| Combinations of chromium or vanadium with antidiabetics for glucose metabolism disorders -> Monitor Keywords |
|
|
  Combinations of chromium or vanadium with antidiabetics for glucose metabolism disordersRelated Patent Categories: Drug, Bio-affecting And Body Treating Compositions, Designated Organic Active Ingredient Containing (doai), Heterocyclic Carbon Compounds Containing A Hetero Ring Having Chalcogen (i.e., O,s,se Or Te) Or Nitrogen As The Only Ring Hetero Atoms Doai, Heavy Metal Containing (including Salts)The Patent Description & Claims data below is from USPTO Patent Application 20060003981. Brief Patent Description - Full Patent Description - Patent Application Claims
RELATED APPLICATION INFORMATION [0001] This application is a Continuation-in-Part of application Ser. No. 09/156,102, filed Sep. 17, 1998, and this application claims the benefit of priority under 35 U.S.C. section 119(e) to Provisional Application 60/126,489, filed Mar. 26, 1999, both of which Applications are hereby incorporated by reference in their entirety. BACKGROUND OF THE INVENTION [0002] Diabetes adversely affects the way the body uses sugars and starches which, during digestion, are converted into glucose. Diabetes mellitus is generally caused in almost all instances by diminished rates of insulin secretion (absolute or relative) by the beta cells of the islets of Langerhans in the pancreas or by reduced insulin sensitivity. Insulin, a hormone produced by the pancreas, makes the glucose available to the body's cells for energy. In muscle, adipose (fat), and connective tissues, insulin facilitates the entry of glucose into the cells by an action on the cell membranes. The ingested glucose is normally converted in the liver to CO.sub.2 and H.sub.2O (50%); to glycogen (5%); and to fat (30-40%), the latter being stored in fat depots. Fatty acids from the adipose tissues are circulated, returned to the liver for re-synthesis of triacylglycerol and metabolized to ketone bodies for utilization by the tissues. The fatty acids are also metabolized by other organs. [0003] The net effect of insulin is to promote the storage and use of carbohydrates, protein and fat. Insulin deficiency is a common and serious pathologic condition. Diabetes is commonly divided into two types: Type 1 diabetes (juvenile-onset, insulin-dependent diabetes mellitus [IDDM]) that usually, but not always, begins in early life, and Type 2 diabetes (maturity-onset diabetes, non-insulin dependent diabetes mellitus [NIDDM]) that usually, but not always, begins in later life. In Type 1 diabetes, the pancreas produces little or no insulin, and insulin must be injected daily. In Type 2 diabetes, the pancreas retains the ability to produce insulin and in fact may produce higher than normal amounts of insulin, but the amount of insulin is relatively insufficient, or less than fully effective, because of cellular resistance to insulin. Type 2 diabetes may present as non-obese NIDDM, obese NIDDM, or maturity-onset diabetes of the young (MODY). Type I is likely to occur in those with a family history of diabetes and is characterized by blurred vision, itching, unusual thirst, drowsiness, obesity, fatigue, skin infections, slow healing, and tingling or numbness in the feet. Type 1 Diabetes [0004] Type 1 diabetes accounts for around ten percent of all cases of diabetes mellitus. The action of Type 1 diabetes is to cause hyperglycemia (elevated blood glucose concentration) and a tendency towards diabetic ketoacidosis (DKA). Currently treatment requires chronic administration of insulin. No single standard exists for patterns of administration of insulin and treatment plans vary and may be selected from one of three treatment regimens: conventional, multiple subcutaneous injections, or continuous subcutaneous insulin infusion. Conventional insulin therapy involves the administration of one or two injections a day of intermediate-activity insulin such as zinc insulin or isophane insulin with or without the addition of small amounts of regular insulin. Regular insulin has a duration of action lasting from 3 to 8 hours, whereas other forms of insulin are absorbed slowly from the injection site and therefore have effects that may last as long as ten to forty-eight hours. The multiple subcutaneous insulin injection technique involves administration of intermediate- or long-acting insulin in the evening as a single dose together with regular insulin prior to each meal. Continuous subcutaneous insulin infusion involves the use of a small battery-driven pump that delivers insulin subcutaneously into the abdominal wall, usually through a butterfly needle. Insulin is delivered at a basal rate continuously throughout the day, with increased rates programmed prior to meals. Insulin may also be delivered by way of an implant that is administered parenterally, or by way of slow-release formulations. Type 2 Diabetes [0005] Type 2 diabetes is marked by hyperglycemia that is not linked with DKA. Sporadic or persistent incidence of hyperglycemia may be controlled by administering insulin. Uncontrolled hyperglycemia may transiently adversely affect the insulin-producing cells of the pancreas (the beta-islet cells), which may eventually result in greater insulin deficiencies. In most Type 2 diabetic subjects, the fundamental defects to which such abnormalities may be traced include (1) a reduced entry of glucose into various "peripheral" tissues, and (2) an increased liberation of glucose