103 results about "Fat diet" patented technology

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 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 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 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 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 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.

One patent obtained in the earlier stage is that the line peptide COX52-69 is cyclized to realize an oral administration route. The invention discovers that the cyclic peptide, namely C * LLPAGWV-[N-Me-Leu]-SHLDSYKKREC *, has the effect of reducing the body weight. In the invention, a diet-induced obesity (DIO) model is established by feeding C57BL / 6J mice with high-fat feed (45% of fat for energy supply) for 14 weeks. After a DIO mouse is obtained, a 17-week administration experiment is carried out by using a PBS buffer solution and a Rybelsus solution as a contrast, and observation finds that the COX52-69 cyclic peptide can relieve weight gain caused by DIO, so that the weight of the DIO mouse is reduced, and multiple metabolic indexes can be improved. Results show that the COX52-69 cyclic peptide has practical application in weight loss and weight gain prevention processes, and also has reagent application in improvement of some metabolic indexes of obese people.

The invention provides a recombinant human lactoferrin milk tablet with weight losing and blood sugar reducing functions and a preparation method thereof, and belongs to the technical field of dairy product processing. The recombinant human lactoferrin milk tablet disclosed by the invention is prepared from the following components in parts by mass: 95 to 105 parts of recombinant human lactoferrin, 3 to 4 parts of zinc gluconate, 1 to 1.5 parts of vitamin E, 0.03 to 0.04 part of folic acid and 1300 to 1400 parts of milk powder. Experiments prove that the recombinant human lactoferrin milk tablet prepared by the invention can slow down the weight gain of mice and relieve the impaired glucose metabolism capability caused by high fat diet, and meanwhile, the recombinant human lactoferrin can regulate the lipid degeneration of the liver to a certain extent, relieve the lipid deposition of the liver and inhibit fat cell hypertrophy. The recombinant human lactoferrin milk tablet has the weight-losing and blood-glucose-reducing effects for the first time, and has a wide application prospect in the field of weight losing and blood glucose reducing in the future.

The composition contains a combination of at least one type of fiber and at least one type of probiotic, and the combination of at least one type of fiber and at least one type of probiotic is formulated for administration to a subject with a stressed gut microbiome to improve and / or maintain optimal cholesterol levels in the subject with a stressed gut microbiome. Preferably, the subject is experiencing one or more microbiome stressors, e.g., dietary stressors, antibiotics, other drugs, infections, strenuous exercise, stress, alcohol, travel, and combinations thereof; more preferably, at least dietary stressors; most preferably, at least a high-fat diet, e.g., a Western high-fat diet or a ketogenic diet. The method can achieve at least one outcome, which is improving and / or maintaining optimal cholesterol levels in a subject with a stressed gut microbiome.

The invention relates to an application of Chinese yam glycoprotein in preparation of a medicine for treating obesity, wherein the obesity is caused by high fat diet. The Chinese yam glycoprotein is derived from a natural plant Chinese yam, the biomacromolecule biological activity of the Chinese yam glycoprotein can be kept to the maximum extent through low-temperature grinding, separation and purification, and the product obtained through extraction and purification can be prepared into various dosage forms such as capsules, tablets, powder and oral liquid. Screening and verification are carried out through animal experiments, and it is proved that the Chinese yam glycoprotein has a remarkable fat reducing effect on obesity caused by high-fat diet, can improve the histological morphology of white adipose tissue, reduces the hypertrophy degree of adipose cells, meanwhile, improves abnormal glucose tolerance induced by the high-fat diet, and has an obvious fat reducing effect on obesity caused by the high-fat diet. And the expression of key factors related to adipogenesis and metabolic homeostasis in adipose tissues is regulated and controlled.

The invention relates to the technical field of traditional Chinese medicine preparations, and discloses a salvia miltiorrhiza salvianolic acid and notoginsenoside composition, and the mass ratio of notoginsenoside to salvianolic acid in the composition is 1: 5 or 5: 3 or 3: 5. The invention further discloses application of the composition in preparation of drugs for preventing and treating vasculopathy related to metabolic syndromes of metabolic organs. The composition disclosed by the invention can be used for remarkably relieving liver lipid deposition induced by high-fat diet and reducing abnormal accumulation of white and beige fat; wherein the optimal compatibility ratio is 1: 5, and the mechanism of playing the role is related to down-regulation of the expression of liver lipid transport key protein CD36; the invention provides a new intervention strategy and compatibility basis for preventing and treating vasculopathy related to metabolic syndrome, and provides a precise intervention thought of'combining diseases and syndromes' for the research of early prevention of atherosclerosis.

