections by pathogens, neutralization of toxins, and regulation of immune system. α-GOS (7.5 kg) was produced from galactose (18 kg; prepared from lactose hydrolyzate) by the reverse reaction of α-galactosidase from Aspergillus niger APC-9319. α-GOS contained 58% disaccharide, 28% trisaccharide and 14% oligosaccharides larger than trisaccharide. The disaccharide in α-GOS consisted largely of α-1,6-galactobiose (73%). α-GOS was stable at neutral and acidic pHs, and high temperatures. The sweetness of α-GOS was 25% of that of sucrose. The taste of α-GOS was mild and mellow. α-GOS reduced acid taste, bitterness, astringency, and harsh taste without spoiling the original taste in various fruit juices, and emphasized the original flavor of food materials in various cooked foods. α-GOS was not hydrolyzed in an in vitro digestion method. In oral tolerance tests of α-GOS, the blood glucose level did not change at all. α-GOS had a strong selective growth activity for Bifidobacterium sp. and Clostridium butyricum. An α-GOS intake in rats made the contents of lactate and n-butyrate in the cecum higher, and pH in the cecum lower than for a control intake. The viable count of Candida albicans in cecum and colon of mouse was decreased by an α-GOS intake more than by a raffinose intake. Therapeutic oral treatment with α-GOS had a potent inhibitory effect on adjuvant arthritis in Wister rats and on type II collagen-induced arthritis in DBA/1 J mice. Dietary α-GOS ameliorated allergic airway eosinophilia at least partly via post-absorptive mechanisms in Brown Norway rats.
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