query: where do fatty acids enter the krebs cycle

pos: Fatty acid metabolism is destined to feed into the fatty acid synthesis pathway. Acetyl-CoA carboxylase is the point of regulation in saturated straight-chain fatty acid synthesis, and is subject to both phosphorylation and allosteric regulation. Regulation by phosphorylation occurs mostly in mammals, while allosteric regulation occurs in most organisms. Allosteric control occurs as feedback inhibition by palmitoyl-CoA and activation by citrate. When there are high levels of palmitoyl-CoA, the final product of saturated fatty acid synthesis, it allosterically inactivates acetyl-CoA carboxylase to prevent a build-up of fatty acids in cells. Citrate acts to activate acetyl-CoA carboxylase under high levels, because high levels indicate

neg: Malonyl-CoA decarboxylase length DFAs). While long and medium chain fatty acids are oxidized mainly in the mitochondria, DFAs are oxidized primarily in peroxisomes, which degrade DFAs completely to malonyl-CoA (in the case of odd chain length DFAs) and oxalyl-CoA (for even chain length DFAs). The peroxisomal form of MCD could function to eliminate this final malonyl-CoA. Malonyl-CoA acts as an intermediary between fatty acids and acetyl-CoA in the mitochondria, where MCD is believed to participate in the elimination of the residual malonyl-CoA, so that acetyl-CoA can enter the Krebs cycle. MCD also plays a role in the regulation of glucose and lipids

neg: Malate synthase skip over the decarboxylation steps of the citric acid cycle. In other words, malate synthase works together with isocitrate lyase in the glyoxylate cycle to bypass two oxidative steps of Krebs cycle and permit carbon incorporation from acetate or fatty acids in many microorganisms. Together, these two enzymes serve to produce succinate (which exits the cycle to be used for synthesis of sugars) and malate (which remains in the glyoxylate cycle). During this process, acetyl-CoA and water are used as substrates. As a result, the cell does not lose 2 molecules of carbon dioxide as it does in the Krebs

neg: Methylisocitrate lyase A. The enzyme 2-methylcitrate synthase adds propionyl coenzyme A to oxaloacetate, yielding methylcitrate instead of citrate. But isomerizing methylcitrate to methylisocitrate and then subjecting it to MICL regenerates succinate, which proceeds as in the Krebs cycle, and pyruvate, which is easily metabolized by other pathways (e.g. decarboxylated to form acetyl coenzyme A and oxidized in the Krebs cycle). This allows catabolism of propionic acid—and, using beta oxidation, other fatty acids with odd numbers of carbons—without relying on coenzyme B12, a complex cofactor often used to metabolize propionate. The methylcitrate cycle is found in many microorganisms. Methylisocitrate lyase plays a regulatory

neg: Biochemistry molecular dynamics simulations. These techniques allowed for the discovery and detailed analysis of many molecules and metabolic pathways of the cell, such as glycolysis and the Krebs cycle (citric acid cycle), and led to an understanding of biochemistry on a molecular level.philip Randle is well-known for his discovery in diabetes research is possibly the glucose-fatty acid cycle in 1963.He confirmed that fatty acids reduce oxidation of sugar by the muscle. High fat oxidation was responsible for the insulin resistance. Another significant historic event in biochemistry is the discovery of the gene, and its role in the transfer of information in

neg: Fatty acid metabolism Thereafter the glucose that is released into the blood by the liver for general use by the body tissues, has to be synthesized from the glucogenic amino acids and a few other gluconeogenic substrates, which do not include fatty acids. Please note however that lipolysis releases glycerol which can enter the pathway of gluconeogenesis. Fatty acids are broken down to acetyl-CoA by means of beta oxidation inside the mitochondria, whereas fatty acids are synthesized from acetyl-CoA outside the mitochondria, in the cytosol. The two pathways are distinct, not only in where they occur, but also in the reactions that occur,

neg: Ketosis coenzyme A is bound to the fatty acid to produce acyl-CoA, which is able to enter the mitochondria. Once inside the mitochondrion, the dominant way that the bound fatty acids are used as fuel in cells is through β-oxidation, which cleaves two carbons off of the acyl-CoA molecule in every cycle to form acetyl-CoA. Acetyl-CoA enters the citric acid cycle, where it undergoes an aldol condensation with oxaloacetate to form citric acid; citric acid then enters the tricarboxylic acid cycle (TCA), which harvests a very high energy yield per carbon in the original fatty acid. Acetyl-CoA can be metabolized through

neg: Fatty acid metabolism that there is enough acetyl-CoA to feed into the Krebs cycle and produce energy. High plasma levels of insulin in the blood plasma (e.g. after meals) cause the dephosphorylation and activation of acetyl-CoA carboxylase, thus promoting the formation of malonyl-CoA from acetyl-CoA, and consequently the conversion of carbohydrates into fatty acids, while epinephrine and glucagon (released into the blood during starvation and exercise) cause the phosphorylation of this enzyme, inhibiting lipogenesis in favor of fatty acid oxidation via beta-oxidation. Disorders of fatty acid metabolism can be described in terms of, for example, hypertriglyceridemia (too high level of triglycerides), or other

