116 results about "Prediabetes" patented technology

The present invention provides compositions and methods for treating and / or preventing diseases and disorders associated with expression of PPAR γ and / or infiltration of macrophages into skeletal muscle tissue and / or white adipose tissue. The method treats such diseases and disorders with abscisic acid (ABA). Exemplary diseases and disorders include diabetes, including type 2 diabetes, prediabetes, glucose intolerance insulin resistance, and diseases and disorders involving the immune system, such as inflammation, including obesity-related inflammation, inflammatory bowel disease, type 1 diabetes, multiple sclerosis, allergies, asthma, cardiovascular disease, and arthritis.

Novel methods for assessing the state of a diabetic condition of a subject are described, comprising determining the amount of a metabolite in a sample from a body fluid or tissue of the subject. The methods may be used, for example, in diagnosing and monitoring insulin resistance, prediabetes, or the response to a drug which alters a diabetic condition.

The present invention is directed to a method for treating a patient suffering from the metabolic syndrome, Type 2 diabetes, obesity, or prediabetes, comprising the step of increasing the ratio of dopaminergic neuronal to noradrenergic neuronal activity within the hypothalamus of the central nervous system of the patient. In another aspect, the present invention is directed to a method for treating a patient suffering from the metabolic syndrome, Type 2 diabetes, obesity, or prediabetes, comprising the step of: administering to a patient suffering from the metabolic syndrome, Type 2 diabetes, obesity, or prediabetes a pharmaceutical composition comprising (1) at least one compound that stimulates an increase in central dopaminergic neuronal activity level in the subject, and (2) at least one compound that stimulates a decrease in central noradrenergic neuronal activity level in the subject. The present invention is also directed to pharmaceutical compositions that include the above compounds and a pharmaceutically acceptable carrier.

Methods are provided for treating or prophylactically preventing metabolic disorders in humans without causing, promoting, or aggravating fluid retention, peripheral edema, pulmonary edema, or congestive heart failure, by administration of a therapeutically effective amount of a compound sufficient to partially or fully activate peroxisome proliferator activated receptors (PPARs) and partially or fully inhibit, antagonize or block the activity of angiotensin II type 1 receptors. Metabolic disorders that can be treated or prevented include but are not limited to type 2 diabetes, the metabolic syndrome, prediabetes, and other insulin resistance syndromes. Compounds are provided that antagonize or block the angiotensin II type 1 (AT1) receptor, function as partial or full activators of peroxisome proliferator activated receptors (PPARs), can be used to treat or prevent diseases known to be treatable or preventable by PPAR activators and were not previously recognized to be therapeutic targets for angiotensin II receptor antagonists.

Methods, systems and circuits evaluate a subject's risk of developing type 2 diabetes or having prediabetes using at least one defined mathematical model of risk of progression that can stratify risk for patients having the same glucose measurement. The model may include NMR derived measurements of GlycA and a plurality of selected lipoprotein components of at least one biosample of the subject.

The present invention relates to methods for modulating the intestinal microbiota by administering one or more defensins and / or GLP-1 / GLP-1 analogs and methods for prevention or treatment of gut inflammation by oral administration of one or more defensins. GLP-1 analogs such as Liraglutide, as well as mammalian and poultry alfa and beta defensins can cause a change in the composition of the microbiota and metabolome in the intestine and can therefore be used to treat or prevent gut inflammation, colorectal cancer, metabolic syndrome, obesity, prediabetes and diabetes or as lean growth promoters in the meat production.

The present invention is directed to a method for treating a patient suffering from the metabolic syndrome, Type 2 diabetes, obesity, or prediabetes, comprising the step of increasing the ratio of dopaminergic neuronal to noradrenergic neuronal activity within the central nervous system and particularly the hypothalamus of the central nervous system of the patient.In another aspect, the present invention is directed to a method for treating a patient suffering from a metabolic disorder such as the metabolic syndrome, Type 2 diabetes, obesity, or prediabetes, and the metabolic sequale of these diseases including cardiovascular, cerebrovascular, renal and hepatic diseases, comprising the step of: administering to a patient suffering from the metabolic syndrome, Type 2 diabetes, obesity, or prediabetes a pharmaceutical composition comprising (1) at least one compound that stimulates an increase in central dopaminergic neuronal activity level in the subject, and (2) at least one compound that stimulates a decrease in central noradrenergic neuronal activity level in the subject. The present invention is also directed to pharmaceutical compositions that include the above compounds and a pharmaceutically acceptable carrier.

Annatto extract composition (AEC), including cis and trans geranyl geraniols (GG) and tocopherol-free C-5 unsubstituted tocotrienols (T3), increases the de novo synthesis of intermediate isoprenoid and distal protein products, including endogenous coenzyme Q10 (CoQ10), dolichols (DL) and all subsequent GG-prenylated and DL-glycosylated proteins, including GG-porphyrinated hemes. This intermediate and distal product replenishment by AEC reverses maladies of myotoxicity (of both drug and non-drug origins), including maladies that affect the muscle, kidney, eye, GI tract and skin, nerve, blood, and CoQ10-related syndromes of energetics and LDL protection. AEC anabolically increases the endogenous de novo CoQ10 synthesis via GG elongation / prenylation of side-chain and conversely CoQ10 catabolically increases the endogenous de novo GG synthesis via beta-oxidation of CoQ10. Also, such AEC decreases de novo synthesis and increases disposal of triglycerides (TG) in humans via PPAR activation and SREBP deactivation. Such drop in TG by AEC reverses maladies of insulin resistance (IR) and metabolic syndrome (MS), prediabetes, diabetes and diabetes-related cardiovascular diseases (CVD). GG activates PPAR and down regulates SREBP transcription factors. This AEC, containing GG, inhibits cancer growth whether or not GG involvement in protein prenylation is required.