42 results about "Beta oxidation" patented technology

Methods and compositions comprising peroxisomal and/or mitochondrial beta oxidation stimulating agents to reverse or resolve, slow the progression of, treat or prevent the development of fatty liver and conditions stemming from fatty liver, such as NASH, liver inflammation, cirrhosis and liver failure. An active agent that by itself is associated with an increased risk of fatty liver development and conditions stemming from fatty liver, such as NASH, liver inflammation, cirrhosis and liver failure, may be administered in combination with peroxisomal and/or mitochondrial beta oxidation stimulating agents. A combination regimen involving such agents, as simultaneous or concomitant therapy, or as a fixed dosage form, is also provided.

This invention relates to one method of improving fermentation efficiency of long chain diacid. In this method, normal alkane is the material, and animalcule fermentation method is adopted to produce correspondent diacid. Its major character is to add catastaltica, which includes halogeno-aliphatic acid, methyl fat acid and one or two kinds of its salt or ester, to reduce beta oxidation ability of bacterial strain. The concentration of the catastaltica is 0.01-5mmol/L. the added catastaltica can efficiently reduce beta oxidation ability of bacterial strain, lowers the alkane consumption, and improves greatly the fermentation efficiency, the acid-producing rapidity and is particularly suitable for long chain diacid.

The invention relates to recombinant microorganisms that have been engineered to produce various chemicals using genes that have been repurposed to create a reverse beta oxidation pathway. Generally speaking, the beta oxidation cycle is expressed and driven in reverse by modifying various regulation points for as many cycles as needed, and then the CoA thioester intermediates are converted to useful products by the action of termination enzymes.

Bacteria that run the beta oxidation cycle in reverse anabolic direction are provided, along with many novel primers to start the reverse cycle, pathways to make such primers, and a large variety of products produced thereby. Methods for making desired product by using such primers in the reverse pathway are also disclosed.

Disclosed are a method for activating lipid metabolism in the small intestine epithelium and also a method for promoting accumulation of fatty acids into the small intestine epithelium, each of which features administering an effective amount of a diacylglycerol. Also disclosed are methods for improving various symptoms in diabetes, which have ingesting a diacylglycerol. Ingestion of the diacylglycerol leads to accumulation of the fatty acids in the small intestine. The fatty acids so accumulated promote induction of beta-oxidation, thereby not only activating lipid catabolism but also making it difficult to allow lipids to accumulate as triacylglycerols. This series of actions eventually results in development of lowering action for blood remnant-like lipoprotein level and also lowering action for blood leptin level, and hence, lipid metabolism is improved. Further, energy consumption is enhanced by promoting the induction of beta-oxidation and activating lipid catabolism.

Genetically modified strains of C. tropicalis, which will not revert to wild-type activity at the POX 4 and/or POX 5 locus, are disclosed. The strains are β-oxidation blocked and have been transformed through homologous recombination with a construct which deletes a portion of the POX 4 and/or POX 5 gene. The modified strains may be used to increase yields of dicarboxylic acids produced in host cells of the strains. Methods for blocking the β-oxidation pathway in a C. tropicalis host cell are also provided.

The invention relates to the genetic manipulation of plants to increase oil accumulation in plant tissues, particularly seeds. Methods for decreasing β-oxidation in plants and optimizing oil accumulation in a seeds are provided. The methods find use in increasing the accumulation of oil or particular oil constituents in plant seeds. Isolated nucleotide molecules, isolated proteins, expression cassettes and transformed plants, plant tissues and plant cells are additionally provided.

The MFE2 gene of a microorganism capable of producing glycolipids, such as, but not limited to C. bombicola is disrupted with the purpose of blocking the beta-oxidation pathway in the strain. Fermentation of a such strain having such disrupted genes on primary or secondary alcohols or diols, preferably on primary alcohols produces short chained glycolipids in high yield and purity.

The present invention relates to a method for increasing the β-oxidation of fatty acids while substantially simultaneously maintaining blood glucose concentration through the inhibition of carbohydrate absorption. Furthermore, the present invention additionally provides a composition for increasing the β-oxidation of fatty acids while substantially simultaneously maintaining blood glucose concentration through the inhibition of carbohydrate absorption comprising an Extract of Green Coffee Bean, and an Extract of Salacia oblonga. The composition may further comprise diacylglycerol.

