Abstract: Embodiments of the present disclosure pertain to methods of treating or preventing Alzheimer's disease or symptoms of Alzheimer's disease in a subject by administering to the subject an active agent that includes an adenovirus-36 E4orf1 protein, a nucleic acid encoding an adenovirus-36 E4orfl protein, or combinations thereof. Additional embodiments of the present disclosure pertain to the active agents of the present disclosure for use in the treatment or prevention of Alzheimer's disease or symptoms of Alzheimer's disease.

Abstract: In an embodiment, the present disclosure pertains to compositions and methods for modulating cellular glucose uptake. In general, the methods include associating cells with the compositions of the present disclosure. In another aspect, the present disclosure pertains to compositions and methods to treat or prevent a disorder in a subject. The methods generally include administering the compositions of the present disclosure to the subject.

Abstract: The invention relates to amino nitrile compounds. Such compounds can increase glucose uptake by cells and preferably do not substantially increase adipogenesis.

Abstract: This invention generally relates to methods for treating or preventing the symptoms of non-alcoholic fatty liver disease, methods for reducing excessive fat from the liver, methods of improving glycemic control, and methods for treating or preventing liver dysfunction, that comprise administering a therapeutically effective amount of Adenovirus 36 E4orf1 protein or functional variant thereof.

Abstract: A compound includes the structure of general Formula II, pharmaceutically acceptable salts thereof, and/or solvates thereof: wherein R1, R2, R3, are independently selected from the group consisting of null, hydroxy, alkoxy, and halo, or R1 and R2 taken together form a cyclic boronate ester and R3 is null; wherein when four bonds to boron are present, boron bears a formal negative charge and the structure further comprises a countercation that is potassium or sodium, X1, X2, X3, and X4 are independently selected from the group consisting of O, CH, and N, with the proviso that no more than two of combined O and N are selected, and Z is selected from the group consisting of hydrogen, alkyl, aryl, heteroaryl, and halogen, any of which may be optionally substituted. Such compounds can increase glucose uptake by cells and preferably do not substantially increase adipogenesis.

Abstract: A compound includes the structure of general Formula II, pharmaceutically acceptable salts thereof, and/or solvates thereof: wherein R1, R2, R3, are independently selected from the group consisting of null, hydroxy, alkoxy, and halo, or R1 and R2 taken together form a cyclic boronate ester and R3 is null; wherein when four bonds to boron are present, boron bears a formal negative charge and the structure further comprises a countercation that is potassium or sodium, X1, X2, X3, and X4 are independently selected from the group consisting of O, CH, and N, with the proviso that no more than two of combined O and N are selected, and Z is selected from the group consisting of hydrogen, alkyl, aryl, heteroaryl, and halogen, any of which may be optionally substituted. Such compounds can increase glucose uptake by cells and preferably do not substantially increase adipogenesis.

Abstract: The invention relates to amino nitrile compounds. Such compounds can increase glucose uptake by cells and preferably do not substantially increase adipogenesis.

Abstract: A method of treating a disease comprising administering to a subject a therapeutically effective amount of a compound that includes the structure of general Formula II, pharmaceutically acceptable salts thereof, and/or solvates thereof: wherein R1, R2, R3, are independently selected from the group consisting of null, hydroxy, alkoxy, and halo, or R1 and R2 taken together form a cyclic boronate ester and R3 is null; wherein when four bonds to boron are present, boron bears a formal negative charge and the structure further comprises a countercation that is potassium or sodium, X1, X2, X3, and X4 are independently selected from the group consisting of O, CH, and N, with the proviso that no more than two of combined O and N are selected, and Z is selected from the group consisting of hydrogen, alkyl, aryl, heteroaryl, and halogen, any of which may be optionally substituted. Such compounds can increase glucose uptake by cells and preferably do not substantially increase adipogenesis.

Abstract: A compound includes the structure of general Formula (II), pharmaceutically acceptable salts thereof, and/or solvates thereof: wherein R1, R2, R3, are independently selected from the group consisting of null, hydroxy, alkoxy, and halo, or R1 and R2 taken together form a cyclic boronate ester and R3 is null; wherein when four bonds to boron are present, boron bears a formal negative charge and the structure further comprises a countercation that is potassium or sodium, X1, X2, X3, and X4 are independently selected from the group consisting of O, CH, and N, with the proviso that no more than two of combined O and N are selected, and Z is selected from the group consisting of hydrogen, alkyl, aryl, heteroaryl, and halogen, any of which may be optionally substituted. Such compounds can increase glucose uptake by cells and preferably do not substantially increase adipogenesis.

