152 results about "High 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 invention discloses an establishment method and application of a damp-heat intestine accumulation type ulcerative colitis animal model, and belongs to the field of animal models.The establishment method comprises the steps that S1, high-fat feed treatment is conducted, specifically, experimental animals freely eat high-fat feed for 6-10 weeks from the first day; s2, DSS treatment: feeding 1.5% (w / v) DSS solution to the experimental animal for 2 weeks; and S3, observing the damp-heat syndrome type and ulcerative colitis related indications of the experimental animals, and selecting the experimental animals meeting the scoring standard, thereby establishing the ulcerative colitis mouse model. Aiming at the situation that most patients induce ulcerative colitis due to excess energy due to the change of dietary structures and lifestyles at present, the invention constructs and evaluates the damp-heat accumulation type ulcerative colitis mouse model by inducing internal dampness by a direct pathogenesis (high fat diet), which is closer to the actual situation of clinical patients. Therefore, a model and reference are provided for research and treatment of pathology of the damp-heat accumulation type ulcerative colitis and pharmacological mechanisms of traditional Chinese medicines.

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 invention relates to application of 9-cis-retinoic acid in preparation of products for treating, preventing or improving obesity, and belongs to the technical field of biological medicine. Experimental evaluation of obese mice induced by high-fat diet proves that the 9-cis-retinoic acid can reduce blood fat and improve the glycometabolism function, and lipid accumulation of the liver is improved mainly by increasing expression of main regulatory protein PPAR-alpha oxidized by liver beta, so that the 9-cis-retinoic acid can be used for preparing medicines for treating obesity. The traditional Chinese medicine composition can be used for treating, preventing or improving metabolic symptoms caused by high fat diet, and a new strategy is provided for treating obesity and related metabolic syndromes. Besides, 9-cis-retinoic acid is a natural active metabolite of vitamin A, does not show obvious toxic reaction in animal experiments, and has better biocompatibility.

The invention belongs to the technical field of natural products, and provides application of fucoxanthin in preparation of oral anti-alopecia drugs. Animal experiments find that long-term high-fat diet can lead to large-piece shedding of hair accompanied by skin inflammation, and fucoxanthin has a treatment effect on high-fat diet induced mouse back hair shedding and skin inflammation, can obviously relieve high-fat diet induced subcutaneous cholesterol crystal accumulation and sebaceous gland cell hypertrophy, and has the effects of preventing and treating the high-fat diet induced mouse back hair shedding and skin inflammation and preventing and treating the high-fat diet induced mouse back hair shedding and the high-fat diet induced sebaceous gland cell hypertrophy. And skin epidermal hyperplasia and cuticle thickening induced by high fat diet can be improved. Besides, cell experiments also find that fucoxanthin intervention can reduce oleic acid infiltration of the hair follicle stem cells and reduce oleic acid induced death and apoptosis of the hair follicle stem cells, and prove that fucoxanthin has a protection effect on the hair follicle stem cells, has low toxic and side effects on cells and animals as a natural algae extract, and has a good application prospect. Good clinical application prospects are realized.

The invention provides an application of liquiritin in preparation of a PPAR gamma receptor partial agonist. Through a structure-based high-throughput virtual screening technology, it is found that liquiritin can be used as a partial agonist of a PPAR gamma receptor, and the relative activation efficiency of liquiritin is 35.9% of that of rosiglitazone; in-vitro experiments prove that liquiritin can remarkably promote glucose uptake and consumption of HepG2 cells and does not induce adipocyte differentiation; in-vivo experiments prove that liquiritin can effectively improve the blood glucose level of an insulin resistance mouse model induced by high fat diet and reduce the level of serum proinflammatory factors. Compared with thiazolidinedione compounds, liquiritin not only can relieve and treat insulin resistance or related metabolic diseases, but also does not cause adverse reactions such as weight gain, fat accumulation and myocardial hypertrophy, provides a new candidate compound for developing safe and effective anti-diabetic drugs, and has a wide application prospect.

