464 results about "NAFLD - Nonalcoholic Fatty Liver Disease" patented technology

The invention relates to the discovery that farnesoid X receptor (FXR) agonists can be used in combination with peroxisome proliferation activated receptor gamma (PPARγ) agonists to reduce drug-induced adverse side effects in patients suffering from conditions such as insulin resistance, Type II diabetes, metabolic syndrome, non-alcoholic fatty liver disease (NAFLD), non-alcoholic steatohepatitis (NASH), and heart disease. Particularly, the present invention encompasses methods for treating patients suffering from drug-induced adverse side effects with selective PPARγ, dual PPARα/γ and pan PPARα/γ/δ agonists in combination with FXR agonists.

A method and system for treating non-alcoholic fatty liver disease (NAFLD) involves the modulation of the gut microbial of a person suffering from NAFLD, and in particular the provision of a probiotic therapy configured to reduce liver aminotransferases, total-cholesterol, TNF-α and to improve insulin resistance in NAFLD patients.

The invention relates to compositions containing cholesterol absorption inhibitors alone or in combination with other therapeutic agents for treating non-alcoholic fatty liver disease-associated disorders by administering a therapeutically effective amount of the compositions to a subject in need thereof.

A method for reducing the likelihood of developing non-alcoholic steatohepatitis (NASH) in an individual diagnosed with non-alcoholic fatty liver disease involves providing in the gut of an individual a population of beneficial bacteria selected from the group consisting of Lactobacillus species, and at least 6 grams per day of fiber to the individual to maintain a therapeutically effective amount of the beneficial bacteria in the gut of the individual. In certain embodiments, monoacylglycerolacyltransferase-3 (MGAT3) synthesis is inhibited to lower triacylglycerol (TAG) production, while in others, expression of diacylglycerolacyltransferase-2 (DGAT-2) is inhibited. The beneficial bacteria are preferably modified to produce increased amounts of butyrate and are also encapsulated in a frangible enclosure. Levels of Roseburia are preferably increased while the levels of Akkermansia spp. in the individual's gut microbiome are reduced.

The present invention provides methods of treating a subject with non-alcoholic fatty liver disease (NAFLD), insulin resistance, obesity or hyperlipidemia, comprising administering to the subject an effective amount of a compound according to Formula I:

or a physiologically acceptable salt thereof.

The present invention provides methods of treating, stabilizing or lessening the severity or progression of a non-alcoholic fatty liver disease using an ACC inhibitor alone or with one or more additional therapeutic agents.

Evidence is emerging that lipid accumulation in the liver and the muscle contributes to insulin resistance in type II diabetes and the metabolic syndrome (1). This has prompted an investigation of the relationship between lipid accumulation in the liver, serum triglyceride levels, and glucose disposal. These studies demonstrate that liver fat positively correlated to fasting triglyceride levels and negatively correlated to glucose diposal (2). Therefore, strategies to prevent lipid accumulation in liver would have therapeutic value for treatment of type II diabetes, metabolic syndrome and non-alcoholic fatty liver disease. The invention described here relates to continuous administration of GLP-1 or its analogs obtained by either gene or cell therapy that results in reduction serum triglycerides and reduction of lipid accumulation in the liver for treatment of type II diabetes, the metabolic syndrome or non-alcoholic fatty liver disease.

Methods of determining levels of unbound metabolites are disclosed. Probes derived from fatty acid binding protein muteins are described that bind preferentially to a number of unbound metabolites including oleate, stearate, linoleate, palmitate, arachidonate and unconjugated bilirubin. A profile for a patient is determined using one or more of the described probes. The profile is useful in diagnosis of disease, particularly myocardial infarction, non-alcoholic fatty liver disease (NAFLD), diabetes, stroke, sepsis and neonatal jaundice. The responses of multiple probes to a test sample are used to classify the degree of acute coronary syndrome by comparison to multi-probe profiles generated from unstable angina, non ST elevation myocardial infarction, and ST elevation myocardial infarction.

