114 results about "Insulin dependent" patented technology

A method for individualized management of diabetes in insulin-dependent patients provides a period of evaluation as the patient adheres to a structured pattern of eating, sleeping, and physical activity. Glucose is monitored with a continuous glucose monitoring system, insulin doses are metered, carbohydrate consumption is quantified, and glucose, carbohydrate, and insulin data are collected and analyzed. Insulin dosage is adjusted in three steps: (1) an insulin dosage is estimated from conventional formulas, (2) adjustments are made according to the patient's clinical specifics, and (3) further insulin dose adjustments are made according to glucose data obtained during the evaluation period. By the end of the evaluation period, substantially normal glucose values are achieved, and quantitative relationships from data are calculated that are then applied to determine insulin dosages for an ensuing period of therapy. By this method, diabetic patients achieve a near normal glycemic profile, and without significant occurrence of hypoglycemic episodes.

The present invention relates to compounds that are inhibitors of the 11-beta-hydroxysteroid dehydrogenase Type 1 enzyme. The present invention further relates to the use of inhibitors of 11-beta-hydroxysteroid dehydrogenase Type 1 enzyme for the treatment of non-insulin dependent type 2 diabetes, insulin resistance, obesity, lipid disorders, metabolic syndrome and other diseases and conditions that are mediated by excessive glucocorticoid action.

The present invention relates to compounds which are inhibitors of the 11-beta-hydroxysteroid dehydrogenase Type 1 enzyme. The present invention further relates to the use of inhibitors of 11-beta-hydroxysteroid dehydrogenase Type 1 enzyme for the treatment of non-insulin dependent type 2 diabetes, insulin resistance, obesity, lipid disorders, metabolic syndrome, and other diseases and conditions that are mediated by excessive glucocorticoid action.

Techniques are provided for use with an implantable medical device such as a pacemaker or implantable cardioverter / defibrillator (ICD) for predicting and detecting hypoglycemia. In one example, the device tracks changes in a paced depolarization integral (PDI). A significant increase in PDI over a relatively short period of time indicates the onset of hypoglycemia (this can also be confirmed with QT changes). Upon detection of hypoglycemia, appropriate warning signals are generated to alert the patient. Certain therapies automatically provided by the implantable device may also be controlled in response to hypoglycemia. For example, if the patient is an insulin-dependent diabetic and the implantable device is equipped with an insulin pump capable of delivering insulin directly into the bloodstream, insulin delivery is automatically suspended until blood glucose levels return to acceptable levels. If the device is an ICD, it may be controlled to begin charging defibrillation capacitors upon detection of hypoglycemia so as to permit prompt delivery of a defibrillation shock, which may be needed if hypoglycemia triggers ventricular fibrillation. The detection techniques may be used in conjunction with other hypoglycemia detection techniques to improve detection specificity.

The present invention relates to the use of inhibitors of the 11-beta-hydroxysteroid dehydrogenase Type 1 enzyme. The present invention further relates to the use of inhibitors of 11-beta-hydroxysteroid dehydrogenase Type 1 enzyme for the treatment or prophylactically treatment of non-insulin dependent type 2 diabetes, insulin resistance, obesity, lipid disorders, metabolic syndrome, and other diseases and conditions mediated by excessive glucocorticoid action.

The invention relates to a method for minimizing mean blood glucose levels in an insulin dependent patient by administering insulin to the patient in a sufficiently fast manner to provide a difference of 50% or less between high and low blood glucose levels. Advantageously, the insulin is administered to the patient by jet injection and the high and low blood glucose levels differ by an amount that is less than that which would be obtained after injection of insulin by a conventional needle syringe. The invention also relates to a method for reducing mean blood glucose levels in an insulin dependent patient that is receiving insulin through a conventional syringe and needle arrangement. This method provides for administration of the insulin to the patient by jet injection rather than by the syringe by substituting a jet injector for the syringe.

Methods and compositions for preserving the function of insulin-producing cells and to furthering the lifespan of insulin-producing cells in non-insulin dependent patients with insulin-related disorders are provided.