Annatto extract composition (AEC), including cis and trans geranyl geraniols (GG) and tocopherol-free C-5 unsubstituted tocotrienols (T3), increases the de novo synthesis of intermediate isoprenoid and distal protein products, including endogenous coenzyme Q10 (CoQ10), dolichols (DL) and all subsequent GG-prenylated and DL-glycosylated proteins, including GG-porphyrinated hemes. This intermediate and distal product replenishment by AEC reverses maladies of myotoxicity (of both drug and non-drug origins), including maladies that affect the muscle, kidney, eye, GI tract and skin, nerve, blood, and CoQ10-related syndromes of energetics and LDL protection. AEC anabolically increases the endogenous de novo CoQ10 synthesis via GG elongation/prenylation of side-chain and conversely CoQ10 catabolically increases the endogenous de novo GG synthesis via beta-oxidation of CoQ10. Also, such AEC decreases de novo synthesis and increases disposal of triglycerides (TG) in humans via PPAR activation and SREBP deactivation. Such drop in TG by AEC reverses maladies of insulin resistance (IR) and metabolic syndrome (MS), prediabetes, diabetes and diabetes-related cardiovascular diseases (CVD). GG activates PPAR and down regulates SREBP transcription factors. This AEC, containing GG, inhibits cancer growth whether or not GG involvement in protein prenylation is required.

The invention provides a complex microbial inoculant for a grease-rich raw material medium-temperature biogas fermentation system and a preparation method and application thereof. The complex microbial inoculant is mainly used for strengthening degradation (beta-oxidation) of long-chain fatty acid and methane production of a degradation product (acetic acid+CO2+H2) of the long-chain fatty acid, improving gas production rate of a grease-rich raw material, shortening fermentation dwell time and meanwhile avoiding severed accumulation of fermentation liquid upper-layer grease.

The invention discloses a saccharomyces cerevisiae strain for synthesizing squalene and an application of the saccharomyces cerevisiae strain, and belongs to the technical field of genetic engineering. According to the invention, tHMG1 and IDI1 are integrated at a multi-copy site Ty2 of saccharomyces cerevisiae, so that synthesis and accumulation of squalene are remarkably promoted, NADH-dependent HMG1 is heterologously expressed, the redox level in yeast cells is balanced, a promoter HXT1 with a remarkable inhibition effect on ERG1 transcription is further replaced, conversion of squalene to the downstream is hindered, ACL1 and ACL2 are heterologously expressed, PEX11 and FOX3 are over-expressed, accumulation of a squalene synthesis precursor acetyl coenzyme A in cytoplasm is enhanced through beta oxidation, accumulation of squalene is further promoted, and the squalene yield can reach 1253.4 mg/L after saccharomyces cerevisiae is fermented for 96 h.

The invention discloses a natamycin fermentation technology based on addition of exogenous saturated fatty acid. By adding a slow-release precursor source, namely the saturated fatty acid, which has no toxic or side effects on cells, when beta-oxidation utilization is conducted in the cells, the exogenous saturated fatty acid generates a large quantity of acetyl CoA precursors and NADH, thus supply of natamycin macrolide precursors and ATP is guaranteed, and product synthesis is promoted. Since the saturated fatty acid is in a solid state under normal temperature and is not dissolved in water,the concentration of the saturated fatty acid cannot influence cell growth and metabolism in a fermentation liquor, and therefore, in the technology, rigid control over the concentration of the saturated fatty acid is not needed. By means of the technology, the biosynthesis level of the natamycin can be effectively improved, the detection and material supply operation load of precisely regulatingthe precursor concentration in the fermentation liquor is greatly lowered, and the technology has important application value in the industry.

The use of microorganisms to make omega- and/or omega-l-functionalized products through an iterative carbon chain elongation pathway that we call a reverse beta oxidation pathway. The pathway uses omega-functionalized CoA thioesters as primers and acetyl-CoA as the extender unit in a non-decarboxylative Claisen condensation, and then uses beta oxidation or fatty acid synthesis enzymes to complete the cycle, via reductase, dehydratase and reductase reactions. Various termination enzymes that act on the functionalized beta-keto acyl-CoA intermediates of the pathway and produce omega or omega-1 functionalized products. The action of termination enzymes on such intermediates yield a large variety of products.