The application discloses a method for relieving obesity cardiomyopathy lipid toxicity by Chemerin and belongs to the technical field of pharmacological research. Mice are selected to establish an obesity mouse model, and are equally divided into a control group, a high-fat diet group, an AAV CMKLR1 virus group, and a high-fat + AAV CMKLR1 virus group. In succession, mouse heart ultrasound, TSE system detection, glucose tolerance test, and insulin tolerance test are carried out, and mouse blood glucose is measured at intervals. Then, tissue protein is extracted for protein immunoblotting, and tissue RNA is extracted for reverse transcription, and then qPCR is used to detect the expression of related genes. After paraffin embedding and slicing of mouse tissues, HE, WGA, immunofluorescence and other pathological staining are carried out. MTBE method is used for lipid extraction and detection of lipid content. ELISA method is used to measure serum Chemerin, and Acyl-RAC method is used to detect protein palmitoylation. Finally, the experimental results are analyzed to draw a conclusion. The present application proves by clinical data and mouse models that Chemerin compensatorily increases in the process of obesity, and Chemerin can relieve cardiac lipid toxicity caused by obesity and protect cardiac function.

The invention relates to the technical field of biological medicines, in particular to polypeptide for treating non-alcoholic fatty liver diseases. The invention provides a novel octapeptide P3-1 (SEQ ID NO: 1) derived from macadamia nuts. The novel octapeptide P3-1 (SEQ ID NO: 1) can remarkably improve liver lipid metabolism disorder, restore liver functions, relieve inflammatory response and increase abundance of probiotics in mice with non-alcoholic fatty liver diseases induced by high fat diet. The polypeptide is small in molecular weight, safe in source and easy to absorb, has good medicinal and health-care food development potential, and provides a safe and effective new way for targeted intervention of the non-alcoholic fatty liver disease.

Light is fundamental for biological life, with most mammals possessing light-sensing photoreceptors in various organs. Opsin3 is highly expressed in adipose tissue which has extensive communication with other organs, particularly with the brain through the sympathetic nervous system (SNS). Our study reveals a new light-triggered crosstalk between adipose tissue and the hypothalamus. Direct blue-light exposure to subcutaneous white fat improves high-fat diet-induced metabolic abnormalities in an Opsin3-dependent manner. Metabolomic analysis shows that blue light increases circulating levels of histidine, which activates histaminergic neurons in the hypothalamus and stimulates brown adipose tissue (BAT) via SNS. Blocking central actions of histidine and denervating peripheral BAT blunts the effects of blue light. Human white adipocytes respond to direct blue light stimulation in a cell-autonomous manner, highlighting the translational relevance of this pathway. Together, these data demonstrate a light-responsive metabolic circuit involving adipose-hypothalamus communication, offering a potential strategy to alleviate obesity-induced metabolic abnormalities.

The invention discloses an application of bifidobacterium animalis subsp. Lactis SS9 in preparation of a product for preventing and treating stress obesity. The bifidobacterium animalis subsp. Lactis SS9 obtained by screening can remarkably relieve obesity induced by combination of chronic pressure and high-fat diet, and the obesity is represented by slowing down weight increase, reducing appetite, improving blood fat, up-regulating GLP-1 and insulin secretion and effectively relieving anxiety-like and depression-like behaviors. Researches find that the strain can regulate the hypothalamic-pituitary-adrenal axis activation level, improve secretion imbalance of hormones such as CRH, ACTH and CORT, restore expression of appetite regulation factors such as NPY / AgRP / POMC of hypothalamic and relieve emotional eating behaviors. In addition, the strain can also reduce the systemic inflammation level, recover the diversity of intestinal flora and improve the proportion of beneficial bacteria. The invention provides the probiotics with multiple effects of regulating emotion, controlling body weight and improving metabolic disorder, and a new strategy is provided for preventing and treating stress-related obesity.

Use of ganoderic acid A in the preparation of a product for preventing and / or treating non-alcoholic fatty liver disease. Ganoderic acid A can regulate bile acid reabsorption in C57BL / 6J mice induced by a high-fat diet, and reduce the absorption of triglycerides and cholesterol. Ganoderic acid A can also enhance the expression of the gene of cholesterol 7α-hydroxylase, a key enzyme for liver cholesterol decomposition, thereby promoting the conversion of liver cholesterol into bile acid, and alleviating the accumulation of liver cholesterol. Ganoderic acid A has a significant preventive and ameliorative effect on non-alcoholic fatty liver disease induced by a high-fat diet by means of regulating bile acid metabolism, inhibiting lipid absorption, and reducing liver lipid accumulation. Therefore, ganoderic acid A can be used as a health care product, a functional product, or a drug for preventing and treating non-alcoholic fatty liver disease.

The invention relates to the technical field of biology, in particular to application of a Gpr88 gene in treatment and prevention of a non-alcoholic fatty liver disease, the invention reveals that the GPR88 gene is used as a target spot for preventing and treating the non-alcoholic fatty liver disease for the first time, and research finds that deletion of the GPR88 gene can improve sugar tolerance and insulin resistance of a high-fat diet induced mouse, so that the non-alcoholic fatty liver disease can be prevented and treated. The deletion of the GPR88 gene can significantly reduce the weight of the high fat diet induced mouse liver, and the deletion of the GPR88 gene can significantly reduce the lipid deposition of the high fat diet induced mouse liver. The result shows that the GPR88 gene is an effective target for regulating the occurrence of the non-alcoholic fatty liver disease. According to the invention, the biological function of the GPR88 gene is broadened, and a new theoretical basis and a treatment target are provided for preparing medicines for preventing and treating the non-alcoholic fatty liver disease.