The present invention relates to compounds which are inhibitors of the 11-beta-hydroxysteroid dehydrogenase Type 1 enzyme. The present invention further relates to the use of inhibitors of 11-beta-hydroxysteroid dehydrogenase Type 1 enzyme for the treatment of non-insulin dependent type 2 diabetes, insulin resistance, obesity, lipid disorders, metabolic syndrome, and other diseases and conditions that are mediated by excessive glucocorticoid action.

Thiazolidinedione (TZD) and its pharmacologically active derivatives can be used, in combination with agonists of glucagon-like peptide-1 (GLP-1), to treat non-insulin dependent diabetes mellitus, optionally with other therapies, by improving glycemic control while minimizing side effects, such as heart hypertrophy and elevated fed-state plasma glucose, which are associate with both TZD and GLP-1 monotherapies. Thus, the co-administration of TZD and GLP-1 helps regulate glucose homeostasis in Type II diabetic patients.

The present invention relates to the use of inhibitors of the 11-beta-hydroxysteroid dehydrogenase Type 1 enzyme. The present invention further relates to the use of inhibitors of 11-beta-hydroxysteroid dehydrogenase Type 1 enzyme for the treatment or prophylactically treatment of non-insulin dependent type 2 diabetes, insulin resistance, obesity, lipid disorders, metabolic syndrome, and other diseases and conditions mediated by excessive glucocorticoid action.

The present invention relates to compounds which are inhibitors of the 11-beta-hydroxysteroid dehydrogenase Type 1 enzyme. The present invention further relates to the use of inhibitors of 11-beta-hydroxysteroid dehydrogenase Type 1 enzyme for the treatment of non-insulin dependent type 2 diabetes, insulin resistance, obesity, lipid disorders, metabolic syndrome and other diseases and conditions that are mediated by excessive glucocorticoid action.

Methods and compositions are described for the treatment of type I insulin-dependent diabetes mellitus and other conditions using newly identified stem cells that are capable of differentiation into a variety of pancreatic islet cells, including insulin-producing beta cells, as well as hepatocytes. Nestin has been identified as a molecular marker for pancreatic stem cells, while cytokeratin-19 serves as a marker for a distinct class of islet ductal cells. Methods are described whereby nestin-positive stem cells can be isolated from pancreatic islets and cultured to obtain further stem cells or pseudo-islet like structures. Methods for ex vivo differentiation of the pancreatic stem cells are disclosed. Methods are described whereby pancreatic stem cells can be isolated, expanded, and transplanted into a patient in need thereof, either allogeneically, isogeneically or xenogenically, to provide replacement for lost or damaged insulin-secreting cells or other cells.

Flavonoids, especially luteolin, are shown to be effective against insulin dependent (Type I) and insulin independent (Type II) diabetes mellitus. It is demonstrated that luteolin works in mammals by binding and blocking the Kv1.3 potassium channel of T-cell and Beta cells. Antidiabetic and anti-autoimmune compounds can be selected by measuring their ability to bind to and block the Kv1.3 channel.

A compound of formula (I):or a pharmaceutically acceptable salt, prodrug, salt of a prodrug, or a combination thereof. Methods of inhibiting 11-beta-hydroxysteroid dehydrogenase Type 1 enzyme. Methods of treating non-insulin dependent type 2 diabetes, insulin resistance, obesity, lipid disorders, metabolic syndrome and other diseases and conditions that are mediated by excessive glucocorticoid action.

Techniques are provided for use with an implantable medical device such as a pacemaker or implantable cardioverter / defibrillator (ICD) for predicting and detecting hypoglycemia. In one example, the device tracks changes in a paced depolarization integral (PDI). A significant increase in PDI over a relatively short period of time indicates the onset of hypoglycemia (this can also be confirmed with QT changes). Upon detection of hypoglycemia, appropriate warning signals are generated to alert the patient. Certain therapies automatically provided by the implantable device may also be controlled in response to hypoglycemia. For example, if the patient is an insulin-dependent diabetic and the implantable device is equipped with an insulin pump capable of delivering insulin directly into the bloodstream, insulin delivery is automatically suspended until blood glucose levels return to acceptable levels. If the device is an ICD, it may be controlled to begin charging defibrillation capacitors upon detection of hypoglycemia so as to permit prompt delivery of a defibrillation shock, which may be needed if hypoglycemia triggers ventricular fibrillation. The detection techniques may be used in conjunction with other hypoglycemia detection techniques to improve detection specificity.

