78 results about "Hepatic lipid" patented technology

The present invention relates to an oral formulation to lower serum or hepatic lipid and triglyceride concentrations, hepatic inflammation and/or insulin resistance in a patient comprising live feruloyl esterase producing microorganisms alone or in association with a pharmaceutically acceptable carrier resistant to gastric conditions, and wherein the microorganisms are wild type, genetically modified, or combination thereof. The present invention is also directed to an oral formulation to lower serum or hepatic lipid and triglyceride concentrations, hepatic inflammation and/or insulin resistance in a patient, which comprises polymeric microcapsules containing live feruloyl esterase producing microorganisms in suspension in a pharmaceutically acceptable carrier, wherein said microcapsules are semipermeable and resistant to gastro-intestinal conditions, and wherein said microorganism are wild type, genetically modified, or combination thereof as well as methods of preventing or improving liver diseases and disorders and uses thereof.

The invention relates to an application of nicotinamide riboside in preparing drugs for treating non-alcoholic steatohepatitis. According to the application, a non-alcoholic steatohepatitis animal model is adopted to prove that the nicotinamide riboside is capable of reducing the liver lipid content, the liver inflammations and the liver fibrosis degree of the animal model and prompt that the nicotinamide riboside can be applied to preparing the drugs for treating the non-alcoholic steatohepatitis. The application of the nicotinamide riboside is expanded, a new way is provided for treating the non-alcoholic steatohepatitis, and therefore, the non-alcoholic steatohepatitis can be prevented and prognosed favorably.

A method for treating or preventing non-alcoholic fatty liver disease is disclosed. By promoting the expression of six-transmembrane protein of prostate 2 (STAMP2) in liver cells, the method can be useful in improving the abnormalities in lipid metabolism in the liver, and also improving insulin resistance, thereby preventing or treating a non-alcoholic fatty liver disease.

The invention provides an application of GGPPS serving as a target for treating non-alcoholic fatty liver disease. A GGPPS antagonist disclosed by the invention can reduce genetic expression related to lipid accumulation of the liver. The liver-specific knockout GGPPS disclosed by the invention is capable of retarding the lipid accumulation and degeneration of the liver, reducing the level of aspartate transaminase (AST) and alanine aminotransferase (ALT) and protecting the liver functions.

The present invention provides a method for preventing or ameliorating obesity, for inhibiting accumulation of visceral fat, for inhibiting accumulation of liver lipid, for preventing or ameliorating fatty liver, including using a material for a pharmaceutical product or food, which has inhibitory actions on body weight increase, accumulation of visceral fat and accumulation of liver lipid. The present invention is also directed to a method for preventing or ameliorating obesity, a method for inhibiting accumulation of visceral fat, a method for inhibiting accumulation of liver lipid, and a method for preventing or ameliorating fatty liver, which methods include administering potassium alginate to a subject in need thereof or having the subject take potassium alginate.

The invention discloses application of a baicalein extract in preparation of a medicament for controlling hyperlipidemic fatty liver. The baicalein extract is proved to have effect of preventing the hyperlipidemic fatty liver in pharmacological experiments, and is particularly used for reducing the liver weight and the liver coefficient of rats and reducing the content of the blood fat and liver lipid.

The invention discloses an application of dioscin in preparation of a liver-protecting pharmaceutical preparation. The pharmaceutical preparation can obviously inhibit increase of activity of aminotransferase and lactate dehydrogenase due to medicines (carbon tetrachloride or paracetamol) and alcohol, and reduce the liver indices, thereby performing the liver-protecting function; the pharmaceutical preparation can enhance the activity of SOD, reduce the content of MDA, increase the content of GSH and inhibit liver lipide overoxidation induced by medicines (carbon tetrachloride or paracetamol); and the pharmaceutical preparation can also reduce the content of TG and TC and inhibit the liver steatosis caused by alcohol. The dioscin can be used as the raw material to prepare various preparation formulations for clinic applications according to pharmaceutic related requirements and clinic requirements, such as tablets, capsules, injections, oral liquids, granules and the like. The invention is safe (no toxicity or side effect), convenient, economical and the like.

