Comparative structural characterization of 7 commercial galacto-oligosaccharide (GOS) products

Nowadays, dairy waste represents a global challenge as a result of the amount produced worldwide. Initially, one of the major objectives was to transform this waste into a single valuable product, but recently the concept of biorefinery has been applied to convert dairy waste into several valuable bioproducts such as biofuels, feed additives, bioplastics, and chemicals. Despite the potential that represents this kind of waste for the production of bioproducts, it is not a technology used extensively. An important factor that can help to become the biorefinery of dairy waste more attractive is the measure of the biorefinery complexity index (BCI). The BCI is a measure of the technological and economic risk to develop a biorefinery process using specific raw materials, production, extraction and purification processes. Our analysis of a dairy biorefinery gives a BCI of 20, which reflects a sustainable biorefinery. The dairy biorefinery synergistic approach predicted presents a zero-waste generation in the dairy industry. This will provide strength in academic and industrial level towards a biorefinery process design.

Background: Oligosaccharides in milk act as soluble decoy receptors and prevent pathogen adhesion to the infant gut. Milk oligosaccharides reduce infectivity of a porcine rotavirus strain; however, the effects on human rotaviruses are less well understood. Objective: In this study, we determined the effect of specific and abundant milk oligosaccharides on the infectivity of 2 globally dominant human rotavirus strains. Methods: Four milk oligosaccharides—2′-fucosyllactose (2′FL), 3′-sialyllactose (3′SL), 6′-sialyllactose (6′SL), and galacto-oligosaccharides—were tested for their effects on the infectivity of human rotaviruses G1P[8] and G2P[4] through fluorescent focus assays on African green monkey kidney epithelial cells (MA104 cells). Oligosaccharides were added at different time points in the infectivity assays. Infections in the absence of oligosaccharides served as controls. Results: When compared with infections in the absence of glycans, all oligosaccharides substantially reduced the infectivity of both human rotavirus strains in vitro; however, virus strain-specific differences in effects were observed. Compared with control infections, the maximum reduction in G1P[8] infectivity was seen with 2′FL when added after the onset of infection (62% reduction, P < 0.01), whereas the maximum reduction in G2P[4] infectivity was seen with the mixture of 3′SL + 6′SL when added during infection (73% reduction, P < 0.01). The mixture of 3′SL + 6′SL at the same ratio as is present in breast milk was more potent in reducing G2P[4] infectivity (73% reduction, P < 0.01) than when compared with 3′SL (47% reduction) or 6′SL (40% reduction) individually. For all oligosaccharides the reduction in infectivity was mediated by an effect on the virus and not on the cells. Conclusions: Milk oligosaccharides reduce the infectivity of human rotaviruses in MA104 cells, primarily through an effect on the virus. Although breastfed infants are directly protected, the addition of specific oligosaccharides to infant formula may confer these benefits to formula-fed infants.

β-Galactosidase enzymes are used in the dairy industry to convert lactose into galactooligosaccharides (GOS) that are added to infant formula to mimic the molecular sizes and prebiotic functions of human milk oligosaccharides. Here we report a detailed analysis of the clearly different GOS profiles of the commercial β-galactosidases from Bacillus circulans, Kluyveromyces lactis and Aspergillus oryzae. Also the GOS yields of these enzymes differed, varying from 48.3% (B. circulans) to 34.9% (K. lactis), and 19.5% (A. oryzae). Their incubation with lactose plus the monosaccharides Gal or Glc resulted in altered GOS profiles. Experiments with ¹³C₆ labelled Gal and Glc showed that both monosaccharides act as acceptor substrates in the transgalactosylation reactions. The data shows that the lactose isomers β-d-Galp-(1 → 2)-d-Glcp, β-d-Galp-(1 → 3)-d-Glcp and β-d-Galp-(1 → 6)-d-Glcp are formed from acceptor reactions with free Glc and not by rearrangement of Glc in the active site.