neg: Malonyl-CoA decarboxylase for the Krebs cycle. Cytoplasmic MCD is thought to play a role in the regulation of cytoplasmic malonyl-CoA abundance and, therefore, of mitochondrial fatty acid uptake and oxidation. It has been observed that MCD mRNA is most abundant in cardiac and skeletal muscles, tissues in which cytoplasmic malonyl-CoA is a strong inhibitor of mitochondrial fatty acid oxidation and which derive significant amounts of energy from fatty acid oxidation. In peroxisomes, it is proposed that this enzyme could be involved in degrading intraperoxisomal malonyl-CoA, which is produced by the peroxisomal beta oxidation of odd chain length dicarboxylic fatty acids (odd chain

neg: Metabolism plants do, but animals do not, have the necessary enzymatic machinery. As a result, after long-term starvation, vertebrates need to produce ketone bodies from fatty acids to replace glucose in tissues such as the brain that cannot metabolize fatty acids. In other organisms such as plants and bacteria, this metabolic problem is solved using the glyoxylate cycle, which bypasses the decarboxylation step in the citric acid cycle and allows the transformation of acetyl-CoA to oxaloacetate, where it can be used for the production of glucose. Polysaccharides and glycans are made by the sequential addition of monosaccharides by glycosyltransferase from a

neg: Absorptive state main product of fat digestion, are first broken down to fatty acids and glycerol through hydrolysis using Lipoprotein lipase. This allows them to freely pass through capillary walls. Most of this will be reconstituted as triglycerides and stored in adipose tissue. The rest is used for energy in adipose cells, skeletal muscle, and hepatocytes. In a low carb environment, other body cells will also begin to use triglycerides as energy sources. Amino Acids - The liver deaminates amino acids to keto acids to be used in the krebs cycle in order to produce ATP. They may also be converted to

neg: Fatty acid synthesis cells. Citrate acts to activate acetyl-CoA carboxylase under high levels, because high levels indicate that there is enough acetyl-CoA to feed into the Krebs cycle and conserve energy. High plasma levels of insulin in the blood plasma (e.g. after meals) cause the dephosphorylation of acetyl-CoA carboxylase, thus promoting the formation of malonyl-CoA from acetyl-CoA, and consequently the conversion of carbohydrates into fatty acids, while epinephrine and glucagon (released into the blood during starvation and exercise) cause the phosphorylation of this enzyme, inhibiting lipogenesis in favor of fatty acid oxidation via beta-oxidation. Many bacteria use the anaerobic pathway for synthesizing unsaturated

neg: Ketone bodies are high. This occurs between meals, during fasting, starvation and strenuous exercise, when blood glucose levels are likely to fall. Fatty acids are very high energy fuels, and are taken up by all metabolizing cells that have mitochondria. This is because fatty acids can only be metabolized in the mitochondria. Red blood cells do not contain mitochondria and are therefore entirely dependent on anaerobic glycolysis for their energy requirements. In all other tissues the fatty acids that enter the metabolizing cells are combined with co-enzyme A to form acyl-CoA chains. These are transferred into the mitochondria of the cells, where

neg: Lipid metabolism steps of fatty acids catabolism occur in the mitochondria. Long chain fatty acids (more than 14 carbon) need to be converted to Fatty acyl-CoA in order to pass across the mitochondria membrane. Fatty acid catabolism begins in the cytoplasm of cells as Acyl-CoA synthetase uses the energy from cleavage of an ATP to catalyze the addition of Coenzyme A to the fatty acid. The resulting Acyl-CoA cross the mitochondria membrane and enter the process of beta oxidation. The main products of the beta oxidation pathway are Acetyl-CoA (which is used in the Citric acid cycle to produce energy), NADH and

neg: Short-chain fatty acid colon health because it is the primary energy source for colonic cells. Short-chain fatty acid Short-chain fatty acids (SCFAs), also referred to as volatile fatty acids (VFAs), are fatty acids with less than six carbon atoms. Free SCFAs can cross the blood-brain barrier via monocarboxylate transporters. Short-chain fatty acids are produced when dietary fiber is fermented in the colon. Short-chain fatty acids and medium-chain fatty acids are primarily absorbed through the portal vein during lipid digestion, while long-chain fatty acids are packed into chylomicrons and enter lymphatic capillaries, and enter the blood first at the subclavian vein. Short-chain fatty acids

neg: Short-chain fatty acid Short-chain fatty acid Short-chain fatty acids (SCFAs), also referred to as volatile fatty acids (VFAs), are fatty acids with less than six carbon atoms. Free SCFAs can cross the blood-brain barrier via monocarboxylate transporters. Short-chain fatty acids are produced when dietary fiber is fermented in the colon. Short-chain fatty acids and medium-chain fatty acids are primarily absorbed through the portal vein during lipid digestion, while long-chain fatty acids are packed into chylomicrons and enter lymphatic capillaries, and enter the blood first at the subclavian vein. Short-chain fatty acids have diverse physiological roles in body functions. Butyrate is particularly important for

neg: Gluconeogenesis to pyruvate and enter into gluconeogenesis. In plants, specifically seedlings, the glyoxylate cycle can be used to convert fatty acids (acetate) into the primary carbon source of the organism. The glyoxylate cycle produces four-carbon dicarboxylic acids that can enter gluconeogenesis. In 1995, researchers identified the glyoxylate cycle in nematodes. In addition, the glyoxylate enzymes malate synthase and isocitrate lyase have been found in animal tissues. Genes coding for malate synthase have been identified in other metazoans including arthropods, echinoderms, and even some vertebrates. Mammals found to possess these genes include monotremes (platypus) and marsupials (opossum) but not placental mammals. Genes