The application discloses a polypeptide composition for treating obesity and related metabolic diseases and application thereof. The polypeptide composition comprises polypeptide 1 and polypeptide 2, wherein the amino acid sequence of the polypeptide 1 is shown as SEQ ID NO. 1, can be specifically combined with the CD105 receptor on the surface of MSCs and the AdipoR1 receptor of adipocytes; the amino acid sequence of the polypeptide 2 is shown as SEQ ID NO. 2, can target adipose tissue and regulate glycolipid metabolism. The polypeptide composition is combined with fat-derived mesenchymal stem cells (MSCs) and applied to a high-fat-diet obese mouse model, and the results show that the composition has a significant synergistic effect in reducing body fat, improving the morphology of adipose tissue, regulating serum metabolic factors and inflammatory factors, and has no obvious organ toxicity. The application provides a new effective strategy and a safe and reliable pharmaceutical composition for treating obesity and related metabolic diseases.

Compositions and formulations of synthetic MXRA8-Fc fusion proteins are provided, as well as methods of use thereof. Methods include neutralizing TSP1 / MXRA8 interactions in a subject by administering a synthetic MXRA8-Fc fusion protein, such that the synthetic MXRA8-Fc fusion protein binds to TSP1 to inhibit the TSP1 from binding with MXRA8. Methods also include treating obesity such as high fat diet (HFD)-induced obesity, and treating obesity-associated metabolic diseases such as type 2 diabetes by administering a synthetic MXRA8-Fc fusion protein.

The invention discloses an application of an intestinal strain in preparation of a cholesterol-lowering product, and belongs to the technical field of microbial medicines. The intestinal bacterial strain is Oscillibacter ruminant, the viable bacteria concentration of the intestinal bacterial strain is controlled to be (4.8-5.2) * 10 < 9 > CFU / mL, the intestinal bacterial strain can be prepared into bacterial liquid, freeze-dried powder, capsules or tablets and other dosage forms, and pharmaceutically acceptable auxiliary materials such as lactose and microcrystalline cellulose can be added. According to the cholesterol-lowering product, the total cholesterol, triglyceride and low-density lipoprotein cholesterol level of an object can be remarkably reduced under the action of peste des petits ruminants, and meanwhile, the high-density lipoprotein cholesterol level is increased; in addition, abnormal blood glucose induced by high-fat diet can be improved, arterial lipid accumulation is reduced, and the plaque area proportion of atherosclerotic lesions is improved.

The invention relates to the technical field of biological medicines, and discloses application of INHBC as a target spot in prevention and / or treatment of metabolic diseases. Specifically, the invention relates to application of substances for promoting INHBC gene expression or improving protein activity in preparation of products for preventing and / or treating metabolic diseases, and the metabolic diseases comprise diseases caused by energy metabolism disorder, such as obesity, diabetes, fatty liver disease, hyperlipidemia and the like. According to the application disclosed by the invention, liver specific overexpression or INHBC knock-in can improve mouse liver fatty degeneration and abnormal glucose metabolism induced by high fat diet, and in addition, the heat production activity of mouse adipose tissues can be enhanced, so that obesity induced by high fat diet is inhibited; the compound has an important application value in preventing and / or treating metabolic diseases such as obesity, type 2 diabetes and fatty liver diseases.

Disclosed herein are a means to prevent and / or ameliorate age, disease and obesity associated metabolic diseases, such as diabetes and impaired glucose tolerance. Also disclosed are compositions and methods that relate to the findings that GDF11 prevents weight gain, improves glucose tolerance and reduces hepatosteatosis in aged mice administered a high fat diet. In particular, the methods and compositions described herein relate to increasing the level of GDF11 in a subject, thereby treating or preventing the development of obesity in the subject, reducing the metabolic consequences of obesity and improving the subject's metabolic health.

Provided is a Bifidobacterium bifidum strain, Bifidobacterium bifidum ibiome001, which can significantly reduce body weight gain and white adipose tissue weight gain of high fat diet-induced obese and diabetic mice, and enhances expression of lipolytic genes ATGL and HSL. Moreover, Bifidobacterium bifidum ibiome001 can significantly lower fasting blood glucose levels, area under curves (AUCs) of the oral glucose tolerance (OGTT) curve, plasma glycated hemoglobin levels and insulin levels of diabetic mice. It is suggested that Bifidobacterium bifidum ibiome001 is a promising potential probiotic strain for the treatment of metabolic syndrome such as obesity, diabetes and the like, which is more effective than other Bifidobacterium strains / compositions.

