138 results about "Fat diet" patented technology

The application discloses a Weizmannia coagulans with fat-reducing and weight-reducing functions, and belongs to the technical field of microorganisms. The Weizmannia coagulans screened by the application can inhibit the content and activity of fat synthesis enzyme on the basis of reducing blood fat and weight, can relieve liver damage caused by high-fat diet, has excellent acid tolerance, bile salt tolerance and high fat hydrolysis capacity, and is a multifunctional Weizmannia coagulans, and has a wide application prospect in the preparation of fat-reducing, weight-reducing and weight-losing products.

The present application relates to use of Ligilactobacillus salivarius in preparing a drug for preventing and / or treating diseases associated with overweight and / or obesity . The strain can inhibit the weight growth of a high-fat diet-induced obesity model mouse, reduce the blood lipid level of the high-fat diet-induced obesity model mouse, improve the liver injury index of the high-fat diet-induced obesity model mouse, reduce the area of white adipose cells of the high-fat diet-induced obesity model mouse, improve the colon GLP-1 level of the high-fat diet-induced obesity model mouse, improve the intestinal flora imbalance of the high-fat diet-induced obesity model mouse, and improve the liver glycolipid metabolism of the high-fat diet-induced obesity model mouse; and reduce the waist circumference, hip circumference, body fat mass, BMI, and weight of overweight and overweight and / or obesity volunteers, and maintain the muscle content, promoting overweight and overweight and / or obesity people to carry out safe, effective, and sustainable weight management.

The application discloses a method for constructing a mouse model of atherosclerosis induced without high-fat diet, and relates to the technical field of disease model construction.The mouse model construction method provided by the application obtains a mouse model that spontaneously exhibits atherosclerosis symptoms without high-fat diet induction.The mouse model of atherosclerosis induced without high-fat diet can be used for researching the pathogenesis of atherosclerosis and screening and evaluating drugs for atherosclerosis.

The invention provides an application of Fuxia dothidei YG0564 in preparation of a composition for preventing, relieving and / or treating individual sexual precocity, growth and development impairment and / or obesity. It is found that the Fuxia dolferi YG0564 can effectively prevent, relieve and / or treat sexual precocious puberty, growth and development damage and / or obesity of individuals, and especially has a remarkable improvement effect on the diseases caused by high-fat diet. For sexual precocious puberty or damaged growth and development induced by high-fat diet, the Fuxia dolferi YG0564 is applied to individuals in the early stage or early stage of puberty, the protection effect of the Fuxia dolferi YG0564 can be continued to the adult stage, and the fundamental problem of growth and development is solved through staged medication. Therefore, a potential probiotic treatment scheme is provided for precocious puberty, growth and development damage and / or obesity of individuals, and the probiotic composition is convenient to apply, high in patient acceptability and low in treatment cost, so that the probiotic composition has good clinical transformation value and social benefits.

The invention discloses application of a lucid ganoderma extract combined with clostridium butyricum in preparation of fat-reducing food or medicine. The invention finds that the ganoderma lucidum extract is combined with clostridium butyricum for use, so that the weight gain of a mouse induced by high-fat diet can be obviously slowed down, the epididymal fat weight of the high-fat mouse is reduced, and the lipid accumulation in the liver and serum of the mouse is reduced; according to the present invention, with the application of the polypeptide, the fat cell size is reduced, the expression of the key gene mRNA related to lipid metabolism and synthesis in the mouse liver is reduced, the intestinal flora of the mouse is regulated, the obesity can be well improved, and the important application prospect in the preparation of the drugs or food for treating diabetes, reducing blood fat, obesity and non-alcoholic fatty liver disease is provided.