neg: Ketogenic diet do this by using fatty acids. Since amino acids are needed to make proteins, which are essential for growth and repair of body tissues, these cannot be used only to produce glucose. This could pose a problem for the brain, since it is normally fuelled solely by glucose, and most fatty acids do not cross the blood–brain barrier. However, the liver can use long-chain fatty acids to synthesise the three ketone bodies β-hydroxybutyrate, acetoacetate and acetone. These ketone bodies enter the brain and "partially" substitute for blood glucose as a source of energy. The ketone bodies are possibly anticonvulsant; in

neg: Protein catabolism so that they can be processed into the Krebs/Citric Acid (TCA) Cycle. By proceeding into the Citric Acid Cycle, the original proteins will be converted into usable energy for the organism. There are also other processes to convert amino acids into usable molecules to enter the TCA cycle, such as transamination (transfer of amino group), decarboxylation (removal of carboxyl group), and dehydrogenation (removal of hydrogen). The proteins are digested in the intestines to produce the amino acids. The proteins are continuously being broken down and reformed, depending on the current needs that the body has. Proteins have different half-lives: some

neg: Randle cycle from the high concentration of fatty acids and the relationship to abnormalities of carbohydrate metabolism, including starvation, diabetes and Cushing’s syndrome. Randle cycle The Randle cycle, also known as the glucose fatty-acid cycle, is a metabolic process involving the competition of glucose and fatty acids for substrates. It is theorized to play a role in explaining type 2 diabetes and insulin resistance. It was named for Philip Randle, who described it in 1963. The Randle cycle is a biochemical mechanism involving the competition between glucose and fatty acids for their oxidation and uptake in muscle and adipose tissue. The cycle

neg: Flavin adenine dinucleotide positive reduction potential than NAD+ and is a very strong oxidizing agent. The cell utilizes this in many energetically difficult oxidation reactions such as dehydrogenation of a C-C bond to an alkene. FAD-dependent proteins function in a large variety of metabolic pathways including electron transport, DNA repair, nucleotide biosynthesis, beta-oxidation of fatty acids, amino acid catabolism, as well as synthesis of other cofactors such as CoA, CoQ and heme groups. One well-known reaction is part of the citric acid cycle (also known as the TCA or Krebs cycle); succinate dehydrogenase (complex II in the electron transport chain) requires covalently bound

neg: Beta oxidation overall reaction for one cycle of beta oxidation is: Fatty acid catabolism consists of: Free fatty acids cannot penetrate any biological membrane due to their negative charge. Free fatty acids must cross the cell membrane through specific transport proteins, such as the SLC27 family fatty acid transport protein. Once in the cytosol, the following processes bring fatty acids into the mitochondrial matrix so that beta-oxidation can take place. Once the fatty acid is inside the mitochondrial matrix, beta-oxidation occurs by cleaving two carbons every cycle to form acetyl-CoA. The process consists of 4 steps. Fatty acids are oxidized by most

neg: Fatty acid metabolism and the substrates that are used. The two pathways are mutually inhibitory, preventing the acetyl-CoA produced by beta-oxidation from entering the synthetic pathway via the acetyl-CoA carboxylase reaction. It can also not be converted to pyruvate as the pyruvate dehydrogenase complex reaction is irreversible. Instead the acetyl-CoA produced by the beta-oxidation of fatty acids condenses with oxaloacetate, to enter the citric acid cycle. During each turn of the cycle, two carbon atoms leave the cycle as CO in the decarboxylation reactions catalyzed by isocitrate dehydrogenase and alpha-ketoglutarate dehydrogenase. Thus each turn of the citric acid cycle oxidizes an acetyl-CoA unit

neg: Long-chain-fatty-acid—CoA ligase chain fatty acyl-CoAs causes the downregulation of FAS mRNA by vitamin D. Adrenoleukodystrophy (ALD), is the build up of long chain fatty acids in the brain and adrenal cortex, because of the decreased activity of long chain fatty acyl coa synthetase. The oxidation of the long chain fatty acids normally occurs in the peroxisome where the long chain fatty acyl coa synthetase is found. Long chain fatty acids enter the peroxisome via a transporter protein, ALDP, which creates a gate in the membrane of the peroxisome. In ALD the gene for this peroximal membrane transporter, ALDP, is defective, preventing long

neg: Glyoxylate cycle place in the TCA cycle, allowing simple carbon compounds to be used in the later synthesis of macromolecules, including glucose. Glyoxylate is subsequently combined with acetyl-CoA to produce malate, catalyzed by MS. Malate is also formed in parallel from succinate by the action of succinate dehydrogenase and fumarase. Fatty acids from lipids are commonly used as an energy source by vertebrates as fatty acids are degraded through beta oxidation into acetate molecules. This acetate, bound to the active thiol group of coenzyme A, enters the "citric acid cycle" (TCA cycle) where it is fully oxidized to carbon dioxide. This pathway

neg: SLC25A10 SLC25A10 The mitochondrial dicarboxylate carrier (DIC) is an integral membrane protein encoded by the "SLC25A10" gene in humans that catalyzes the transport of dicarboxylates such as malonate, malate, and succinate across the inner mitochondrial membrane in exchange for phosphate, sulfate, and thiosulfate by a simultaneous antiport mechanism, thus supplying substrates for the Krebs cycle, gluconeogenesis, urea synthesis, fatty acid synthesis, and sulfur metabolism. The "SLC25A10" gene is located on the q arm of chromosome 17 in position 25.3 and spans 8,781 base pairs. The gene has 11 exons and produces a 31.3 kDa protein composed of 287 amino acids. Intron