Aptamer oligonucleotides specifically bind to the DNA binding site of proteins such as Sp1 and Sp1-related proteins which regulate the genes which encode costimulatory molecules such as CD28 and cytokines such as IL-2 and GMCSF. The oligonucleotides compete with the DNA-binding sites of regulatory proteins which specifically regulate molecules to modulate T-cell activation. This serves to modulate gene expression by preventing transcription of the gene. Aptamers are administered to provide therapies for diseases which involve aberrant T-cell activation such as psoriasis, Type I (insulin-dependent) diabetes mellitus, multiple sclerosis, autoimmune uveitis, rheumatoid arthritis, systemic lupus erythematosus, inflammatory bowel disease (Crohn's and ulcerative colitis), and septic shock and to regulate normal T-cell activation such as in allograft rejection.

The present invention relates to compounds which are inhibitors of the 11-beta-hydroxysteroid dehydrogenase Type 1 enzyme. The present invention further relates to the use of inhibitors of 11-beta-hydroxysteroid dehydrogenase Type 1 enzyme for the treatment of non-insulin dependent type 2 diabetes, insulin resistance, obesity, lipid disorders, metabolic syndrome, and other diseases and conditions that are mediated by excessive glucocorticoid action.

Methods and compositions are described for the treatment of type I insulin-dependent diabetes mellitus and other conditions using newly identified stem cells that are capable of differentiation into a variety of pancreatic islet cells, including insulin-producing beta cells, as well as hepatocytes. Nestin has been identified as a molecular marker for pancreatic stem cells, while cytokeratin-19 serves as a marker for a distinct class of islet ductal cells. Methods are described whereby nestin-positive stem cells can be isolated from pancreatic islets and cultured to obtain further stem cells or pseudo-islet like structures. Methods for ex vivo differentiation of the pancreatic stem cells are disclosed. Methods are described whereby pancreatic stem cells can be isolated, expanded, and transplanted into a patient in need thereof, either allogeneically, isogeneically or xenogenically, to provide replacement for lost or damaged insulin-secreting cells or other cells.

The present invention relates to compounds which are inhibitors of the 11-beta-hydroxysteroid dehydrogenase Type 1 enzyme. The present invention further relates to the use of inhibitors of 11-beta-hydroxysteroid dehydrogenase Type 1 enzyme for the treatment of non-insulin dependent type 2 diabetes, insulin resistance, obesity, lipid disorders, metabolic syndrome and other diseases and conditions that are mediated by excessive glucocorticoid action.

The object of the present invention is to provide a method of preparing excellent cultured muscle cells having high metabolic capacity and insulin responsiveness, and further provide a method for the measurement of sensitive metabolic capacity using the cells. Moreover, its purpose is to provide a culture system / culture apparatus that can smoothly translocate such highly advanced cultured muscle cells intact to activity evaluation systems of a number of drugs. Moreover, the object of the present invention is to provide cultured muscle cells that are very suitable for measurement of the membrane-translocation activity of GLUT4 in an extraneous stimulus-dependent manner such as insulin, etc., and to provide a method for the measurement of the membrane-translocation activity of GLUT4 using the cells. The present invention is a method of preparing myotube cells, comprising a step (1) of culturing myoblast cells, a step (2) of differentiation-inducing the myotube cells into the myoblast cells in a culture medium with a high content of amino acids, and a step (3) of applying an electric pulse to the differentiation-induced myotube cells, and a method for the measurement of insulin-dependent sugar uptake using the myotube cells prepared by said method, and relates to the method for the measurement, comprising applying insulin stimulation by culturing the cells in a culture medium containing insulin, culturing the cells in the culture medium further supplemented with sugar, and measuring the sugar uptake. Furthermore, the present invention relates to a differentiation-type culture myotube cell constitutively expressing a recombinant GLUT4 having a labeled substance at its extra-cellular site, which is prepared by co-culturing wild-type myoblast cells and recombinant myoblast cells constitutively expressing said recombinant GLUT4, and a method for the measurement of membrane-translocation activity of the recombinant GLUT4 using the cells, and particularly a method for the measurement of insulin-dependent sugar uptake activity.