into the circulation from the liver. There is therefore an extracellular glucose excess and an intracellular glucose deficiency. There is also a decrease in the entry of amino acids into muscle and an increase in lipolysis. The cumulative effect of these diabetes-associated abnormalities may be severe blood vessel and nerve damage. Type 2 diabetic subjects may be treated with insulin, if necessary. [0006] Type 2 often develops in subjects of certain at risk populations. Obesity predisposes an individual to Type 2 diabetes due to long-tern effects on insulin resistance. If the beta-cells are compromised, diabetes may well ensue. Type 2 also develops from the at risk population of individuals with gestational diabetes mellitus (GDM). Pregnancy normally is associated with progressive resistance to insulin-mediated glucose disposal. In fact, insulin sensitivity is lower during late pregnancy than in nearly all other physiological conditions. The insulin resistance is thought to be mediated in large part by the effects of circulating hormones such as placental lactogen, progesterone, and cortisol, all of which are elevated during pregnancy. In the face of the insulin resistance, pancreatic beta-cell responsiveness to glucose normally increases nearly 3-fold by late pregnancy, a response that serves to minimize the effect of insulin resistance on circulating glucose levels. Thus, pregnancy provides a major "stress-test" of the capacity for beta-cells to compensate for insulin resistance. [0007] Other populations thought to be at risk for developing Type 2 diabetes are the elderly; certain minorities; persons with Syndrome X; persons with concomitant hyperinsulinemia; persons with insulin resistance characterized by hyperinsulinemia and by failure to respond to exogenous insulin; and persons with abnormal insulin and/or evidence of glucose disorders associated with excess circulating glucocorticoids, growth hormone, catecholamines, glucagon, parathyroid hormone, and other insulin-resistant conditions. Treatment of Diabetes and its Complications [0008] Diabetes has become a leading health care issue in the United States and other countries, accounting for one seventh of the national health care budget. The incidence of diagnosed diabetes has increased five-fold in America over the past 35 years, with currently 8 million diagnosed diabetic patients, another estimated 8 to 12 million undiagnosed diabetic individuals, and still an additional 23 million Americans with pre-diabetes, or impaired glucose tolerance (IGT). As the American populace continues its trend towards aging, obesity, and greater minority representation, the number of individuals who are diabetic and suffer from other glucose metabolism disorders is likely to increase. Diabetic Complications and Symptoms [0009] Although progress has been made in reducing the short term complications of diabetes, e.g. ketoacidosis, dehydration, and non-ketotic hyperosmolar coma, less progress has been made in preventing or minimizing the chronic complications of the disease, e.g. premature atherosclerosis, retinopathy, nephropathy, and neuropathy. It is estimated that a diabetic patient's life is shortened by 10 to 15 years, and those years of life are distinguished by significantly increased medical care costs as compared to a non-diabetic patient. Some complications of diabetes includes blindness and end-stage renal disease. [0010] Another complication of diabetes mellitus is diabetic neuropathy (also called neuritis), which has been an unusually refractive complication of diabetes. Endoneural hypoxia is the overt cause of diabetic neuropathy. Early symptoms include numbness, irritation, and pain, usually in the extremities, and more advanced ones include gastroparesis and impotence. The conversion of the essential fatty acid (EFA) linolenic acid to gamma-linolenic acid (GLA) appears to be impaired in diabetics because of a lack of the enzymes delta-6-desaturase and/or delta 5-desaturase. Consequently, there is shortage of GLA and its metabolites, prostacyclin and prostaglandins, the chronic deficiencies of which contribute to the pathogenesis of diabetic neuropathy. Prostacyclin (PGI2) is a vasoprotective molecule with multiple physiological functions, and the enzyme cyclooxygenase (cox) is involved in its synthesis. Two isoforms of cox have been identified to date: cox-1, which produces both prostacyclin and anti-inflammatory prostaglandins, and cox-2, which produces both thromboxane A.sub.2 (TxA.sub.2) and some of the prostaglandins responsible for inflammation. Many therapeutics for pain management inhibit both cox-1 and cox-2, thereby reducing inflammation caused by prostagladins produced by cox-2, but also inhibiting production of prostacyclin, which may exacerbate a prostacyclin deficiency resulting in neuropathy. In addition, neurotrophic factors, such as the superfamiliy of neurotrophins including nerve growth factor, may present an alternative pathogenic mechanism that results in neuropathy. [0011] Another complication of diabetes is increased cardiovascular risk factor, especially among women. A man's risk of dying by heart disease doubles upon developing diabetes, whereas a woman's risk increases three to five-fold. [0012] In particular, Type 2 diabetes presents a number of co-existent cardiovascular metabolic risk factors, e.g., insulin resistance, hyperinsulinemia, central obesity, hypertriglyceridemia, low HDL level, quantitatively abnormal LDL (diabetic