The invention discloses application of E3 ubiquitin ligase RNF14 in preparation of a drug for treating fatty liver and related diseases, and belongs to a new use of the RNF14. In the present invention, a L02 cell line overexpressed by human normal liver cell line L02 and the RNF14 is used as an experimental object, and the gene function of the RNF14 is studied by a fatty liver cell model co-induced by palmitic acid (PA) and oleic acid (OA). The study finds that RNF14 overexpression can significantly improve lipid accumulation in liver cells, indicating that the RNF14 can protect the liver cells from fatty degeneration, and the RNF14 plays a protective role in liver lipid metabolic diseases. Since the RNF14 is an endogenous protein kin the body, the RNF14 is highly safe as the drug.

The invention relates to application of great burdock root polysaccharide in preparation of a drug for treating non-alcoholic fatty liver disease (NAFLD). The great burdock root polysaccharide provided by the invention is prepared from great burdock roots, and is prepared by carrying out enzyme inactivation, extraction, filtration, suction filtration, centrifugation, ethanol precipitation, macroporous resin decolorization, trichloroacetic acid deproteinization and the like; and the great burdock root polysaccharide has an average molecular weight of 3000-5000 Da. According to the application of the great burdock root polysaccharide in the preparation of the drug for treating the NAFLD, NAFLD mouse models are established through induction by high fat diet (HFD), and are used for study on activity of the burdock root polysaccharide in NAFLD treatment; and it is found that the great burdock root polysaccharide is capable of significantly reducing liver weight and liver index so as to reduce accumulation of liver lipid, alleviate liver damage and regulate inflammatory factors so as to achieve positive therapeutic effects on the NAFLD.

The present invention provides a method to prepare polysaccharides from Ganoderma lucidum. The prepared polysaccharides can reduce liver weight and liver lipid content in humans and animals. The prepared polysaccharides can therefore be used to prevent and treat fatty liver disease.

The invention discloses a function and application of a (pro) resin receptor [(pro) resin receptor, (P) RR] inhibitor in nonalcoholic fatty livers and fat diseases. Under the background of C57 mice, (P) RR liver specificity knock-out/know-down mice are used as experimental objects, according to a fat mouse model which is induced through high-fat feed, and it is proved through a result that the size of the liver (P) RR knock-out mice is remarkably small, and the fat tissue in the mouse bodies is remarkably reduced; after the mice are fed with the high-fat feed, the increase amplitude of the weight of the mice is low, fat is not generated, the blood glucose content is low, through results of oil red dyeing, liver lipid measurement and the like, it is explained that the liver function of theliver (pro) resin receptor knock-out mice is remarkably better than that of contrasted fatty mice, the fatty liver lesion of the mice is remarkably improved, the stored lipid is remarkably reduced, and the blood glucose content is lowered. Therefore, (P) RR can be used as a medicine target of screening treatment of type-II diabetes, nonalcoholic fatty livers and fat diseases, and the inhibitor of(P) RR can be applied to preparation of medicine for treating type-II diabetes, nonalcoholic fatty livers and fat diseases.

The invention discloses application of PSMB8 and a PSMB8 inhibitor to preparation of medicine for treating fatty liver and related diseases. Primary hepatocytes of C57BL/6 wild type mice and PSMB8 knock-down C57BL/6 mice are separated; the functions of PSMB8 gene are studied by a palmitate and oleic acid stimulation induced liver cell lipid accumulation model. The result proves that when the PSMB8expression is lowered, the PA+OA stimulation induced primary hepatocyte lipid accumulation is obviously reduced, i.e., the PSMB8 gene can promote the development and progression of fatty liver and related diseases; in an HFHC (high fat and high cholesterol) induced WT mouse fatty liver disease model, PR-957 can obviously inhibit HFHC induced weight increase, white grease increase and liver lipidaccumulation; the development and progression of the fatty liver and related diseases are inhibited. Therefore the PSMB8 provides a target for developing medicine for preventing, relieving and/or treating the fatty liver and related diseases.

