Abstract: One aspect of the present invention relates to a method of treating or preventing pathologic sequelae of acute hyperglycemia and/or increased fatty acid flux in a subject. This method involves administering an ROS inhibitor to the subject. In addition, methods of promoting neovascularization, inhibiting oxidation or excessive release of free fatty acids, and identifying compounds suitable for treatment or prevention of ROS-mediated injury are also disclosed.

Abstract: One aspect of the present invention relates to a method of treating or preventing pathologic effects of hyperglycemia and/or increased fatty acid flux in a subject in need of such treatment or preventive therapy. This method involves administering a composition containing a therapeutically effective amount of a ROS inhibitor to a subject in need thereof.

Abstract: One aspect of the present invention relates to a method of treating or preventing pathologic effects of hyperglycemia and/or increased fatty acid flux in a subject in need of such treatment or preventive therapy. This method involves administering a composition containing a therapeutically effective amount of a ROS inhibitor to a subject in need thereof.

Abstract: One aspect of the present invention relates to a method of treating or preventing pathologic sequelae of acute hyperglycemia and/or increased fatty acid flux in a subject. This method involves administering an ROS inhibitor to the subject. In addition, methods of promoting neovascularization, inhibiting oxidation or excessive release of free fatty acids, and identifying compounds suitable for treatment or prevention of ROS-mediated injury are also disclosed.

Abstract: One aspect of the present invention relates to a method of treating or preventing pathologic sequelae of acute hyperglycemia and/or increased fatty acid flux in a subject. This method involves administering an ROS inhibitor to the subject. In addition, methods of promoting neovascularization, inhibiting oxidation or excessive release of free fatty acids, and identifying compounds suitable for treatment or prevention of ROS-mediated injury are also disclosed.

Abstract: Methods of inhibiting hyperglycemia-induced or free fatty acid-induced reactive oxygen formation in mammalian cells and mammals using the degradation product of glucagon-like peptide 1, GLP-1 (9-36) are provided. Various GLP-1 (9-36) compositions are also provided.

Abstract: Methods of inhibiting hyperglycemia-induced or free fatty acid-induced reactive oxygen formation in mammalian cells and mammals using the degradation product of glucagon-like peptide 1, GLP-1 (9-36) are provided. Various GLP-1 (9-36) compositions are also provided.

Abstract: The present invention relates to methods for inhibiting protein aging. Accordingly, methods are disclosed for treating an animal to inhibit the formation of advanced glycosylation end products of target proteins with the animal by adminstering a pharmaceutical composition comprising an agent capable of reacting with the carbonyl moiety of the early glycosylation product, whereby the subsequent cross-linking of the early glycosylation product is inhibited. Agents of the present invention comprise aminoguanidine, its pharmaceutically acceptable salts, and mixtures thereof.

Abstract: The present invention relates to methods for inhibiting protein aging. Accordingly, methods are disclosed for treating an animal to inhibit the formation of advanced glycosylation end products of target proteins with the animal by adminstering a pharmaceutical composition comprising an agent capable of reacting with the carbonyl moiety of the early glycosylation product, whereby the subsequent cross-linking of the early glycosylation product is inhibited. Agents of the present invention comprise aminoguanidine, its pharmaceutically acceptable salts, and mixtures thereof.

Abstract: The present invention relates to compositions and methods for inhibiting protein aging. Accordingly, a composition is disclosed which comprises an agent or compound capable of inhibiting the formation of advanced glycosylation end products of target proteins by reacting with the carbonyl moiety of the early glycosylation product of such target proteins formed by their initial glycosylation. Suitable agents may contain an active nitrogen-containing group, such as a hydrazine group. Particular agents comprise aminoguanidine, .alpha.-hydrazinohistidine and mixtures thereof. The method comprises contacting the target protein with the composition. Both industrial and therapeutic applications for the invention are envisioned, as food spoilage and animal protein aging can be treated.