The present invention relates to methods of enhancing the potency of incretin-based drugs in subjects in need thereof. Through different animal models, the inventors identified that a specific gut microbiota signature impairs GLP-1-activated gut-brain axis which could be transferred to germ free mice. The dysbiotic gut microbiota induces enteric neuropathy, reduces GLP-1 receptor and nNOS mRNA concentration, GLP-1-induced nitric oxide production for the control of insulin secretion and gastric emptying. The frequency of Lactobacilli in the ileum microbiota was tightly correlated with nMOS mRNA concentration, which is a mode of action of GLP-1, of the enteric nervous system opening a novel route for the improvement of GLP-1 based therapies in type 2 diabetic patients. In particular, the present invention relates to a method of enhancing the potency of an incretin-based drug administered to a diabetic subject as part of a treatment regimen.

Methods are provided for the simple, fast, effective and safe directed differentiation of embryonic stem cells into the mature beta cells of enriched beta clusters, wherein the beta cells rapidly and reliably secrete insulin in response to glucose levels. The cells are useful transplant therapeutics for diabetic individuals. These cells can also be used for drug screening purposes to identify factors/chemicals capable of increasing beta cell functions, proliferation, survival, and resistance to immune assault.

Methods are provided for the simple, fast, effective and safe directed differentiation of embryonic stem cells into the mature beta cells of enriched beta clusters, wherein the beta cells rapidly and reliably secrete insulin in response to glucose levels. The cells are useful transplant therapeutics for diabetic individuals. These cells can also be used for drug screening purposes to identify factors/chemicals capable of increasing beta cell functions, proliferation, survival, and resistance to immune assault.

There is provided an activator of peroxisome proliferator-activated receptor α which contains: a compound represented by the following Formula (I); a tautomer or stereoisomer of the compound; or a pharmaceutically acceptable salt or solvate thereof (where, in a case where R.sup.1, R.sup.2, R.sup.3, and R.sup.8 do not constitute a ring, in the Formula, R.sup.1, R.sup.2, R.sup.3, R.sup.6, R.sup.7, and R.sup.8 may be the same as or different from each other and represent a hydrogen atom, a halogen atom, an alkyl group having 1 to 8 carbon atoms, an alkoxy group having 1 to 8 carbon atoms, an alkyl group having 1 to 8 carbon atoms substituted with 1 to 3 halogen atoms, an alkoxy group having 1 to 8 carbon atoms substituted with 1 to 3 halogen atoms, a hydroxy group, an amino group, a carboxyl group, a mercapto group, an alkylsulfanyl group having 1 to 8 carbon atoms, a nitro group, or a cyano group).

Compounds that inhibit PI3Kδ activity, including compounds that selectively inhibit PI3Kδ activity, are disclosed. Methods of inhibiting phosphatidylinositol 3-kinase delta isoform (PI3Kδ) activity, and methods of treating diseases, such as disorders of immunity and inflammation in which PI3Kδ plays a role in leukocyte function, using the compounds also are disclosed.

The present invention relates to the use of a galactooligosaccharide composition for preventing or reducing the risk of developing metabolic syndrome.

This invention provides compositions comprising a byetta, fish oil, and a protease inhibitor, method for treating diabetes mellitus, comprising administering same, and methods for oral or rectal administration of a byetta.

The invention provides compositions and methods for ameliorating symptoms associated with hyperglycemia by administering a Zn-α2-glycoprotein or a functional fragment thereof, methods of decreasing plasma insulin levels, methods of increasing skeletal muscle mass, and methods of bringing about a weight reduction or reduction in obesity, Also provided are pharmaceutical compositions for use thereof.

Wnt signaling agonist compositions and methods for their use are provided. Wnt signaling agonists of the invention comprise a frizzled binding moiety, which is fused or conjugated to an LRP5 or LRP6 binding moiety.

Described are macro-capsules, barriers, and devices that can be used to prepare therapeutic cell implants, methods of encapsulating therapeutic cells, and methods of using the encapsulated cells in the treatment of disease.