The invention discloses functions and applications of RECS1 in the fatty liver and the diabetes mellitus, and belongs to the field of functions and applications of genes. An RECS1 gene knockout mouse and a wild type C57 mouse are used as experimental subjects, through a model of the fatty liver and the diabetes mellitus which are induced by high-fat diets, the result shows that compared with the wild type C57 mouse, glycometabolism of the RECS1 gene knockout mouse is disorderly, fatty liver lesion is severe, and lipid accumulation is remarkably increased. It explains that the RECS1 has the adjustment and control capacity for maintaining the steady state of glycometabolism and has the liver lipid removal capacity and fatty liver forming resistance. Thus, the functions of the RECS1 in the fatty liver and the diabetes mellitus are found and the functions are mainly reflected in the effects on alleviating fatty liver and diabetes mellitus. For the functions of the RECS1, the RECS1 can be used for preparing medicine for treating the fatty liver and the diabetes mellitus.

The invention relates to Crtc2/Creb compound blocking polypeptide and derivative medicinal polypeptide and application thereof. The amino acid sequence of the Crtc2/Creb compound blocking polypeptideis shown in SEQ ID NO:1, and the Crtc2/Creb compound blocking polypeptide can be used for preparing drugs for treating obesity, fatty liver, hyperlipemia and type-2 diabetes. The medicinal polypeptidecomprises a blocking function structure area and a membrane penetrating function structure area which are formed by a targeted-inhibition Crtc2/Creb compound, wherein the amino acid sequence of the blocking function structure area formed by targeted-inhibition Crtc2/Creb compound is shown in SEQ ID NO:1. The medicinal polypeptide has obvious effects on adjustment of blood sugar and blood fat andinhibition of liver lipid deposition and can be used as a treatment drug for treating metabolic diseases such as obesity, fatty liver and type-2 diabetes alone or in other auxiliary treatment modes.

The present invention discloses an application of a pleurotus eryngii mycelium polysaccharide from solid-state fermentation (PESF). The active polysaccharide (PESF) with a hypolipidemic function is produced by a solid-state fermentation method of pleurotus eryngii mycelia. In a mouse model in vivo hypolipidemic mechanism, an oral administration of a certain dose of the PESF can regulate intestinalmicroflora, significantly promotes growth of Lactobacillus and inhibits major micro-organism genus of staphylococcus, corynebacterium, aerococcus, etc., thus restores intestinal flora imbalance caused by a high-fat diet to a certain degree, finally inhibits absorption of exogenous lipids in intestinal tract, and thus reduces accumulation of blood lipids and liver lipids in body. The pleurotus eryngii polysaccharide is analyzed and confirmed to have biofunctional activity of regulating structure and functions of the intestinal microflora, and a significant correlation is found between polysaccharide hypolipidemic activity and polysaccharide intestinal microflora-regulating function.

The invention relates to an extract for promoting lipid metabolism of the liver, resisting inflammation and reducing the enzyme content, and a preparation thereof. The preparation method comprises thesteps that firstly, multiple active substances in matsutake are extracted; and then the active substances are mixed with yeast for fermentation culture, so that the live yeast digests, absorbs and converts the active substances into substances of an organic mode closer to original biological activity and nutrition, accordingly the absorption mechanism is enhanced, and the biological value is improved. Animal experiments prove that the extract provided by the invention has a positive effect on regulating the blood lipid level, can inhibit amplification of inflammatory signals so as to improvelipid accumulation of the liver and inflammatory responses, and accordingly plays a inflammation resistant role; and the extract can effectively reduce the content of GOT and GPT in serum of a mouse with non-alcohol fatty liver disease and has the effect of relieving hepatocyte injury. In the preparation method provided by the invention, extracting the active components of the matsutake through chemical components is avoided, the preparation process is simple, and the large-scale production requirement is met.

The invention relates to an application of a cordate houttuynia extract as an adenylate-activated protein kinase activator in preparing a medicine for improving metabolic syndrome. The cordate houttuynia extract is a water-soluble extract of a dried part of a houtuynia sulfite plant, an extraction solvent is distilled water, an extraction ratio is 20:1, and the appearance of the product is yellow-brown powder; The cordate houttuynia extract acts to protect mitochondrial function and anti-oxidation by activating an AMPK-PGC-1alpha/Nrf2 signaling pathway and simultaneously up-regulating mitochondrial production and biphasic enzyme pathways, further improves the metabolic disorders associated with hyperlipidemia, liver lipid accumulation and cardiac dysfunction, and delays the occurrence anddevelopment of metabolic syndrome. The cordate houttuynia extract has no obvious side effects, and is a safe, simple and effective drug.