The invention belongs to the field of biotechnology and nutritional medicine, relates to a maternal obesity intervention preparation, and particularly relates to a preparation method of a plant embryo fermentation product and application of the plant embryo fermentation product in blocking of trans-generation delivery metabolic diseases. FWG is prepared through a probiotic fermentation technology, obesity, glucose and lipid metabolism disorder and oxidative stress induced by high-fat diet of a parent body can be remarkably improved, and cross-generation transmission of metabolic diseases is blocked by adjusting composition of intestinal flora of the parent body and offspring and a hypothalamic PI3K-Akt signal channel. The invention reveals that maternal FWG intervention passes through a mechanism that a PI3K-Akt pathway is dominated and multiple pathways are coordinated on the transcriptome level for the first time, the HFD-induced offspring hypothalamus metabolism programming abnormality is reversed, and a new central regulation target is provided for cross-generation metabolic disease prevention. The FWG is a wheat processing byproduct, is free of chemical additives, is suitable for long-term dietary supplement, is a natural and safe nutrition intervention scheme, and is suitable for the field of maternal and infant health.

The application discloses application of O-acyl-alpha-hydroxy acid compounds in weight loss and lipid reduction, and belongs to the fields of biological medicine manufacturing, biological medicine use and functional food development. The O-acyl-alpha-hydroxy acid compounds can inhibit weight growth of high-fat diet-induced obese model mice and reduce body fat. Compared with GLP-1 receptor weight loss drugs which achieve the effect of reducing weight by inhibiting appetite, the O-acyl-alpha-hydroxy acid compounds are not dependent on appetite inhibition, and can reduce side effects such as gastrointestinal discomfort and muscle loss caused by inhibiting appetite. When combined or sequentially administered with GLP-1 drugs, the O-acyl-alpha-hydroxy acid compounds can maintain or enhance the weight loss effect while improving the side effects caused by GLP-1, and can prevent the risk of significant weight rebound after stopping GLP-1 by maintaining body weight. The application provides a safe and effective new strategy for weight loss and lipid reduction.

The application discloses a construction method of a fat-targeted gene therapy vector. The method comprises the following steps: obtaining a fat tissue-specific promoter sequence; obtaining a shRNA coding sequence targeting a Tks4 gene; cloning the promoter sequence and the shRNA coding sequence into an adeno-associated virus vector skeleton to construct a recombinant expression vector; and co-transfecting the recombinant expression vector and an auxiliary plasmid into a packaging cell to package and purify a recombinant adeno-associated virus particle. The vector constructed by the application adopts an adiponectin promoter to drive the expression of miR30-shRNA targeting the Tks4, and can be specifically expressed in fat tissues and livers after being injected through a tail vein, significantly inhibits fat cell hypertrophy and systemic fat accumulation induced by a high-fat diet, reduces the serum cholesterol level, does not cause an immune inflammatory reaction, does not affect sugar metabolism, and is not expressed in non-target tissues. The application provides a safe and efficient new strategy for the gene therapy of obesity, hyperlipidemia, fatty liver and related metabolic diseases.

The invention discloses an application of isoquercitrin in preparation of a medicine for improving insulin resistance and diabetes-related liver diseases, and belongs to the technical field of medicines. According to the application, a high-glucose and high-fat diet and streptozotocin combined method is adopted to successfully construct a type 2 diabetes mouse model; experiments find that the isoquercitrin can effectively relieve the symptoms of weight loss and water intake increase of T2DM mice, significantly reduce the fasting blood-glucose level and improve abnormal glucose tolerance; the isoquercitrin can reduce the liver index of a T2DM mouse, relieve fatty degeneration of the liver and repair a liver cell structure; by activating a PI3K / AKT signal channel, the isoquercitrin up-regulates the expression levels of PI3K, p-AKT, p-GSK3 and GLUT4 and down-regulates the expressions of GSK3 and PEPCK at the same time, so that the insulin resistance of T2DM mice is effectively improved, the fatty degeneration of the liver is improved, and the isoquercitrin has a protection or repair effect on liver injury.

The present invention relates to a Korean microbiome-derived Clostridium butyricum strain having anti-obesity efficacy and a use thereof. The strain has an excellent effect of reducing the body weight and adipose tissue weight of experimental animals compared to a control group (strain-untreated) under high-fat diet conditions, has an excellent effect of reducing the content of total cholesterol, triglycerides, low-density lipoprotein (LDL), leptin, alanine aminotransferase (ALT), and aspartate aminotransferase (AST) in serum, and has an excellent effect of reducing blood glucose and increasing the content of glucagon-like peptide-1 (GLP-1) in an oral glucose load test, and is thus expected to be effectively used as an ingredient in a composition for preventing, alleviating, or treating obesity and metabolic diseases caused by obesity.