Abstract: A method of treating a disease comprising administering to a subject a therapeutically effective amount of a compound that includes the structure of general Formula II, pharmaceutically acceptable salts thereof, and/or solvates thereof: wherein R1, R2, R3, are independently selected from the group consisting of null, hydroxy, alkoxy, and halo, or R1 and R2 taken together form a cyclic boronate ester and R3 is null; wherein when four bonds to boron are present, boron bears a formal negative charge and the structure further comprises a countercation that is potassium or sodium, X1, X2, X3, and X4 are independently selected from the group consisting of O, CH, and N, with the proviso that no more than two of combined O and N are selected, and Z is selected from the group consisting of hydrogen, alkyl, aryl, heteroaryl, and halogen, any of which may be optionally substituted. Such compounds can increase glucose uptake by cells and preferably do not substantially increase adipogenesis.

Abstract: A compound includes the structure of general Formula (II), pharmaceutically acceptable salts thereof, and/or solvates thereof: wherein R1, R2, R3, are independently selected from the group consisting of null, hydroxy, alkoxy, and halo, or R1 and R2 taken together form a cyclic boronate ester and R3 is null; wherein when four bonds to boron are present, boron bears a formal negative charge and the structure further comprises a countercation that is potassium or sodium, X1, X2, X3, and X4 are independently selected from the group consisting of O, CH, and N, with the proviso that no more than two of combined O and N are selected, and Z is selected from the group consisting of hydrogen, alkyl, aryl, heteroaryl, and halogen, any of which may be optionally substituted. Such compounds can increase glucose uptake by cells and preferably do not substantially increase adipogenesis.

Abstract: This invention generally relates to methods for treating or preventing the symptoms of non-alcoholic fatty liver disease, methods for reducing excessive fat from the liver, methods of improving glycemic control, and methods for treating or preventing liver dysfunction, that comprise administering a therapeutically effective amount of Adenovirus 36 E4orf1 protein or functional variant thereof.

Abstract: This invention generally relates to methods for improving glycemic control by administering an Ad36 composition and an AKT1 inhibitor.

Abstract: This invention generally relates to methods for treating or preventing the symptoms of non-alcoholic fatty liver disease, methods for reducing excessive fat from the liver, methods of improving glycemic control, and methods for treating or preventing liver dysfunction, that comprise administering a therapeutically effective amount of Adenovirus 36 E4orf1 protein or functional variant thereof.

Abstract: Expression of the E4 orf 1 gene of Ad-36 alone has been discovered to be responsible for the increased insulin sensitivity observed in Ad-36 infected animals, including increased adipogenesis. Ad-36 E4 orf 1 protein can be used to increase insulin sensitivity and ameliorate diabetes. Additionally, drugs that mimic the action of Ad-36 E4 orf 1 protein could be found. Ad-36 E4 orf 1 could also be used to increase fat cells in lipodystrophy. We have also discovered that Ad-36 infection in human skeletal muscle cells increased differentiation and insulin independent glucose uptake. It is expected that infection with Ad-36 E4 orf 1 gene will also cause these effects.

Abstract: Expression of the E4 orf 1 gene of Ad-36 alone has been discovered to be responsible for the increased insulin sensitivity observed in Ad-36 infected animals, including increased adipogenesis. Ad-36 E4 orf 1 protein can be used to increase insulin sensitivity and ameliorate diabetes. Additionally, drugs that mimic the action of Ad-36 E4 orf 1 protein could be found. Ad-36 E4 orf 1 could also be used to increase fat cells in lipodystrophy. We have also discovered that Ad-36 infection in human skeletal muscle cells increased differentiation and insulin independent glucose uptake. It is expected that infection with Ad-36 E4 orf 1 gene will also cause these effects.

Abstract: Expression of the E4 orf 1 gene of Ad-36 alone has been discovered to be responsible for the increased insulin sensitivity observed in Ad-36 infected animals, including increased adipogenesis. Ad-36 E4 orf 1 protein can be used to increase insulin sensitivity and ameliorate diabetes. Additionally, drugs that mimic the action of Ad-36 E4 orf 1 protein could be found. Ad-36 E4 orf 1 could also be used to increase fat cells in lipodystrophy. We have also discovered that Ad-36 infection in human skeletal muscle cells increased differentiation and insulin independent glucose uptake. It is expected that infection with Ad-36 E4 orf 1 gene will also cause these effects.

Abstract: Infection with obesifying adenoviruses in animals and humans may be used to predict changes in body weight and disease status. More particularly, infection with certain adenoviruses, such as adenovirus type 36 (Ad-36) and adenovirus type 37 (Ad-37) may cause removal of the normal equilibrium factors that control fat cell metabolism and may make individuals more responsive than normal individuals to perturbations, which cause body composition change including weight gain or weight loss.

Abstract: A source of viral induced obesity has been discovered. A virus known as AD-36P adenovirus type 36 has been found to be associated with obesity in both animals and humans. Diagnostic DNA sequences are presented so that DNA based tests for the presence of the obesity associated virus can be conducted.

Abstract: A source of viral induced obesity has been discovered. A virus known as AD-36P adenovirus type 36 has been found to be associated with obesity in both animals and humans. Diagnostic DNA sequences are presented so that DNA based tests for the presence of the obesity associated virus can be conducted.