neg: Beta oxidation of the tissues in the body. However, some tissues such as the red blood cells of mammals (which do not contain mitochondria), and cells of the central nervous system do not use fatty acids for their energy requirements, but instead use carbohydrates (red blood cells and neurons) or ketone bodies (neurons only). Because many fatty acids are not fully saturated or do not have an even number of carbons, several different mechanisms have evolved, described below. Once inside the mitochondria, each cycle of β-oxidation, liberating a two carbon unit (acetyl-CoA), occurs in a sequence of four reactions: This process continues

neg: Fatty acid degradation fatty acids, the reaction continues. Once inside the mitochondria, the β-oxidation of fatty acids occurs via five recurring steps: Fatty acid degradation Fatty acid degradation is the process in which fatty acids are broken down into their metabolites, in the end generating acetyl-CoA, the entry molecule for the citric acid cycle, the main energy supply of animals. It includes three major steps: Initially in the process of degradation, fatty acids are stored in fat cells (adipocytes). The breakdown of this fat is known as lipolysis. The products of lipolysis, free fatty acids, are released into the bloodstream and circulate throughout

neg: Fatty acid degradation Fatty acid degradation Fatty acid degradation is the process in which fatty acids are broken down into their metabolites, in the end generating acetyl-CoA, the entry molecule for the citric acid cycle, the main energy supply of animals. It includes three major steps: Initially in the process of degradation, fatty acids are stored in fat cells (adipocytes). The breakdown of this fat is known as lipolysis. The products of lipolysis, free fatty acids, are released into the bloodstream and circulate throughout the body. During the breakdown of triacylglycerols into fatty acids, more than 75% of the fatty acids are converted

neg: Fatty acid of beta-oxidation followed by further combustion in the citric acid cycle to CO and water. Cells in the central nervous system, which, although they possess mitochondria, cannot take free fatty acids up from the blood, as the blood-brain barrier is impervious to most free fatty acids, excluding short-chain fatty acids and medium-chain fatty acids. These cells have to manufacture their own fatty acids from carbohydrates, as described above, in order to produce and maintain the phospholipids of their cell membranes, and those of their organelles. The following table gives the fatty acid, vitamin E and cholesterol composition of some common

neg: Randle cycle Randle cycle The Randle cycle, also known as the glucose fatty-acid cycle, is a metabolic process involving the competition of glucose and fatty acids for substrates. It is theorized to play a role in explaining type 2 diabetes and insulin resistance. It was named for Philip Randle, who described it in 1963. The Randle cycle is a biochemical mechanism involving the competition between glucose and fatty acids for their oxidation and uptake in muscle and adipose tissue. The cycle controls fuel selection and adapts the substrate supply and demand in normal tissues. This cycle adds a nutrient-mediated fine tuning on

neg: Peroxisome synthesis in animals. Other known peroxisomal functions include the glyoxylate cycle in germinating seeds ("glyoxysomes"), photorespiration in leaves, glycolysis in trypanosomes ("glycosomes"), and methanol and/or amine oxidation and assimilation in some yeasts. Peroxisomes were identified as organelles by the Belgian cytologist Christian de Duve in 1967 after they had been first described by a Swedish doctoral student, J. Rhodin in 1954. A major function of the peroxisome is the breakdown of very long chain fatty acids through beta oxidation. In animal cells, the long fatty acids are converted to medium chain fatty acids, which are subsequently shuttled to mitochondria where

neg: Fatty acid synthesis each turn of the citric acid cycle oxidizes an acetyl-CoA unit while regenerating the oxaloacetate molecule with which the acetyl-CoA had originally combined to form citric acid. The decarboxylation reactions occur before malate is formed in the cycle. This is the only substance that can be removed from the mitochondrion to enter the gluconeogenic pathway to form glucose or glycogen in the liver or any other tissue. There can therefore be no net conversion of fatty acids into glucose. Only plants possess the enzymes to convert acetyl-CoA into oxaloacetate from which malate can be formed to ultimately be converted to

neg: Omega oxidation β oxidation. The steps of the process are as follows: After these three steps, either end of the fatty acid can be attached to coenzyme A. The molecule can then enter the mitochondrion and undergo β oxidation. The final products after successive oxidations include succinic acid, which can enter the citric acid cycle, and adipic acid. The first step in ω-oxidation, i.e. addition of a hydroxy residue to the omega carbon of short, intermediate, and long chain unsaturated or saturated fatty acids, can serve to produce or inactivate signaling molecules. In humans, a subset of Cytochrome P450 (CYP450) microsome-bound ω-hydroxylases

neg: Citric acid cycle transported out of the mitochondrion to be converted into cytosolic oxaloacetate and ultimately into glucose. These are the so-called "glucogenic" amino acids. De-aminated alanine, cysteine, glycine, serine, and threonine are converted to pyruvate and can consequently either enter the citric acid cycle as "oxaloacetate" (an anaplerotic reaction) or as "acetyl-CoA" to be disposed of as CO and water. In fat catabolism, triglycerides are hydrolyzed to break them into fatty acids and glycerol. In the liver the glycerol can be converted into glucose via dihydroxyacetone phosphate and glyceraldehyde-3-phosphate by way of gluconeogenesis. In many tissues, especially heart and skeletal muscle tissue,