The invention relates to the technical field of biological medicines, in particular to application of tetramer-form pyruvate kinase type 2 (PKM2) in preparation of a medicine for treating obesity. Pyruvate kinase type 2 is a key enzyme in a glycolytic pathway and has two conformations of dimer and tetramer, and the tetramer-form enzyme has high activity. The invention discovers that the PKM2 tetramer stabilizer TEPP-46 can stabilize PKM2 in a high-activity tetramer state and improve obesity-related metabolic disorder induced by high fat diet. The invention discloses a new way for regulating and controlling energy metabolism by stabilizing the form of the PKM2 tetramer, and provides a new medicine application direction for treating obesity and related metabolic diseases.

This invention discloses the application of α-hydroxyisocaproic acid in weight loss and lipid reduction, belonging to the fields of biopharmaceutical manufacturing, biomedical applications, and functional food development. This invention confirms the application of α-hydroxyisocaproic acid in weight loss; this compound can inhibit weight gain in high-fat diet-induced obese mouse models, reduce body fat, and decrease the area of ​​adipocytes in high-fat diet-induced obese mouse models. Compared to GLP-1 receptor weight-loss drugs that reduce weight by suppressing appetite, the compound α-hydroxyisocaproic acid intervenes in and prevents obesity by accelerating fat metabolism, thereby achieving weight reduction. This invention provides a safe and effective new strategy for weight loss and lipid reduction.

The invention relates to a construction method and application of a high-fat diet induced mouse model with abnormal reproductive endocrine metabolism. The method comprises the following steps that after being born, a mouse is fed with high-fat milk for 3 weeks and then fed with high-fat feed for 5 weeks, and the high-fat diet induced abnormal reproduction metabolism mouse model is obtained when the mouse is 8 weeks old. According to the scheme provided by the invention, the high-fat mouse can be at the optimal fertility age in the modeling period and is closer to the condition of a clinically right-age obese patient, the fertility women in the clinical fertility age period are accurately simulated, and the age interference caused by the long modeling period of a traditional model is overcome.

The invention discloses application of knockout or inhibition of intestinal epithelium Ufbp1 gene expression in preparation of medicines for preventing and / or treating obesity, and belongs to the technical field of biological medicines. In order to solve the problems of limited effect, many side effects and the like of the existing obesity treatment means, the invention provides Ufbp1 specifically expressed by intestinal epithelial cells as a new anti-obesity intervention target for the first time. By knocking out or inhibiting intestinal epithelium Ufbp1, weight gain, adipose tissue accumulation, hyperlipidemia, liver fatty degeneration and insulin resistance induced by high fat diet can be effectively resisted. The action mechanism is related to influence on secretion of intestinal apolipoprotein ApoB48 / ApoA1 and further regulation and control of whole body lipid metabolism. The invention provides a clear target and theoretical basis for developing novel anti-obesity therapies such as small-molecule inhibitors and nucleic acid drugs of targeted intestinal epithelium Ufbp1, and has important clinical transformation prospects.

The invention relates to the technical field of traditional Chinese medicine extracts, in particular to an application of a ligusticum wallichii alcohol extract and an active monomer thereof in preparation of a product for relieving or treating food-borne obesity. Experimental research finds that when the ligusticum wallichii alcohol extract is singly used, the mRNA expression level of POMC in hypothalamus of a high-fat diet induced food-borne obesity mouse can be reduced, the alpha-MSH level in the hypothalamus can be improved, appetite can be effectively inhibited, body weight can be reduced, meanwhile, the number of lipid droplets in the liver can be reduced, and the ligusticum wallichii alcohol extract has the effects of relieving and treating food-borne obesity, preventing and treating hyperlipidemia and the like. And the application potential of liver tissues is improved, and a new direction and theoretical support are provided for treating food-borne obesity and expanding the medication range of ligusticum wallichii.

