U.S. Department of Health & Human Services Divider Arrow National Institutes of Health Divider Arrow NCATS

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Showing 1671 - 1680 of 1957 results

Calcitonin-salmon is a polypeptide hormone secreted by the parafollicular cells of the ultimobranchial gland of salmon fish. Calcitonin-salmon Nasal Spray is a polypeptide of 32 amino acids manufactured by recombinant DNA technology and is identical to calcitonin produced by salmon fish or chemical synthesis. Calcitonin acts primarily on bone, but direct renal effects and actions on the gastrointestinal tract are also recognized. Calcitonin-salmon appears to have actions essentially identical to calcitonins of mammalian origin, but its potency per mg is greater and it has a longer duration of action. The actions of calcitonin on bone and its role in normal human bone physiology are still not completely elucidated, although calcitonin receptors have been discovered in osteoclasts and osteoblasts. Single injections of calcitonin cause a marked transient inhibition of the ongoing bone resorptive process. With prolonged use, there is a persistent, smaller decrease in the rate of bone resorption. Histologically, this is associated with a decreased number of osteoclasts and an apparent decrease in their resorptive activity. In vitro studies have shown that calcitonin-salmon causes inhibition of osteoclast function with loss of the ruffled osteoclast border responsible for resorption of bone. Calcitonin-salmon Nasal Spray is indicated for the treatment of postmenopausal osteoporosis in females greater than 5 years postmenopause with low bone mass relative to healthy premenopausal females.
Cosyntropin (ACTH (1–24)) is a synthetic peptide that is identical to the 24-amino acid segment at the N-terminal of adrenocorticotropic hormone. It is intended for use as a diagnostic agent in the screening of patients presumed to have adrenocortical insufficiency. Cosyntropin may bind to sites located on the adrenergic nerve endings associated with the cardiac tissue, and such binding would interfere with the neuronal reuptake of the catecholamines
Glucagon is a polypeptide hormone identical to human glucagon that increases blood glucose and relaxes smooth muscle of the gastrointestinal tract. Glucagon is synthesized in a special non-pathogenic laboratory strain of Escherichia coli bacteria that has been genetically altered by the addition of the gene for glucagon. Glucagon generally elevates the concentration of glucose in the blood by promoting gluconeogenesis and glycogenolysis. Glucagon also decreases fatty acid synthesis in adipose tissue and the liver, as well as promoting lipolysis in these tissues, which causes them to release fatty acids into circulation where they can be catabolised to generate energy in tissues such as skeletal muscle when required. Glucose is stored in the liver in the form of the polysaccharide glycogen, which is a glucan (a polymer made up of glucose molecules). Liver cells (hepatocytes) have glucagon receptors. When glucagon binds to the glucagon receptors, the liver cells convert the glycogen into individual glucose molecules and release them into the bloodstream, in a process known as glycogenolysis. As these stores become depleted, glucagon then encourages the liver and kidney to synthesize additional glucose by gluconeogenesis. Glucagon turns off glycolysis in the liver, causing glycolytic intermediates to be shuttled to gluconeogenesis. Glucagon also regulates the rate of glucose production through lipolysis. Glucagon induces lipolysis in humans under conditions of insulin suppression (such as diabetes mellitus type 1). Glucagon increases blood glucose concentration and is used in the treatment of hypoglycemia. Glucagon administered through a parenteral route relaxes smooth muscle of the stomach, duodenum, small bowel, and colon. Glucagon is also indicated as a diagnostic aid in the radiologic examination of the stomach, duodenum, small bowel, and colon when diminished intestinal motility would be advantageous.
Corticotropin is indicated as monotherapy for the treatment of exacerbations of multiple sclerosis in adults and infantile spasms in infants and children under 2 years of age. Controlled clinical trials have shown Corticotropin to be effective in speeding the resolution of acute exacerbations of multiple sclerosis. However, there is no evidence that it affects the ultimate outcome or natural history of the disease. The mechanism of action of Corticotropin in the treatment of infantile spasms is unknown.

Showing 1671 - 1680 of 1957 results