neg: Free fatty acid receptor 1 of the FFA1 gene, which has made these receptors a new target for the treatment of type II diabetes. While fatty acids themselves do not elicit insulin secretion, FFA1 activation increases the amount of insulin being secreted through various linked pathways. It has also been shown that chronic exposure to high amounts of free fatty acids, like on a high fat diet, can impair the function and secretory capacity of pancreatic β-cells. As stated previously, FFA1 has an affinity for long chain fatty acids. Such fatty acids are also present in the brain, where FFA1 has also been found in

neg: Glyoxylate cycle gluconeogenesis. The net result of the glyoxylate cycle is therefore the production of glucose from fatty acids. Succinate generated in the first step can enter into the citric acid cycle to eventually form oxaloacetate. In plants the glyoxylate cycle occurs in special peroxisomes which are called glyoxysomes. This cycle allows seeds to use lipids as a source of energy to form the shoot during germination. The seed cannot produce biomass using photosynthesis because of lack of an organ to perform this function. The lipid stores of germinating seeds are used for the formation of the carbohydrates that fuel the growth

neg: Acyl-CoA cytosol, but oxidation occurs in the mitochondria. Because there is no transport protein for CoA adducts, acyl groups must enter the mitochondria via a shuttle system involving the small molecule carnitine. Acyl-CoA Acyl-CoA is a group of coenzymes involved in the metabolism of fatty acids. It is a temporary compound formed when coenzyme A (CoA) attaches to the end of a long-chain fatty acid inside living cells. The compound undergoes beta oxidation, forming one or more molecules of acetyl-CoA. This, in turn, enters the citric acid cycle, eventually forming several molecules of ATP. To be oxidatively degraded, a fatty acid

neg: Fatty acid cytosol where the synthesis of fatty acids occurs. This cannot occur directly. To obtain cytosolic acetyl-CoA, citrate (produced by the condensation of acetyl-CoA with oxaloacetate) is removed from the citric acid cycle and carried across the inner mitochondrial membrane into the cytosol. There it is cleaved by ATP citrate lyase into acetyl-CoA and oxaloacetate. The oxaloacetate is returned to the mitochondrion as malate. The cytosolic acetyl-CoA is carboxylated by acetyl CoA carboxylase into malonyl-CoA, the first committed step in the synthesis of fatty acids. Malonyl-CoA is then involved in a repeating series of reactions that lengthens the growing fatty acid

neg: Lipid triglycerides, sterols, and membrane phospholipids. The process of lipid metabolism synthesizes and degrades the lipid stores and produces the structural and functional lipids characteristic of individual tissues. In animals, when there is an oversupply of dietary carbohydrate, the excess carbohydrate is converted to triglycerides. This involves the synthesis of fatty acids from acetyl-CoA and the esterification of fatty acids in the production of triglycerides, a process called lipogenesis. Fatty acids are made by fatty acid synthases that polymerize and then reduce acetyl-CoA units. The acyl chains in the fatty acids are extended by a cycle of reactions that add the

neg: Flavobacterium psychrophilum result in a mixture of amino acids and oligopeptides that comprise the main source of carbon, nitrogen, and energy. Peptidases degrade imported peptides to amino acids, which are then processed by amino acids catabolic pathways. The degradation of lipids to fatty acids is achieved by a phospholipase and by three enzymes of the esterase-lipase-thioesterase family. Beta-oxidation of fatty acids is performed by a long-chain fatty acid-CoA ligase, three fatty acid dehydrogenases, a crotonase and three thiolases. Most of the degradation products of host proteins and lipids by the "F. psychrophilum" are available as citric acid cycle precursors. Because of its

neg: Fatty acid metabolism Fatty acid metabolism Fatty acid metabolism consists of catabolic processes that generate energy, and anabolic processes that create biologically important molecules (triglycerides, phospholipids, second messengers, local hormones and ketone bodies). Fatty acids are a family of molecules classified within the lipid macronutrient class. One role of fatty acids in animal metabolism is energy production, captured in the form of adenosine triphosphate (ATP). When compared to other macronutrient classes (carbohydrates and protein), fatty acids yield the most ATP on an energy per gram basis, when they are completely oxidized to CO and water by beta oxidation and the citric acid cycle.

neg: Lipid metabolism small intestines. Once the triglycerides are broken down into individual fatty acids and glycerols, along with cholesterol, they will aggregate into structures called micelles. Fatty acids and monoglycerides leave the micelles and diffuse across the membrane to enter the intestinal epithelial cells. In the cytosol of epithelial cells, fatty acids and monoglycerides are recombined back into triglycerides. In the cytosol of epithelial cells, triglycerides and cholesterol are packaged into bigger particles called chylomicrons which are amphipathic structures that transport digested lipids. Chylomicrons will travel through the blood stream to enter adipose and other tissues in the body. Due to the

neg: Triheptanoin Triheptanoin Triheptanoin is a triglyceride that is composed of three seven-carbon (C7:0) fatty acids. These odd-carbon fatty acids are able to provide anaplerotic substrates for the TCA cycle. Triheptanoin is used clinically in humans to treat inherited metabolic diseases, such as pyruvate carboxylase deficiency and carnitine palmitoyltransferase II deficiency. It also appears to increase the efficacy of the ketogenic diet as a treatment for epilepsy. Since triheptanoin is composed of odd-carbon fatty acids, it can produce ketone bodies with five carbon atoms, as opposed to even-carbon fatty acids which are metabolized to ketone bodies with four carbon atoms. The five-carbon

neg: Fatty acid synthesis in the liver and adipose tissue, as well as in the mammary glands during lactation. The pyruvate produced by glycolysis is an important intermediary in the conversion of carbohydrates into fatty acids and cholesterol. This occurs via the conversion of pyruvate into acetyl-CoA in the mitochondrion. However, this acetyl CoA needs to be transported into cytosol where the synthesis of fatty acids and cholesterol occurs. This cannot occur directly. To obtain cytosolic acetyl-CoA, citrate (produced by the condensation of acetyl CoA with oxaloacetate) is removed from the citric acid cycle and carried across the inner mitochondrial membrane into the cytosol.