The present application provides a polypeptide composition with anti-obesity effect, which is composed of capsaicin and polypeptides, and the amino acid sequence of the polypeptides comprises any one or more of SEQ ID NO. 1 to SEQ ID NO. 8. The polypeptides of sequences 1-8 are mixed uniformly at a mass ratio of 1-20:1-4:1-2:1-4:1:1:1:1, and the capsaicin is mixed with the mixed polypeptides at a ratio of 2-12:100 (w / w). The polypeptide composition proposed in the present application, in combination with capsaicin, not only promotes the weight loss effect of capsaicin, but also significantly reduces the fat index of the test mice after use, and can significantly reduce the total cholesterol concentration in the liver and the liver triglyceride concentration under a high-fat diet.

The invention discloses application of rebaudioside B in preparation of a medicine for preventing and treating metabolism-related osteoarthritis, and belongs to the technical field of biological medicine. Animal experiments prove that the application of the natural micromolecular monomer rebaudioside B in preventing and treating osteoarthritis induced by high fat diet shows that the rebaudioside B can realize a cartilage protection effect by improving lipid deposition, regulating inflammatory response and promoting cartilage matrix synthesis; the method is suitable for intervention and prevention and treatment of metabolism-related osteoarticular diseases. The invention provides a set of intervention scheme with clear structure, multi-target action, clear mechanism and controllable path for the prevention and treatment of metabolism-related osteoarthritis, and provides a scientific basis for the application of rebaudioside B in the prevention and treatment of metabolism-related osteoarthritis.

The invention relates to the technical field of medicines, in particular to application of an integrin beta3 inhibitor RGDfK in preparation of a medicine for treating metabolic dysfunction related fatty liver diseases. The RGDfK provided by the invention can inhibit palmitoylation and membrane localization of CD36 in liver tissues of mice with fatty liver diseases related to metabolic dysfunction induced by high fat diet feeding, so that lipid uptake of the liver is inhibited. Experimental results show that RGDfK can improve obesity and insulin resistance of mice with metabolic dysfunction-related fatty liver diseases, can improve fat accumulation, fibrosis and inflammatory infiltration of liver tissues of the mice with fatty liver diseases, and is expected to become a new medicine for treating the metabolic dysfunction-related fatty liver diseases.

Embodiments of the methods of the disclosure and compositions related to managing the microbiota in an individual having at least one social behavior deficit. In particular embodiments, an individual has at least one social behavior deficit and was born to a mother who was obese, overweight, or consumed a high-fat diet during pregnancy or carries mutations associated with neurodevelopmental behaviors. In particular embodiments, an effective amount of Lactobacillus reuteri is provided to the individual having at least one social behavior deficit to improve at least one symptom of a social behavior deficit.

The application belongs to the technical field of cell biology, and particularly relates to a solution rich in Sargassum fusiforme nano-vesicles and a preparation method and application thereof. The solution rich in Sargassum fusiforme nano-vesicles is prepared by a differential centrifugation combined with hollow fiber membrane concentration, and the obtained solution rich in Sargassum fusiforme nano-vesicles can play an anti-inflammatory role, inhibit high-fat diet induced fatty liver and osteoporosis, and can also be used for preparing a mask with soothing, moisturizing and anti-wrinkle effects.

The invention provides a bisphenol A induced rat benign prostatic hyperplasia model and a construction method, and relates to the technical field of animal models. The method comprises the following steps: S1, selecting rats which are 8-9 months old and 9-10 weeks old, and adaptively feeding the rats in a suitable environment for 7 days or more; s2, jointly applying high-fat feed and bisphenol A to the adaptively fed rats to induce benign prostatic hyperplasia; the induction time is 60-80 days, and performing biological index evaluation after the induction is completed. The exposure level of low-dose BPA adopted by the invention is closer to the actual environment exposure level of people, and a main exposure way is simulated through oral gavage. The model constructed by the method can better simulate the real process of chronic and low-dose exposure pathopoiesis of the environmental endocrine disrupter in etiology, and provides an experimental tool with more practical significance for related risk evaluation.