The present invention provides an azulene derivative and a salt thereof, wherein an azulene ring is bonded to a benzene ring directly or via a lower alkylene which may be substituted with a halogen atom and the benzene ring is directly bonded to the glucose residue, and it is usable as a Na<+>-glucose cotransporter inhibitor, especially for a therapeutic and / or preventive agent for diabetes such as insulin-dependent diabetes (type 1 diabetes) and insulin-independent diabetes (type 2 diabetes), as well as diabetes-related diseases such as insulin-resistant diseases and obesity.

The present invention relates to inhibitors of 11-β-hydroxysteroid dehydrogenase type 1 enzyme and their use in treatment of non-insulin dependent type 2 diabetes, insulin resistance, obesity, lipid disorders, metabolic syndrome, central nervous system disorders, and diseases and conditions that are related to excessive glucocorticoids.

There are disclosed derivatives of 3-chromancarboxylic acid represented by formula Itheir pharmaceutically acceptable salts thereof and prodrugs thereof which are useful for treatment and control of non-insulin dependent diabetes mellitus (type II diabetes) and its related vascular disease as well as obesity and lipid disorders.

The invention provides the immunomodulator with the free adjuvant having the function of preventing and curing the insulin-dependent diabetes mellitus. Aiming at the weak immunogenicity, the antigen epitope polypeptide gene (a length of antigen epitope p277 rooted from human HSP60) is associated repeatedly six times and inserted repeatedly into the backward position of the heat shock protein HSP65 gene rooted from the mycobacterium bovis, the fusing expression between the repeat series connecting antigen polyeptide and the HSP65 is realized. The produced fusing albumen did not need the adjuvant; the antigen polyeptide don't need be coupled with the carrier chemistry to the immunity. The fusing albumen can inspire the organism to produce the high titer aiming at p277 by means of the mucous membrane immunity, so the nosogeny of NOD chmice diabetic are depressed highly. The invention can prevent the 1 type and 1.5 type diabete characterized in depending on the insulin.

A therapeutic or an edible composition comprising at least three of the five herbs selected from Prunus amygdales, Ocimum sanctum, Azadirachta indica, Aegle marelose and Vitus vinefera, is provided for the treatment of hyperglycemia, especially for non-insulin dependent diabetic subjects, and the herbal composition has significantly reduced the blood glucose levels in both diabetic and non-diabetic experimental subjects having elevated blood glucose levels.

The present invention relates to inhibitors of 11-beta-hydroxysteroid dehydrogenase Type 1 enzyme and their use in treatment of non-insulin dependent type 2 diabetes, insulin resistance, obesity, lipid disorders, metabolic syndrome, central nervous system disorders, and diseases and conditions that are related to excessive glucocorticoids.

A compound of formula (I): or a pharmaceutically acceptable salt, prodrug, salt of a prodrug, or a combination thereof. Methods of inhibiting 11-beta-hydroxysteroid dehydrogenase Type 1 enzyme. Methods of treating non-insulin dependent type 2 diabetes, insulin resistance, obesity, lipid disorders, metabolic syndrome and other diseases and conditions that are mediated by excessive glucocorticoid action.

The present invention relates to compounds which are inhibitors of the 11-beta-hydroxysteroid dehydrogenase Type 1 enzyme. The present invention further relates to the use of inhibitors of 11-beta-hydroxysteroid dehydrogenase Type 1 enzyme for the treatment of non-insulin dependent type 2 diabetes, insulin resistance, obesity, lipid disorders, metabolic syndrome, and other diseases and conditions that are mediated by excessive glucocorticoid action.