neg: Randle cycle leads to a bigger proportion of electrons being transported to complex 2 rather than complex 1 of the respiratory chain. This difference leads to a less efficient oxidative phosphorylation. By oxidizing fatty acids, mitochondria increase their respiration while increasing the production of ROS. Fatty acids may act directly upon the pancreatic β-cell to regulate glucose-stimulated insulin secretion. This effect is biphasic. Initially fatty acids potentiate the effects of glucose. After prolonged exposure to high fatty acid concentrations this changes to an inhibition. Randle suggested that the term fatty acid syndrome would be appropriate to apply to the biochemical syndrome resulting

neg: Essential fatty acid is attributed to arachidonic acid. Arachidonic acid is the major precursor of prostaglandins, leukotrienes that play a vital role in cell signaling, and an endogenous cannabinoid anandamide. Metabolites from the ω-3 pathway, mainly from eicosapentaenoic acid, are mostly inactive, and this explains why ω-3 fatty acids do not correct the reproductive failure in rats where arachidonic is needed to make active prostaglandins that cause uterine contraction. To some extent, any ω-3 or ω-6 can contribute to the growth-promoting effects of EFA deficiency, but only ω-6 fatty acids can restore reproductive performance and correct the dermatitis in rats. Particular fatty acids

neg: Citric acid cycle rate of ATP production by the mitochondrion, and thus the availability of ATP to the cell. "Acetyl-CoA", on the other hand, derived from pyruvate oxidation, or from the beta-oxidation of fatty acids, is the only fuel to enter the citric acid cycle. With each turn of the cycle one molecule of "acetyl-CoA" is consumed for every molecule of "oxaloacetate" present in the mitochondrial matrix, and is never regenerated. It is the oxidation of the acetate portion of "acetyl-CoA" that produces CO and water, with the energy thus released captured in the form of ATP. The three steps of beta-oxidation resemble

neg: Randle cycle is stimulated. The LCFAs are then rerouted to esterification. These conditions exist in tissues rich in oxygen, in which AMPK is inactive and glucose inactivates the AMPK (researched in skeletal muscle). The inhibition of MCD suppresses the oxidation of fatty acids and stimulates glucose oxidation. In a study on MCD deficient mice there was no difference in the oxidation of fatty acids and glucose in the heart under aerobic conditions. It is theorized that the overexpression of fatty acids being used makes up for the lack of MCD. Long chain fatty acid uptake is mediated by several transporters, including FAT

neg: Fatty acid tissues) are distributed to cells to serve as a fuel for muscular contraction and general metabolism. They are broken down to CO and water by the intra-cellular mitochondria, releasing large amounts of energy, captured in the form of ATP through beta oxidation and the citric acid cycle. Fatty acids that are required for good health but cannot be made in sufficient quantity from other substrates, and therefore must be obtained from food, are called essential fatty acids. There are two series of essential fatty acids: one has a double bond three carbon atoms away from the methyl end; the other

neg: Fatty acid dietary fats. Fatty acids exhibit reactions like other carboxylic acids, i.e. they undergo esterification and acid-base reactions. Fatty acids do not show a great variation in their acidities, as indicated by their respective p"K". Nonanoic acid, for example, has a p"K" of 4.96, being only slightly weaker than acetic acid (4.76). As the chain length increases, the solubility of the fatty acids in water decreases, so that the longer-chain fatty acids have minimal effect on the pH of an aqueous solution. Even those fatty acids that are insoluble in water will dissolve in warm ethanol, and can be titrated with

neg: Nutrition useful in the food processing industry, such as rancidity resistance. Most fatty acids are non-essential, meaning the body can produce them as needed, generally from other fatty acids and always by expending energy to do so. However, in humans, at least two fatty acids are essential and must be included in the diet. An appropriate balance of essential fatty acids—omega-3 and omega-6 fatty acids—seems also important for health, although definitive experimental demonstration has been elusive. Both of these "omega" long-chain polyunsaturated fatty acids are substrates for a class of eicosanoids known as prostaglandins, which have roles throughout the human body.

neg: Ketogenesis further oxidized by the citric acid cycle (TCA/Krebs cycle) and then by the mitochondrial electron transport chain to release energy. However, if the amounts of acetyl-CoA generated in fatty-acid β-oxidation challenge the processing capacity of the TCA cycle; i.e. if activity in TCA cycle is low due to low amounts of intermediates such as oxaloacetate, acetyl-CoA is then used instead in biosynthesis of ketone bodies via acetoacyl-CoA and β-hydroxy-β-methylglutaryl-CoA (HMG-CoA). Furthermore, since there is only a limited amount of coenzyme A in the liver the production of ketogenesis allows some of the coenzyme to be freed to continue fatty-acid β-oxidation.