The invention relates to application of DOP (dioctyl phthalate) in preparation of medicines for regulating lipid metabolism, resisting diabetes and resisting intestinal microorganisms. The DOP significantly alleviates DIO by inhibiting the expansion of lipid droplets (LD) in white adipose tissue (WAT) and down-regulating LD-related genes (including PLIN2 and PLIN3). DOP can target visceral fat, significantly improve visceral fat hypertrophy and hyperplasia (especially epididymal fat EAT is taken as aboriginal) induced by high fat diet (HFD), inhibit formation of lipid droplets, reduce expression of lipid droplet coating protein PLIN2 / 3, and block the accumulation process of lipid droplets (LD). Consistent with we have observed that DOP also inhibits the expression of genes associated with lipid synthesis and adipogenesis, including Fabp1, Fast, Ldlr, Cebpb, and Dio2. These findings show that DOP can improve diet-induced obesity by regulating lipid droplet-related pathways.

The invention discloses a method for establishing a cross-generation genetic model of rats attacking nutritional imbalance twice, and relates to the technical field of animal model establishment, and the key points of the technical scheme are as follows: starting from the angle of paternal line, selecting SD male rats of 3 weeks old, adaptively feeding for 1 week, then starving and feeding for 4 weeks, and finally feeding for 17 weeks with high fat, evaluating the phenotype of fatty liver, and establishing the cross-generation genetic model of rats attacking nutritional imbalance twice. And establishing a parent (F0) which attacks the nutritional imbalance twice. After the parent generation (F0) and the normal exposed parent generation (F0) are mated, the male offspring (F1) is given with common diet and high-fat diet respectively, then after the parent generation (F0) and the normal exposed female generation (F0) are mated, the male offspring (F2) is given with common diet and high-fat diet respectively. According to the method, the fatty liver phenotype of the male rat of the F0-F2 model can be determined, and the glucolipid metabolism pathway and function change of the parental generation and the offspring generation can be known through an isotopic tracing technology, metabonomics and transcriptomics.

Targeting mitochondrial function is a strategy for preventing metabolic disorders, but restoring mitochondria diurnal regulation remains to be explored. Using targeted metabolomics, we identified 24-hour mitochondrial rhythms promoted by nocturnal time-restricted feeding (TRF) in mice fed a high-fat diet (HFD). Preceding its metabolic benefits, TRF promoted mitochondrial daily rhythms by converging on the enzyme dihydroorotate dehydrogenase (DHODH), which coordinates pyrimidine biosynthesis and mitochondrial oxidative metabolism. The inhibition of DHODH activity by the short half-life inhibitor BAY-2402234 modulated mitochondrial oxidative metabolism, thereby preventing diet-induced obesity, but only when injected at the transition between night and day. This timed inhibition of DHODH promoted oscillations in mitochondrial metabolic pathways and oscillations in the CoQ / CoQH2 ratio, improving metabolic adaptation to the HFD challenge. Our results highlight the role of mitochondrial daily rhythms in the pathophysiology of obesity and open avenues for chronopharmacological treatments targeting these rhythms. Thus, the present invention pertains to a method for treating or preventing obesity in a subject in need thereof. This method includes administering to the subject, at a specific time of the circadian rhythm, a therapeutically effective amount of a dihydroorotate dehydrogenase inhibitor that exhibits an inhibitory duration of less than 24 hours, and more specifically, a short half-life of less than 24 hours.

The invention relates to an application of a traditional Chinese medicine composition in preparation of a medicine for treating hypertension, which is characterized in that the traditional Chinese medicine composition is prepared from gypsum, rehmannia, ophiopogon root, rhizoma anemarrhenae and achyranthes root. The composition disclosed by the invention can be used for remarkably reducing systolic pressure of spontaneously hypertensive rats and reducing blood pressure rise of the rats caused by feeding of high-fat feed, so that the traditional Chinese medicine composition has a relatively good treatment effect on hypertension.