A compound of Formula (I):

or a metabolite thereof, or an ester of the compound of Formula (I) or the metabolite thereof, or a pharmaceutically acceptable salt of each thereof, wherein m, n, X¹ and X² are as defined herein, is useful for treating non-alcoholic fatty liver disease (NAFLD) or non-alcoholic steatohepatitis (NASH).

The invention provides various novel compositions of berberine in combination with pharmacologically active organic acids, and related methods of their use in treating various diseases or disorders. The invention further provides various novel compounds prepared from berberine and pharmacologically active organic acids and prepared from ursodeoxycholic acid and pharmacologically active organic bases, and pharmaceutical compositions thereof, and methods of their preparation and therapeutic use in treating and/or preventing various diseases or disorders. The compounds and pharmaceutical compositions of the invention can be utilized to treat various diseases or disorders, such as diabetes, diabetic complications, dyslipidemia, hyperlipidemia, obesity, metabolic syndromes, pre-diabetes, atherosclerosis, heart diseases, neurodegenerative diseases, sarcopenia, muscle atrophy, inflammation, cancer and liver diseases and conditions such as fatty liver, non-alcoholic fatty liver disease, non-alcoholic steatohepatitis, cholestatic liver diseases or graft-versus-host disease of the liver. The compounds of this invention are also useful in improving liver functions in chronic viral associated liver diseases and alcohol-related liver diseases.

Novel MCH-1 receptor antagonists are disclosed. These compounds are used in the treatment of various disorders, including obesity, anxiety, depression, non-alcoholic fatty liver disease, and psychiatric disorders. Methods of making these compounds are also described in the present invention.

The invention relates to the treatment and reduction of fibrosis, specifically hepatic fibrosis. More specifically, embodiments of the invention provide compositions and methods useful for the treatment and inhibition of hepato-fibrotic conditions associated with Non-Alcoholic Fatty Liver Disease (NAFLD) and Non-Alcoholic Steatohepatitis (NASH), employing the use of 3β-arachidylamido-7α,12α-dihydroxy-5β-cholan-24-oic acid (Aramchol) or a pharmaceutically acceptable salt thereof. In other embodiments, the treatment and inhibition of hepato-fibrotic conditions caused by contact with hepatotoxic chemical substances or by mechanical obstruction is contemplated.

The present invention relates to the discovery that acetylsalicylic acid (ASA or aspirin), salicylic acid (SA) and related salicylate esters and their pharmaceutically acceptable salts, when coadministered in effective amounts with a drug or other bioactive agent which typically (in the absence of the salicylate compound) produces significant hepatotoxicity as a secondary indication, will substantially reduce or even eliminate such hepatotoxicity. Favorable therapeutic intervention results from the use of the present invention having the effect of reducing hepatotoxicity associated with the administration of certain drugs and other bioactive agents and in certain instances of allowing the administration of higher doses of a compound which, without the coadministration, would produce hepatotoxicity which limits or even negates the therapeutic value of the compound. The invention also relates to methods of reducing the likelihood of a patient at risk for non-alcoholic fatty liver diseases (NAFLD), including non-alcoholic steatohepatitis (NASH), or treating NAFLD or NASH including primary NASH, NASH secondary to liver transplantation (NASH post-liver transplantation) or cirrhosis represent alternative aspects of the present invention.

The disclosure relates, in general, to treatment of fatty liver disorders comprising administering compositions comprising cysteamine products. The disclosure provides administration of enterically coated cysteamine compositions to treat fatty liver disorders, such as non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH).

The sulfated oxysterol 5-cholesten-3β, 25-diol 3-sulphate, a nuclear cholesterol metabolite that decreases lipid biosynthesis and increases cholesterol secretion and degradation, is provided as an agent to lower intracellular and serum cholesterol and/or triglycerides, and to prevent or treat lipid accumulation-associated inflammation and conditions associated with such inflammation. Methods which involve the use of this sulfated oxysterol to treat conditions associated with high cholesterol and/or high triglycerides and/or inflammation (e.g. hypercholesterolemia, hypertriglyceridemia, non-alcoholic fatty liver diseases, atherosclerosis, etc.) are also provided.

