250 results about "Pancreatic beta Cells" patented technology

It is intended to provide a method of forming pancreatic β cells from mesenchymal cells characterized by comprising using mammal-origin mesenchymal cells as starting cells, culturing these cells in the presence of, for example, a pancreatic β cell-forming agent, and selecting and separating the thus obtained pancreatic βcells with the use of a gene expressed specifically in such cells as a selection marker; a remedy for glucose intolerance which comprises pancreatic β cells obtained by the above method as the active ingredient; a pancreatic β cell-forming agent such as a cytokine to be used in the above method; a method of screening a candidate compound promoting the formation of pancreatic β cells from mesenchymal cells; and a pancreatic β cell formation promoter obtained by this screening method.

The invention provides a method of modulating blood glucose levels by treating or preventing pancreas-related disorders with thyrotropin-releasing hormone (TRH) or a TRH derivative. Diabetes mellitus, pancreatic islet destruction, pancreatic beta cell malfunction, and hyperglycemia-related malfunction are preferably treated or prevented.

A composition of bio-active compounds and methods for facilitating and supporting the metabolism and transport of glucose and carbohydrates into muscle cells, promoting muscle function and growth, promoting glycogen synthesis, enhancing glucose disposal, stimulating pancreatic beta cells, promoting metabolic recovery, promoting muscle recovery, promoting lean body mass, and promoting fat burning. Preferably, the composition of bio-active compounds includes a combination of 4-hydroxyisoleucine with at least one amino acid selected from the group consisting of arginine, aspartate, threonine, serine, glutamate, proline, glycine, alanine, cysteine, valine, methionine, isoleucine, leucine, tryptophan, phenylalanine, ornithine, lysine, histidine, gamma-amino butyrate and tyrosine. In one presently preferred embodiment of the present invention, the combination is derived, isolated, and/or extracted from fenugreek seeds. Methods for using a novel composition of bio-active compounds from fenugreek seed for facilitating and supporting the metabolism and transport of glucose and carbohydrates into muscle cells, promoting muscle function and growth, promoting glycogen synthesis, enhancing glucose disposal, stimulating pancreatic beta cells, promoting metabolic recovery, promoting muscle recovery, promoting lean body mass, and promoting fat burning are also disclosed, wherein methods comprise the steps of: (1) providing an effective amount of a composition of bio-active compounds derived, isolated, and/or extracted from fenugreek seeds; and (2) administering the composition to a human or animal.

Provided are methods for determining concurrently with a simple, minimally invasive test, the adequacy of pancreatic beta-cell compensation and/or the presence of tissue insulin resistance in a subject human or an experimental animal. The methods allow for the determination of a subject's or experimental animal's susceptibility to developing type 2 diabetes mellitus (DM2) or to progression to more advanced forms of DM2. Among other uses, the methods allow for diagnostic classification of subjects for decisions regarding therapeutic interventions, clinical differentiation between type 1 DM and DM2, clinical monitoring of treatments intended to reduce risk of developing DM2 in non-diabetic subjects, clinical monitoring of agents intended to improve existing DM2 and to prevent progression of DM2, clinical development and testing of new compounds, candidate agents, or candidate therapies for preventing progression to DM2 or disease progression in existing DM2, and preclinical screening of candidate agents or candidate therapies in experimental animals to identify and characterize agents having insulin-sensitizing properties, pancreatic stimulatory or regenerative properties or other desirable actions.

This invention relates to human adipose tissue-derived multipotent adult stem cells. More particularly, the invention relates to human adipose tissue-derived multipotent stem cells, which can be maintained in an undifferentiated state for a long period of time by forming spheres and have high proliferation rates, as well as methods for isolating and maintaining the adult stem cells, and methods for differentiating the multipotent adult stem cells into nerve cells, fat cells, cartilage cells, osteogenic cells and insulin-releasing pancreatic beta-cells. Also, the invention relates to cellular therapeutic agents for treating osteoarthritis, osteoporosis and diabetes and for forming breast tissue, which contain the differentiated cells or the adult stem cells. Although the multipotent stem cells are adult stem cells, they have the ability to differentiate into osteogenic cells, nerve cells, astrocytes, fat cells, chrondrogenic cells or insulin-releasing pancreatic beta-cells, and so are effective in treating osteoporosis, osteoarthritis, nerve disease, diabetes, etc. Also, the stem cells form spheres in a serum-free medium containing CORM-2, and thus can be maintained in an undifferentiated state for a long period of time. Also, the stem cells have very high proliferation rates. Accordingly, the stem cells are useful as cellular therapeutic agents.

