A method for treating metabolic disorders includes determining a treatment group comprising obese non-infant humans; formulating a composition comprising one or more synthetic non-fucosylated human milk oligosaccharides (HMOs) selected from lacto-N-tetraose (LNT), lacto-N-neotetraose (LNnT) and/or 2′-fucosyllactose (2′-FL), 3-fucosyllactose (3-FL), difucosyllactose (DFL), and lacto-N-fucopentaose I (LNFP-I), that are effective for: increasing in the gastrointestinal microbiota of a non-infant human during a treatment period, the relative abundance of Bifidobacterium adolescentis and reducing a precursor condition for a metabolic disorder associated with development of one or more of obesity-induced pre-diabetes and type 2 diabetes, the precursor condition selected from gut permeability, metabolic endotoxemia, low-grade metabolic inflammation, and body fat percentage; and reducing the precursor condition in at least one non-infant human in the treatment group by providing the composition to the at least one non-infant human during the treatment period.

A method for treating metabolic disorders includes determining a treatment group comprising obese non-infant humans; formulating a composition comprising one or more synthetic non-fucosylated human milk oligosaccharides (HMOs) selected from lacto-N-tetraose (LNT), lacto-N-neotetraose (LNnT) and/or 2′-fucosyllactose (2′-FL), 3-fucosyllactose (3-FL), difucosyllactose (DFL), and lacto-N-fucopentaose I (LNFP-I), that are effective for: increasing in the gastrointestinal microbiota of a non-infant human during a treatment period, the relative abundance of Bifidobacterium adolescentis and reducing a precursor condition for a metabolic disorder associated with development of one or more of obesity-induced pre-diabetes and type 2 diabetes, the precursor condition selected from gut permeability, metabolic endotoxemia, low-grade metabolic inflammation, and body fat percentage; and reducing the precursor condition in at least one non-infant human in the treatment group by providing the composition to the at least one non-infant human during the treatment period.

The present invention relates to a composition comprising 1) a preparation of Punica granatum L. and/or another source of ellagitannins and/or ellagic acid and 2) one or more human milk oligosaccharides (HMOs). Also disclosed herein is a method of increasing the production of urolithin A and/or other urolithins in the gut by administering said composition to a human subject.

The present invention relates to a composition comprising 1) a preparation of Punica granatum L. and/or another source of ellagitannins and/or ellagic acid and 2) one or more human milk oligosaccharides (HMOs). Also disclosed herein is a method of increasing the production of urolithin A and/or other urolithins in the gut by administering said composition to a human subject.

The present invention relates to a composition comprising 1) a preparation of Punica granatum L. and/or another source of ellagitannins and/or ellagic acid and 2) one or more human milk oligosaccharides (HMOs). Also disclosed herein is a method of increasing the production of urolithin A and/or other urolithins in the gut by administering said composition to a human subject.

Provided herein are compositions, methods, strategies, kits, and articles of manufacture that are useful, inter alia, in the treatment or prevention of diseases or conditions such as those which may be associated with inflammation, infection, allergy, immune dysfunction, or dysbiosis of the intestinal microbiome. In some aspects, the invention provides a synergistic combination of a prebiotics, e.g., a mixture of human milk oligosaccharides, and a probiotic strain, such as a strain capable of internalizing and consuming the rebiotics, e.g., B. longum subsp. infantis.

Provided herein are compositions, methods, strategies, kits, and articles of manufacture that are useful, inter alia, in the treatment or prevention of diseases or conditions such as those which may be associated with inflammation, infection, allergy, immune dysfunction, or dysbiosis of the intestinal microbiome. In some aspects, the invention provides a synergistic combination of a prebiotics, e.g., a mixture of human milk oligosaccharides, and a probiotic strain, such as a strain capable of internalizing and consuming the rebiotics, e.g., B. longum subsp. infantis.

Provided herein are compositions, methods, strategies, kits, and articles of manufacture that are useful, inter alia, in the treatment or prevention of diseases or conditions such as those which may be associated with inflammation, infection, allergy, immune dysfunction, or dysbiosis of the intestinal microbiome. In some aspects, the invention provides a synergistic combination of a prebiotics, e.g., a mixture of human milk oligosaccharides, and a probiotic strain, such as a strain capable of internalizing and consuming the rebiotics, e.g., B. longum subsp. infantis.

Disclosed are a food composition containing 2′-fucosyllactose and a pharmaceutical composition containing 2′-fucosyllactose that are effective in ameliorating, preventing or treating various cerebrovascular diseases caused by thrombogenesis, and a method for ameliorating a cerebrovascular disease caused by a thrombus by administering a composition including 2′-fucosyllactose (2′-FL) to a subject in need thereof. The 2′-fucosyllactose (2′-FL) exhibits antagonistic (inhibitory) activity against CRP and collagen, which are agonists of platelets, and thus can be used to inhibit thrombogenesis due to abnormal platelet activity.

Disclosed are a food composition containing 2′-fucosyllactose and a pharmaceutical composition containing 2′-fucosyllactose that are effective in ameliorating, preventing or treating various cerebrovascular diseases caused by thrombogenesis, and a method for ameliorating a cerebrovascular disease caused by a thrombus by administering a composition including 2′-fucosyllactose (2′-FL) to a subject in need thereof. The 2′-fucosyllactose (2′-FL) exhibits antagonistic (inhibitory) activity against CRP and collagen, which are agonists of platelets, and thus can be used to inhibit thrombogenesis due to abnormal platelet activity.