The present invention discloses compounds of Formula (I), and pharmaceutically acceptable salts and esters thereof:

which inhibit the Apoptosis signal-regulating kinase 1 (ASK-1), which associated with autoimmune disorders, neurodegenerative disorders, inflammatory diseases, chronic kidney disease, cardiovascular disease. The present invention further relates to pharmaceutical compositions comprising the aforementioned compounds for administration to a subject suffering from ASK-1 related disease. The invention also relates to methods of treating an ASK-1 related disease in a subject by administering a pharmaceutical composition comprising the compounds of the present invention. The present invention specifically relates to methods of treating ASK-1 associated with hepatic steatosis, including non-alcoholic fatty liver disease (NAFLD) and non-alcohol steatohepatitis disease (NASH).

The invention discloses a method for establishing a non-alcoholic fatty liver disease combined with viral hepatitis mouse model. The method comprises the steps that high-fat feed is used for feeding a C3H/HeN small mouse for 12 weeks, the body weight, the liver weight, transaminase, the glucolipid metabolism index and liver histological change of the small mouse are observed, and a non-alcoholic fatty liver disease small mouse is cultivated. Then 10 PFU of MHV-3 infected mice are selected, and the survival rate, the liver histology and intrahepatic virus replication of the infected mice are observed, so that the non-alcoholic fatty liver disease combined with viral hepatitis mouse model similar to a human disease process is established. The established model provides a forceful tool for virus dynamics, immunological changes and prevention and control measures systematically studying non-alcoholic fatty liver disease combined with viral hepatitis.

The present invention provides a compound of Formula (I) or pharmaceutical acceptable thereof, wherein ‘R’ is herein described. In addition, the invention relates to composition comprising effective therapeutic amount of compound of formula (I) and methods of using the compounds for treating or prevention disorder such as nonalcoholic fatty liver disease (NAFLD) including fatty liver (steatosis), nonalcoholic steatohepatitis (NASH), and cirrhosis (advanced scarring of the liver).

Embodiments of the present invention provide a magnetic anastomosis device (MAD), a delivery catheter for the MAD, and a method for treating at least one of diabetes, obesity, digestive disease, and non-alcoholic fatty liver disease. In embodiments of the present invention, a pair of the MADs are delivered in body lumen by endoscopic and/or laparoscopic techniques. An anastomosis between two adjacent body lumens is formed by compression of the pair of MADs followed by necrosis and regeneration of the lumen tissue. The bodily fluids are then redirected through the formed anastomosis to relieve disease symptoms.

The invention relates to an enzymatically decomposed clam oligopeptide having a recovery effect on a non-alcoholic fatty liver disease (NAFLD) cell model. The clam oligopeptide is characterized by comprising an amino acid sequence of Gln Leu Asn Trp Asp. The invention also relates to a preparation method of the enzymatically decomposed clam oligopeptide having the recovery effect on the NAFLD cell model. Compared with the prior art, the following advantages can be achieved: the NAFLD cell model is established by virtue of induction of palmitic acid and the damaged liver cells in a body are simulated sufficiently, and the result indicates that the TG content of the in-vitro NAFLD cell model established 48 hours after induction by 15 micrograms/milliliter palmitic acid increased remarkably in comparison with that of normal liver cells; oil red O staining shows that the number of intracellular lipid droplets of the model group is increased in contrast with that of the cells of a normal group, and the cell mortality rate is low and the repeatability is good, and therefore, the modeling method is simple, convenient and feasible; meanwhile, the enzymatically decomposed clam oligopeptide having the obvious recovery effect on the NAFLD cell model can be separated out from clams.