The present invention provides a method for treating type 1 diabetes, hyperlipidemia or hepatic lipid accumulation by using dehydroeburicoic acid, as well as a method for decreasing levels of blood glucose, plasma total cholesterol, and triglyceride, and increasing insulin levels; and a method for decreasing hepatic balloon degeneration; and increasing expression levels of membrane GLUT4 and phospho-Akt in myotubes; and enhancing expression levels of membrane glucose transporter 4 (GLUT4) in skeletal muscle, and phospho-AMPK in both skeletal muscle and liver tissue using dehydroeburicoic acid.

The invention discloses magnolol and honokiol and a method for preventing and treating fatty liver syndrome of laying hens by using the magnolol and the honokiol. When the magnolol and the honokiol are applied to daily ration of laying hens, liver lipid accumulation can be effectively reduced, and the serum triglyceride level can be reduced. The expression of genes FASN and SCD1 related to fatty acid synthesis of the liver of the laying hen is remarkably reduced. The egg laying performance reduction of the cage-rearing laying hens caused by the fatty liver syndrome is relieved; the death and culling rate is reduced. And the magnolol and the honokiol have a synergistic effect in regulating liver lipid metabolism. The invention discloses an appropriate composition proportion of the magnololand the honokiol in preparation of feed additives or medicines for preventing and treating fatty liver syndrome of laying hens for the first time.

The invention discloses application of malonic-acid-modified fullerene C70 in preparation of a medicine for treating the non-alcoholic fatty liver disease. The medicine that uses the C70-malonic acidderivative as the active ingredient and is used for preventing, relieving and/or treating the non-alcoholic fatty liver disease and related diseases has the following advantages: firstly, the pharmacodynamic effect is obvious, the C70-malonic acid derivative can obviously inhibit lipid accumulation in primary hepatocytes of mice and obvious changes can be seen in 10 micrometers; in addition, the C70-malonic acid derivative also has an obvious improvement effect on liver lipid accumulation and fibrosis generated by HFHC diet induction; secondly, the malonic-acid-modified fullerene C70 can effectively reduce the damage of a carbon cage in a fullerene modification process, so that the pharmacodynamic activity of the fullerene body is better retained; and thirdly, the C70-malonic acid derivative has a determined molecular structure, problems that other water-soluble fullerene derivatives have no determined structure and are difficult in quality control are solved, and the patent medicine is realized conveniently.

The invention belongs to the field of pharmaceutical chemistry, and in particular relates to novel applications of pegylated curcumin derivative, especially the applications of the pegylated curcumin derivative in preparing medicines for preventing or treating fatty liver diseases and atherosclerosis. The experiment proves that the pegylated curcumin derivative can reduce the level of triglyceride in the blood, activate the phosphorylation of cyclic-AMP response element binding protein (CREB), negatively regulate nuclear transcription receptor PPAR gamma closely related to lipid metabolism, reduce the CD36 expression of the lever tissue caused by high fat diet, reduce the intake of fatty acid of the liver, reduce the lipid formation of the liver, and improve the fatty degeneration of the liver. The pegylated curcumin derivative further can improve the level of high density lipoprotein cholesterol, promote the reverse cholesterol transport, reduce the CD36 expression of macrophages, reduce the intake of oxidized low density lipoprotein, alleviate the bubblization of the macrophages, and reduce the deposition of lipid on the endangium and the formation of artery atherosclerotic plaque.

The present invention provides an agent for preventing the increase in a body weight (or for decreasing a body weight) or an anti-obesity agent each comprising at least one component selected from the group consisting of EPA and pharmaceutically acceptable salts, esters and derivatives thereof as an active ingredient for obesity in which the increase in the formation of hepatic lipid or the occurrence of fatty liver is mild, preferably the increase in the formation of hepatic lipid or the occurrence of fatty liver is not observed.