neg: Phosphatidylserine Phosphatidylserine Phosphatidylserine (abbreviated Ptd-L-Ser or PS) is a phospholipid and is a component of the cell membrane. It plays a key role in cell cycle signaling, specifically in relation to apoptosis. It is a key pathway for viruses to enter cells via viral apoptotic mimicry. Phosphatidylserine is a phospholipid (more specifically a glycerophospholipid). It consists of two fatty acids attached in ester linkage to the first and second carbon of glycerol and serine attached through a phosphodiester linkage to the third carbon of the glycerol. Phosphatidylserine coming from plants and phosphatidylserine coming from animals differ in fatty acid composition. Phosphatidylserine(s)

neg: Citric acid cycle fatty acids are broken down through a process known as beta oxidation, which results in the production of mitochondrial "acetyl-CoA", which can be used in the citric acid cycle. Beta oxidation of fatty acids with an odd number of methylene bridges produces propionyl-CoA, which is then converted into "succinyl-CoA" and fed into the citric acid cycle as an anaplerotic intermediate. The total energy gained from the complete breakdown of one (six-carbon) molecule of glucose by glycolysis, the formation of 2 "acetyl-CoA" molecules, their catabolism in the citric acid cycle, and oxidative phosphorylation equals about 30 ATP molecules, in eukaryotes. The

neg: Gluconeogenesis facilitates entering of their carbon skeleton into the cycle directly (as pyruvate or oxaloacetate), or indirectly via the citric acid cycle. The contribution of Cori cycle lactate to overall glucose production increases with fasting duration. Specifically, after 12, 20, and 40 hours of fasting by human volunteers, the contribution of Cori cycle lactate to gluconeogenesis was 41%, 71%, and 92%, respectively. Whether even-chain fatty acids can be converted into glucose in animals has been a longstanding question in biochemistry. It is known that odd-chain fatty acids can be oxidized to yield propionyl-CoA, a precursor for succinyl-CoA, which can be converted

neg: Fatty alcohol mg per day of mixed C–C alcohols, including octacosanol and triacontanol, lower low-density lipoprotein (LDL) cholesterol by 21%–29% and raise high-density lipoprotein cholesterol by 8%–15%. Wax esters are hydrolyzed by a bile salt–dependent pancreatic esterase, releasing long-chain alcohols and fatty acids that are absorbed in the gastrointestinal tract. Studies of fatty alcohol metabolism in fibroblasts suggest that very long-chain fatty alcohols, fatty aldehydes, and fatty acids are reversibly inter-converted in a fatty alcohol cycle. The metabolism of these compounds is impaired in several inherited human peroxisomal disorders, including adrenoleukodystrophy and Sjögren–Larsson syndrome. Fatty alcohols are relatively benign materials, with LD

neg: Lipid fatty acids are broken down in the mitochondria or in peroxisomes to generate acetyl-CoA. For the most part, fatty acids are oxidized by a mechanism that is similar to, but not identical with, a reversal of the process of fatty acid synthesis. That is, two-carbon fragments are removed sequentially from the carboxyl end of the acid after steps of dehydrogenation, hydration, and oxidation to form a beta-keto acid, which is split by thiolysis. The acetyl-CoA is then ultimately converted into ATP, CO, and HO using the citric acid cycle and the electron transport chain. Hence the citric acid cycle can

neg: Randle cycle acids as the preferred fuel source for respiration. In the liver β-oxidation of fatty acids fulfills the local energy needs and may lead to ketogenesis (creating ketone bodies out of fatty acids.) The ketone bodies are then used to meet the demands of tissues other than the liver. The inhibition of glucose oxidation causes fatty acids and ketone bodies to contribute to a glucose-sparing effect, which is an essential survival mechanism for the brain during times of starvation. This inhibition of glucose oxidation at the level of pyruvate dehydrogenase preserves pyruvate and lactate, both of which are gluconeogenic precursors. The

neg: Dietary fiber fermented to short-chain fatty acids (chiefly acetic, propionic and n-butyric), and carbon dioxide, hydrogen and methane. Almost all of these short-chain fatty acids will be absorbed from the colon. This means that fecal short-chain fatty acid estimations do not reflect cecal and colonic fermentation, only the efficiency of absorption, the ability of the fiber residue to sequestrate short-chain fatty acids, and the continued fermentation of fiber around the colon, which presumably will continue until the substrate is exhausted. The production of short-chain fatty acids has several possible actions on the gut mucosa. All of the short-chain fatty acids are readily

neg: Mesopelagic zone consumption. Additionally, the demand for nutraceuticals is also rapidly growing, stemming from the popular human consumption of Omega-3 Fatty Acids in addition to the aquaculture industry that requires a specific marine oil for feed material. Lanternfish are of much interest to the aquaculture market, as they are especially high in fatty acids. The mesopelagic region plays an important role in the global carbon cycle, as it is the area where most of the surface organic matter is respired. Mesopelagic species also acquire carbon during their diel vertical migration to feed in surface waters, and they transport that carbon to the

neg: Randle cycle (fatty acid translocase)/CD36. CD36 deletion rescues lipotoxic cardiomyopathy. FAT/CD36 may be controlled by insulin and AMPK. Increased transport coupled to the formation of the CoA derivatives and the resulting AMPK activation should ensure efficient fatty acid uptake and metabolism. Fatty acids are preferentially oxidized because of the inactivation of PDH by fatty acid oxidation inhibiting glucose oxidation. This suggests that mitochondrial metabolism may control fuel selection. Cellular respiration is stimulated by fatty acids and this relates to an increase in the mitochondrial NADH to NAD+ ratio, suggesting that energy provision overtakes energy consumption. Switching from glucose to fatty acid oxidation