The present invention demonstrates a method for inhibiting O-linked protein glycosylation in a tissue or cell, comprising the step of contacting said tissue or cell with (Z)-1-[N-(3-Ammoniopropyl)-N-(n-propy- l)amino] diazen-ium-1,2-diolate or a derivative thereof. The present invention is also directed to a method of treating or inhibiting the onset of diabetes mellitis in an individual in need of such treatment, comprising the step of admininstering to said individual a pharmacological dose of a compound which inhibiting O-linked protein glycosylation in a tissue or cell of said individual. Further, the present invention provides a pharmaceutical composition, comprising (Z)-1-[N-(3-Ammoniopropyl)-N-(n-propyl)amino] diazen-ium-1,2-diolate and a pharmaceutically acceptable carrier or a derivative thereof.

The present invention relates to a method to stimulate reversal of a diabetic state in a patient; a method to prevent autoimmune destruction of new insulin-producing cells (pancreatic beta-cells) in a patient; a method to promote survival of the newly regenerated insulin-producing cells (pancreatic beta-cells); and an in vivo method for the induction of islet cell neogenesis and new islet formation and the prevention of autoimmune destruction of said new cells.

Co-culture compositions and methods are described for identifying agents that modulate a cellular phenotype, particularly of neurons or pancreatic beta cells are provided herein, where the methods include co-culturing differentiated cells, wherein at least one of the cell-types are derived from human induced pluripotent stem cells from a subject having or predisposed to a neurodegenerative or metabolic disorder. Co-culture compositions of differentiated cells from two different human subjects are also described.

The present invention relates to one or more SGLT2 inhibitors or pharmaceutically acceptable forms thereof for use in the treatment and/or prevention of a metabolic disorder in a feline animal, preferably wherein the metabolic disorder is one or more selected from the group consisting of: ketoacidosis, pre-diabetes, diabetes mellitus type 1 or type 2, insulin resistance, obesity, hyperglycemia, impaired glucose tolerance, hyperinsulinemia, dyslipidemia, dysadipokinemia, subclinical inflammation, systemic inflammation, low grade systemic inflammation, hepatic lipidosis, atherosclerosis, inflammation of the pancreas, neuropathy and/or Syndrome X (metabolic syndrome) and/or loss of pancreatic beta cell function and/or wherein the remission of the metabolic disorder, preferably diabetic remission, is achieved and/or maintained.

The present invention relates to novel heterocyclic compounds of the general formula (I), their derivatives, analogs, tautomeric forms, stereoisomers, polymorphs, hydrates, solvates, pharmaceutically acceptable salts and compositions, metabolites and prodrugs thereof. The present invention more particularly provides novel hetereocycles of the general formula (I). Also included is a method of treatment of immunological diseases, inflammation, pain disorder, rheumatoid arthritis; osteoporosis; multiple myeloma; uveititis; acute and chronic myelogenous leukemia; ischemic heart disease; atherosclerosis; cancer; ischemic-induced cell damage; pancreatic beta cell destruction; osteoarthritis; rheumatoid spondylitis; gouty arthritis; inflammatory bowel disease; adult respiratory distress syndrome (ARDS); psoriasis; Crohn's disease; allergic rhinitis; ulcerative colitis; anaphylaxis; contact dermatitis; muscle degeneration; cachexia; asthma; bone resorption diseases; ischemia reperfusion injury; brain trauma; multiple sclerosis; sepsis; septic shock; toxic shock syndrome; fever, and myalgias due to infection in a mammal comprising administering an effective amount of a compound of formula (I) as described above.

This invention provides novel peptides that function in vivo to stimulate insulin release from pancreatic beta cells in a glucose-dependent fashion. These insulin secretagogue peptides are shown to stimulate insulin release in rat islet cells in vitro, and in vivo. The peptides of the present invention provide a new therapy for patients with decreased endogenous insulin secretion, in particular type 2 diabetics. In particular, the invention is a polypeptide selected from a specific group of VIP/PACAP-related polypeptides, or functional equivalents thereof. The invention is also directed to a method of treating a metabolic disease in a mammal comprising administering a therapeutically effective amount of the insulin secretagogue peptides to said mammal. Also disclosed are methods of making the peptides, both recombinant and synthetic.

Type 1 diabetes mellitus is characterized by loss of pancreatic insulin-producing beta cells, resulting in insulin deficiency. The usual cause of this beta cell loss is autoimmune destruction. Coxsackie virus has been detected in human pancreatic beta cells and causes insulitis. This non-destructive islet inflammation does not itself cause diabetes, but this disease will occur if viral infection is followed by a separate autoimmune response. The insulitis is mediated mainly by natural killer cells. Islets from coxsackie virus positive samples displayed reduced insulin secretion in response to glucose and other secretagogues. Virus extracted from positive islets was able to infect beta cells from human islets of non-diabetic donors, causing viral inclusions and signs of pyknosis.