The application discloses a norchizhiol triterpenoid compound, a preparation method and application thereof. The norchizhiol triterpenoid compound norchizhiol A can be quickly prepared from Ganoderma lucidum. The test proves that the norchizhiol A can inhibit the accumulation of triglyceride in the differentiation process of 3T3L1 preadipocytes. The norchizhiol A can also effectively reduce the weight increase and liver coefficient of high-fat-diet-induced obese mice, regulate the blood lipid level of the obese mice, and significantly intervene and improve the lipoprotein distribution of the body. The compound can be used for preparing anti-obesity and lipid-lowering medicines.

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 research finds that the SUMOylation level of the liver in a clinical specimen and an animal model of the metabolic dysfunction fatty liver disease is obviously reduced. UBC9 is used as the only key E2 ligase for SUMOylation to regulate and control the SUMOylation level. The invention discloses application of a UBC9 gene overexpression preparation in drugs for treating or preventing metabolic dysfunction fatty liver diseases. Through overexpression of liver specificity UBC9 mediated by an AAV adeno-associated virus vector or overexpression of UBC9 in HepG2 cells by a lentiviral vector, lipid deposition of a C57 mouse liver induced by high fat diet and a cell model treated by palmitate can be remarkably improved, and reduction of the SUMOylation level of the mouse liver and the human HepG2 cells under the high fat background can be reversed. Therefore, the UBC9 gene overexpression preparation can be used for developing drugs for treating metabolic dysfunction fatty liver diseases.

The invention discloses an application of a SUMO agonist N106 (the molecular formula is C17H14N4O3S, and the molecular weight is 354.38) in treatment or prevention of metabolic dysfunction related fatty liver disease (MASLD). The early-stage research of the invention finds that the liver SUMOylation level in MASLD clinical specimens and animal models is significantly reduced. In-vivo experiments show that in a high-fat diet induced C57BL / 6 mouse model, N106 (10mg / kg, intraperitoneal injection, once a day) can significantly improve liver lipid deposition and blood fat level of a high-fat diet mouse; in in-vitro experiments, N106 (10 mu M for 24 hours) can effectively reduce lipid droplet accumulation of HepG2 cells. The research reveals that N106 regulates lipid metabolism by activating an SUMOylation modification pathway for the first time, and a novel treatment strategy is provided for MASLD.

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 vitexin in preparation of medicines for preventing and treating obesity. According to the application of the vitexin in preparation of the medicine for preventing and treating the obesity, the prevention and treatment comprise one or more of prevention, relieving or treatment of the obesity induced by high fat diet, and the medicine can be generally a solution and contains pharmaceutically acceptable auxiliary materials. The vitexin disclosed by the invention can promote the heat production of brown adipocytes and increase the oxygen consumption; the expression of heat production marker protein UCP1 of brown fat and subcutaneous white fat tissues is increased, the metabolic rate of an organism is increased, obesity induced by high fat diet is resisted, and then insulin resistance is improved.

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 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 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.

The present invention provides a method for preparing an animal model of insulin resistance and abnormal glucose metabolism caused by mild to moderate hypertriglyceridemia, by injecting poloxamer 407 solution into the mouse peritoneal cavity at a dose of 25-100 mg per kilogram of mouse, administering the drug once every other day for 12 consecutive weeks, and continuously monitoring blood lipid and blood glucose levels. The preferred dose of the present invention is 75 mg per kilogram of mouse. The present invention also provides the use of the animal model in screening and preparing drugs for treating insulin resistance and abnormal glucose metabolism caused by mild to moderate hypertriglyceridemia. The present invention simulates insulin resistance and abnormal glucose metabolism directly caused by mild to moderate hypertriglyceridemia. Compared with traditional high-fat diets or gene knockout models, triglyceride levels are precisely regulated by chemical intervention, avoiding factors such as obesity and inflammation and the risk of genetic manipulation, and having high controllability and efficiency.

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.

A composition contains a combination of at least one fiber and at least one probiotic and is formulated for administration to a subject in a condition of challenged gut microbiome such that the combination of at least one fiber and at least one probiotic improves and / or maintains optimal cholesterol levels in a subject in a condition of challenged gut microbiome. Preferably the subject is experiencing a microbiome stressor, such as one or more of a dietary stressor, antibiotic, other medications, infections, intense exercise, stress, alcohol, travel and combinations thereof; more preferably at least a dietary stressor; most preferably at least a high fat diet, such as a Western high fat diet or a ketogenic diet. The method can achieve at least one result that is improving and / or maintaining optimal cholesterol levels in a subject in a condition of challenged gut microbiome.