The invention belongs to the technical field of animal model establishment, and particularly relates to a non-alcoholic fatty liver animal model and an establishment method, and the method comprises the following steps: constructing an ABHD17a gene knockout mouse model; and hybridizing the mouse with the knockout ApoE gene and the mouse with the knockout ABHD17a gene to obtain the mouse with the knockout ApoE gene and the knockout ABHD17a gene, and feeding the mouse with high fat for 16 weeks to obtain the non-alcoholic fatty liver animal model.

The invention belongs to the field of medicines, and particularly discloses application of ImP (Imidazole Propionic Acid) in preparation of medicines for preventing or treating metabolic syndrome related diseases, aiming at the problems that the existing anti-obesity medicines are large in side effect, limited in curative effect and the like, and metabonomics research finds that the peripheral blood ImP level in a high-fat diet induced obesity model is remarkably reduced. A zebra fish model (250 [mu] M) and a human fat cell experiment (10-1000 [mu] M) prove that ImP significantly reduces the lipid accumulation rate by more than 40% (Plt; 0.01) of the substrate. The pharmaceutical composition can be prepared into dosage forms such as oral tablets (for example, each tablet containing 50 mg of ImP), sustained-release injections and the like, and can be theoretically combined with orlistat and other medicines for use. Compared with the traditional therapy, the invention reveals the lipid metabolism regulation function of ImP for the first time, and the ImP has the advantages of strong targeting property (IC50 = 120 mu M), high safety (LD50gt; 2000mg / kg) and the like, and a brand new microbial metabolite intervention strategy is provided for obesity and related metabolic diseases.

The invention belongs to the technical field of medicines, and particularly relates to application of urolithin A and beta-nicotinamide mononucleotide in preparation of a medicine for treating diabetes. The invention finds that when the urolithin A and the beta-nicotinamide mononucleotide are independently used, the hypoglycemic effect on diabetic mice cannot be realized, and when the urolithin A and the beta-nicotinamide mononucleotide are jointly used, the symptoms of diabetes and insulin resistance caused by high fat diet can be remarkably improved; the glucose tolerance and the insulin tolerance are improved; meanwhile, the content of low-density lipoprotein and cholesterol in a mouse body is reduced, so that the risk of thrombus occurrence is reduced; in addition, combined medication can significantly reduce liver cell lipid accumulation and improve mitochondrial morphological abnormality. The invention provides a brand new technical scheme and experimental basis for treating diabetes caused by high fat diet and relieving insulin resistance, and has important medical application value.

This invention belongs to the field of pharmaceutical technology, specifically relating to the use of a 4-(4-diethylamino-1-methylbutanamino)-7-chloroquinoline derivative or its pharmaceutically acceptable salt, or its tautomer, meso compound, racemic compound, enantiomer, diastereomer, or pharmaceutical composition thereof as an active ingredient in the preparation of drugs for the prevention or treatment of obesity and obesity-related metabolic diseases. The 4-(4-diethylamino-1-methylbutanamino)-7-chloroquinoline derivative of this invention has significant therapeutic effects on obesity and related metabolic diseases. In obese mice induced by a high-fat diet and high-fructose water intake, gavage administration for 6 weeks showed that, compared with the high-fat control group, it inhibited more than 70% of the mice's weight gain, with no significant difference in food intake and water intake, demonstrating good clinical application prospects.

This application discloses the application of pyridostigmine in the preparation of drugs for the prevention and treatment of non-alcoholic fatty liver disease (NAFLD). Validation was conducted using animal models of NAFLD induced by three different etiologies: methionine-choline deficiency diet, high-fat diet, and leptin gene knockout. Pyridostigmine significantly improved vagal nerve activity in the model animals (e.g., improving high-frequency and baroreflex sensitivity in heart rate variability), effectively corrected serum lipid metabolism disorders (reducing LDL cholesterol), alleviated hepatocyte damage (reducing ALT and AST), and at the histopathological level, reduced hepatic steatosis, decreased inflammatory cell infiltration, and inhibited collagen deposition, thereby achieving the prevention and treatment of NAFLD.