This disclosure describes enzymes from the type II (a discrete set of enzymes) fatty acid synthesis (“FAS”) pathway that can be used in combination with thiolases to operate a functional reversal of the β-oxidation cycle. A combination of thiolases with one or more of 3-oxoacyl-[acyl-carrier-protein] reductase (FabG, others), 3-hydroxyacyl-[acp] dehydratase (FabA, FabZ, others), and enoyl-[acyl-carrier-protein] reductase (FabI, FabK, FabL, FabV, others) yields a functional reversal of the β-oxidation cycle. If only one or two enzymes are used, the remaining enzymes will be traditional beta oxidation enzymes. Once this cycle is coupled with the appropriate priming and termination pathways, the production of carboxylic acids, alcohols, hydrocarbons, amines and their α-, β-, and ω-functionalized derivatives from renewable carbon sources can be achieved.

Disclosed herein are microorganism and methods that can be used for the synthesis of cannabigerolic acid (CBGA) and cannabinoids. The methods disclosed can be used to produce CBGA, Δ⁹-tetrahydrocannabinolic acid (THCA), cannabidiolic acid (CBDA), cannabichromenic acid (CBCA), Δ⁹-tetrahydrocannabinol (THC), cannabidiol (CBD), cannabichromene (CBC). Enzymes useful for the synthesis of CBGA and cannabinoids, include but are not limited to acyl activating enzyme (AAE1), polyketide synthase (PKS), olivetolic acid cyclase (OAC), prenyltransferase (PT), THCA synthase (THCAS), CBDA synthase (CBDAS), CBCA synthase (CBCAS), HMG-Co reductase (HMG1), and/or farnesyl pyrophosphate synthetase (ERG20). The microorganisms can also have one or more genes disrupted, such as gene that that controls beta oxidation of long chain fatty acids.

The invention relates to the field of gene function, and in particular, relates to an application of an ASB3 gene in preparation of drugs for treatment of non-alcoholic fatty liver disease. The advantages comprise that by constructing an ASB3 gene fully knockout mouse model, the content of E3 ubiquitin ligase ASB3 in vivo can be inhibited, and the beta-oxidation and oxygen consumption of long-chain fatty acids can be enhanced, so as to reduce lipid accumulation in hepatocytes. The invention discloses new functions of the ASB3 gene and provides new targets and ideas for treatment of non-alcoholic fatty liver disease.

The use of microorganisms to make omega- and/or omega-1-functionalized products through an iterative carbon chain elongation pathway that we call a reverse beta oxidation pathway. The pathway uses omega-functionalized CoA thioesters as primers and acetyl-CoA as the extender unit in a non-decarboxylative Claisen condensation, and then uses beta oxidation or fatty acid synthesis enzymes to complete the cycle, via reductase, dehydratase and reductase reactions. Various termination enzymes that act on the functionalized beta-keto acyl-CoA intermediates of the pathway and produce omega or omega-1 functionalized products. The action of termination enzymes on such intermediates yield a large variety of products.

DPN is an intractable and tormenting neurovascular and dermal disorder.

Two patients of DPN of stocking-glove pattern were treated with SAG for treatment of microvascuar coagulopathy, induction of vasodilation and possible induction of angioneogenesis; with ALC for ATP generation through mitochondrial beta-oxidation of fats; and with ALA for antioxidative stress to prevent precipitation of vascular damage and to prevent DPN recurrence. SAG+ALC was to cure maceration.

Thus, SAG+ALC+ALA was effective in mitigating and curing their distresses. It shall be one of the logical and practical means of prompt DPN therapy not only to alleviate DPN but also to lead to “cure.”

The invention discloses a compound formula for preventing and treating obesity by comprehensively correcting metabolic disorders based on gamma-aminobutyric acid. The compound formula comprises the components: gamma-aminobutyric acid (50-500 mg/d), nicotinic acid (20-200 mg/d), riboflavin (3-20 mg/d), pantothenic acid (5-30 mg/d), carnitine (300-2000 mg/d) and magnesium aspartate (30-500 mg/d). The gamma-aminobutyric acid in the formula inhibits nutrient absorption, protects mitochondria from being less continuously damaged by metabolic reactive oxygen species, and plays a role in less absorption and more consumption; the rest components are added to form the compound formula, beta oxidation of a fat-splitting core path is nutritionally supported, metabolism is adjusted in a mild mode, anda safe and healthy weight losing effect is achieved. In formula development, a high-throughput cell experiment and a random double-blind control multi-center volunteer experiment are comprehensivelyutilized; the action range and the toxicity threshold value of each component are accurately detected, so that the use dosage of each component has extremely high tolerance and safety, and the compound formula is suitable for being used as a core formula of a health care product or a nutritional supplement, and is beneficial to development and marketing of subsequent related products.