The present invention relates to differentiation of stem cells into a homogeneous endocrine progenitor cell population suitable for further differentiation into pancreatic beta-cells. The present invention provides methods for obtaining NGN3/NKX2.2 double positive endocrine progenitor cells by exposing precursor cells to a TGF-β type I receptor inhibitor, a BMP antagonist, an adenylate cyclase activator and nicotinamide and/or exposing to the precursor cells to a selection of small molecules.

Compositions, methods of using and methods of making a cyclic peptide analog imaging agent that includes at least portions of a peptide or protein that binds specifically to the GLP-1 receptor (GLP-1R) and the cyclic analog has one or more conformational restrictions including, but not limited to, lactam bridges, disulfide bridges, hydrocarbon bridges, and their combinations, salts and derivatives thereof wherein the cyclic analog is more stable than a non-cyclic analog when incubated in the presence of enzymes that degrade GLP-1 and have an increased serum half-live, wherein the cyclic analog comprises at least a portion of a GLP-1 peptide or at least a portion of an Exendin peptide salts, derivatives or combinations thereof.

The invention provides for methods of differentiating pancreatic endocrine cells into pancreatic beta cells expressing PDX1, NKX6.1, MAFA, UCN3 and SLC2A. These pancreatic beta cells may be obtained by step-wise differentiation of pluripotent stem cells. The pancreatic beta cells exhibit glucose-dependent mitochondrial respiration and glucose-stimulated insulin secretion similar to islet cells.

The invention provides a method for establishing an SD mouse fat and diabetes research model through diet and STZ induction. Through high-fat feed and STZ induction, the attacking characteristics of fat and diabetes of humans are induced, and an animal model for establishing pathogenesis of fat and type-2-diabetes caused by insulin resistance and partial defects of pancreatic beta cells is provided. Mice are divided into a normal control group, a fat group and a diabetes group, and each group has six SD male mice. The high-fat feed is adopted for feeding mice for eight weeks, a pure-fat insulin resistance model is induced, after the mice are fed with the high-fat feed for eight weeks, injection of STZ small doze in batch is conducted, and establishment of the diabetes animal model is induced. The method can better simulate the attacking characteristics of human type-2-diabetes caused by improper diet and enjoinment factors currently, and compared with other modeling, the method has better scientific significance of clinical and fundamental research combination.

The present invention relates to a controller unit and methods for controlling an insulin pump. The controller unit includes a user input that receives a gain factor. The gain factor has been calculated based on historical data in relation to a patient. The controller unit includes a measurement input for receiving data representative of a measured blood glucose level for the patient. Processing logic of the controller unit is configured to apply the measured blood glucose level to a pancreatic beta-cell insulin secretion computational model to predict an insulin output level, apply the gain factor to the predicted insulin output level to determine a patient insulin deficiency level, and calculate a control signal for controlling the insulin output level of the insulin pump based on the patient insulin deficiency level.; Methods are provided for optimising the gain factor based on the historical data in relation to the patient.

The invention relates to methods that allow for the efficient differentiation to form pancreatic endoderm cells from pluripotent stem cells such as human embryonic stem cells and definitive endoderm cells. The invention is directly applicable to the ultimate generation of pancreatic beta cells that could be used as part of a therapy to treat or even cure diabetes. Additionally, the present invention may be used to generate liver endoderm cells from human embryonic stem cells and definite endoderm cells as well. This invention relates to a method for generating definitive endoderm and pancreatic endoderm cells from stem cells, preferably human embryonic stem cells using defined media in the absence of feeder cells. A simply two step procedure to provide pancreatic endoderm cells from embryonic stem cells represents further embodiments of the present invention.

The present invention is directed to the identification of a biomarker specifically located in the plasma membrane of pancreatic beta cells. It was selected by a Systems Biology approach on Massively Parallel Signal Sequencing datasets obtained in human islets and Affymetrix microarray datasets on human islets, purified rat primary beta and non beta cells and insulinoma cells. Based on a set of specific features the biomarker is a unique candidate for imaging and targeting strategies to study the pancreatic beta cell mass in health and disease (T1 D, T2D, pancreatic cancers, obesity, islet transplantation, beta cell regeneration). The five specific features of the selected biomarkers are: 1) Preferentially expressed in pancreatic islets as compared to surrounding tissues; 2) Higher expression in pancreatic beta cells than in pancreatic alpha cells or than in other islet non-beta cells; 3) Expression levels in pancreatic beta cells are higher or comparable to glucokinase which is an enzyme specifically expressed in the pancreatic beta cell; 4) Located in the membrane and as such targetable with antibodies, peptides or small molecules which allows imaging, targeting and immunohistochemistry; and 5) Expression is not induced during the process of inflammation of the beta cell mass and the protein is not enriched in T-cells and dendritic cells or in other cells participating in the inflammation process.