dyslipidemia), hypertension, glucose intolerance, and elevated blood pressure. This state has been identified as "Syndrome X." These cardiovascular risk factors may precede the onset of diabetes by as much as a decade, and they may explain the presence of overt clinical cardiovascular disease in as many as 60% of newly diagnosed diabetic patients. For example, elevated glycated hemoglobin (HbA1c) is believed to be a risk marker for short-term mortality following acute myocardial infarction in non-diabetic subjects. [0013] Diabetic dyslipidemia is another complication of diabetes and is of import to cardiovascular health. Plasma cholesterol and triglycerides are transported in lipoproteins (HDL, VLDL, and LDL). Dyslipoproteinemias are conditions in which the concentration and composition of these cholesterol- or triglyceride-carrying lipoproteins are abnormal. Elevated concentration of lipoproteins LDL and VLDL may accelerate the development of atherosclerosis, with the secondary possibilities of thrombosis and infarction. Evidence suggests that reduction of the concentration of lipoproteins LDL and VLDL in plasma may diminish the increased risk of atherosclerosis that accompanies hyperlipoproteinemia. Dyslipoproteinemias have been designated as either primary or secondary. Secondary dyslipoproteinemias involve complications of a more generalized metabolic disturbance, such as diabetes mellitus or excessive intake of ethanol. In contrast, primary dyslipoproteinemias are typically caused either by an inherited single-gene defect (monogenic dyslipoproteinemias) or a combination of multiple subtle genetic factors that act together with environmental ones (multifactorial or polygenic dyslipoproteinemias). [0014] Evidence suggests that treatment of hyperlipoproteinemia may diminish or prevent atherosclerotic complications. For example, populations studies have shown that an elevated concentration of total cholesterol or LDL-cholesterol in plasma constitutes a major risk factor for the occurrence of atherosclerotic events. In the case of monogenic disorders, family studies have documented a markedly increased risk of vascular disease among affected members. These is evidence that reduction in plasma concentrations of LDL-cholesterol may reduce the risk of coronary heart disease (CHD). [0015] Furthermore, there may be an excessive risk of cardiac mortality in diabetic patients even after adjusting for the co-existence of other cardiov-ascular risk factors such as hypertension, dyslipidemia, and cigarette smoking. This increase risk of cardiac mortality is secondary to both the atherogenicity of insulin resistance, which may precede the onset of diabetes by at least 8 years, and the atherogenicity of undiagnosed and uncontrolled hyperglycemia, which may be present for 9-12 years before diabetes is first diagnosed. [0016] One means of attenuating the cardiovascular effects of diabetes, would involve earlier diagnosis and improved management of diabetes to reduce insulin resistance and control blood glucose. To this end, screening for risk factors for vascular complications followed by appropriate treatment may be appropriate. Pharmacologic Interventions [0017] Current drugs or anti-diabetic agents used for managing Type 2 diabetes that are well-known in the art generally fall within a number of categories: the biguanides, thiazolidinediones, the sulfonylureas, benzoic acid derivatives and glucosidase inhibitors. This drugs usually have distinct modes of action. The biguanides, e.g., metformin, are believed to prevent excessive hepatic gluconeogenesis. The thiazolidinediones are believed to act by increasing the rate of peripheral glucose disposal. The sulfonylureas, e.g., tolbutamide and glyburide, and the benzoic acid derivatives, e.g. repaglinide, lower plasma glucose by stimulating insulin secretion. The alpha-glucosidase inhibitors competitively inhibit alpha-glucosidase, which metabolizes carbohydrates, thereby delaying carbohydrate absorption and attenuating post-prandial hyperglycemia. In addition, there are a number of proposed therapies for treatment of diabetes that have not yet been approved for human use. Continue reading... Full patent description for Combinations of chromium or vanadium with antidiabetics for glucose metabolism disorders Brief Patent Description - Full Patent Description - Patent Application Claims Click on the above for other options relating to this Combinations of chromium or vanadium with antidiabetics for glucose metabolism disorders patent application. ###  How KEYWORD MONITOR works... a FREE service from FreshPatents1. Sign up (takes 30 seconds). 2. Fill in the keywords to be monitored. 3. Each week you receive an email with patent applications related to your keywords. Start now! - Receive info on patent apps like Combinations of chromium or vanadium with antidiabetics for glucose metabolism disorders or other areas of interest. ### Previous Patent Application: Cobalt(ii) complexes as protein tyrosine kinase inhibitors Next Patent Application: Photosensitizer and method for production thereof Industry Class: Drug, bio-affecting and body treating compositions ### FreshPatents.com Support Thank you for viewing the Combinations of chromium or vanadium with antidiabetics for glucose metabolism disorders patent info. IP-related news and info Results in 0.38446 seconds Other interesting Feshpatents.com categories: Novartis , Pfizer , Philips , Polaroid , Procter & Gamble , |
||
