Compositions are conducive to the promotion of a feeling of relaxation. The compositions of the present invention comprise a combination of hops extract, lemon balm extract, magnolia bark extract, and L-theanine to promote a feeling of relaxation in an individual. Methods of making and using the same are further provided.

Bone mineral content, 25(OH) vitamin D3, or 1,25(OH).sub.2 vitamin D3 in a companion animal can be improved by adjusting the diet of the animal to increase the amount of a compound which positively or negatively modulates the bone mineral content, 25(OH) vitamin D3, or 1,25(OH).sub.2 vitamin D3 or adjusting the diet of the animal to decrease the amount of a compound which positively or negatively modulates the bone mineral content, 25(OH) vitamin D3, or 1,25(OH).sub.2 vitamin D3.

Bone mineral content, 25(OH) vitamin D3, or 1,25(OH).sub.2 vitamin D3 in a companion animal can be improved by adjusting the diet of the animal to increase the amount of a compound which positively or negatively modulates the bone mineral content, 25(OH) vitamin D3, or 1,25(OH).sub.2 vitamin D3 or adjusting the diet of the animal to decrease the amount of a compound which positively or negatively modulates the bone mineral content, 25(OH) vitamin D3, or 1,25(OH).sub.2 vitamin D3.

The present disclosure relates to compositions including a phenylbutyrate compound and a bile acid, and methods of processing such compositions.

The present disclosure relates to compositions including a phenylbutyrate compound and a bile acid, and methods of processing such compositions.

The present disclosure pertains to a composition for treatment of glutaric aciduria and an administration method therefor and, specifically, to a pharmaceutical composition comprising recombinant human glutaryl-CoA dehydrogenase (rhGCDH) for treatment of glutaric aciduria and a method for treating glutaric aciduria, the method comprising a step of administering the pharmaceutical composition. Provided according to an aspect of the present disclosure are a pharmaceutical composition comprising recombinant human glutaryl-CoA dehydrogenase (rhGCDH) for treating glutaric aciduria and a novel method for treating glutaric aciduria through in vivo administration of the pharmaceutical composition (intravenously and subcutaneously; i.v. and s. c.), whereby an excellent effect is brought about through in vivo administration remarkably easier than intraventricular administration, with the expectation of more effectively regulating and treating glutaric aciduria.

The present disclosure pertains to a composition for treatment of glutaric aciduria and an administration method therefor and, specifically, to a pharmaceutical composition comprising recombinant human glutaryl-CoA dehydrogenase (rhGCDH) for treatment of glutaric aciduria and a method for treating glutaric aciduria, the method comprising a step of administering the pharmaceutical composition. Provided according to an aspect of the present disclosure are a pharmaceutical composition comprising recombinant human glutaryl-CoA dehydrogenase (rhGCDH) for treating glutaric aciduria and a novel method for treating glutaric aciduria through in vivo administration of the pharmaceutical composition (intravenously and subcutaneously; i.v. and s. c.), whereby an excellent effect is brought about through in vivo administration remarkably easier than intraventricular administration, with the expectation of more effectively regulating and treating glutaric aciduria.

A drug that contains chlorogenic acid is effective in treating chordoma. When administered to a patient in need thereof, chlorogenic acid can significantly inhibit the proliferation of chordoma cells, reduce the expression level of multi-drug resistance gene MDR1 of chordoma cells, reverse the multi-drug resistance of chordoma cells, and effectively treat chordoma disease.

The present invention provides methods of treating obesity, pre-diabetes, diabetes, and/or obese breast cancer, by increasing mitochondrial metabolism by increasing the activity of uncoupling protein 1 (UCP1) in adipocytes. The disclosed methods comprise contacting an adrenergic receptor agonist with an adipocyte in which the genomic activity of estrogen receptor beta (ERβ) has been inhibited or inactivated. In certain aspects, inhibition or inactivation of the genomic activity of ERβ is achieved by contacting the adipocyte with an ERβ ligand that selectively inhibits or inactivates the ERβ genomic activity.

The present disclosure is directed to methods of treating a steatosis-associated disorder by administering a therapeutic agent selected from a lysosomal enzyme, an autophagy-inducing agent, or a combination thereof. Steatosis-associated disorders discussed herein include GSD Ia, GSD Ib, GSD Ic, NAFLD, and NASH. Other embodiments are directed to methods of reversing steatosis, modulating autophagy, inducing autophagy, and reversing glycogen storage.