neg: Mitochondrion into the other. Hence, the addition of any one of them to the cycle has an anaplerotic effect, and its removal has a cataplerotic effect. These anaplerotic and cataplerotic reactions will, during the course of the cycle, increase or decrease the amount of oxaloacetate available to combine with acetyl-CoA to form citric acid. This in turn increases or decreases the rate of ATP production by the mitochondrion, and thus the availability of ATP to the cell. Acetyl-CoA, on the other hand, derived from pyruvate oxidation, or from the beta-oxidation of fatty acids, is the only fuel to enter the citric

neg: Glucose oxygen available for this, the glucose degradation in animals occurs anaerobic to lactate via lactic acid fermentation and releases less energy. Muscular lactate enters the liver through the bloodstream in mammals, where gluconeogenesis occurs (Cori cycle). With a high supply of glucose, the metabolite acetyl-CoA from the Krebs cycle can also be used for fatty acid synthesis. Glucose is also used to replenish the body's glycogen stores, which are mainly found in liver and skeletal muscle. These processes are hormonally regulated. In other living organisms, other forms of fermentation can occur. The bacterium "Escherichia coli" can grow on nutrient media

neg: Glycolysis cytosol where the synthesis of fatty acids and cholesterol occurs. This cannot occur directly. To obtain cytosolic acetyl-CoA, citrate (produced by the condensation of acetyl CoA with oxaloacetate) is removed from the citric acid cycle and carried across the inner mitochondrial membrane into the cytosol. There it is cleaved by ATP citrate lyase into acetyl-CoA and oxaloacetate. The oxaloacetate is returned to mitochondrion as malate (and then back into oxaloacetate to transfer more acetyl-CoA out of the mitochondrion). The cytosolic acetyl-CoA can be carboxylated by acetyl-CoA carboxylase into malonyl CoA, the first committed step in the synthesis of fatty acids,

neg: Metabolism to free fatty acids and glycerol. The glycerol enters glycolysis and the fatty acids are broken down by beta oxidation to release acetyl-CoA, which then is fed into the citric acid cycle. Fatty acids release more energy upon oxidation than carbohydrates because carbohydrates contain more oxygen in their structures. Steroids are also broken down by some bacteria in a process similar to beta oxidation, and this breakdown process involves the release of significant amounts of acetyl-CoA, propionyl-CoA, and pyruvate, which can all be used by the cell for energy. "M. tuberculosis" can also grow on the lipid cholesterol as a

neg: Triheptanoin ketones produced from triheptanoin are beta-ketopentanoate and beta-hydroxypentanoate. Each of these ketone bodies easily crosses the blood–brain barrier and enters the brain. Triheptanoin Triheptanoin is a triglyceride that is composed of three seven-carbon (C7:0) fatty acids. These odd-carbon fatty acids are able to provide anaplerotic substrates for the TCA cycle. Triheptanoin is used clinically in humans to treat inherited metabolic diseases, such as pyruvate carboxylase deficiency and carnitine palmitoyltransferase II deficiency. It also appears to increase the efficacy of the ketogenic diet as a treatment for epilepsy. Since triheptanoin is composed of odd-carbon fatty acids, it can produce ketone bodies

neg: Gluconeogenesis for isocitrate lyase are found only in nematodes, in which, it is apparent, they originated in horizontal gene transfer from bacteria. The existence of glyoxylate cycles in humans has not been established, and it is widely held that fatty acids cannot be converted to glucose in humans directly. However, carbon-14 has been shown to end up in glucose when it is supplied in fatty acids. Despite these findings, it is considered unlikely that the 2-carbon acetyl-CoA derived from the oxidation of fatty acids would produce a net yield of glucose via the citric acid cycle – however, acetyl-CoA can be

neg: Medium-chain triglyceride MCTs passively diffuse from the GI tract to the portal system (longer fatty acids are absorbed into the lymphatic system) without requirement for modification like long-chain fatty acids or very-long-chain fatty acids. In addition, MCTs do not require bile salts for digestion. Patients who have malnutrition, malabsorption or particular fatty-acid metabolism disorders are treated with MCTs because MCTs do not require energy for absorption, use, or storage. Medium-chain triglycerides are generally considered a good biologically inert source of energy that the human body finds reasonably easy to metabolize. They have potentially beneficial attributes in protein metabolism, but may be contraindicated

neg: Fatty acid degradation activated, the acyl CoA is transported into the mitochondrial matrix. This occurs via a series of similar steps: It is important to note that "carnitine acyltransferase I" undergoes allosteric inhibition as a result of malonyl-CoA, an intermediate in fatty acid biosynthesis, in order to prevent futile cycling between beta-oxidation and fatty acid synthesis. The mitochondrial oxidation of fatty acids takes place in three major steps: 1.β-oxidation: conversion of fatty acids into 2-carbon acetyl Co-A units. 2.entry of acetyl Co-A into TCA cycle to yield energy. 3.finally, the electron transport chain in the mitochondria.though in this step, no direct participation of

neg: Human nutrition always by expending energy to do so. However, in humans, at least two fatty acids are essential and must be included in the diet. An appropriate balance of essential fatty acids – omega-3 and omega-6 fatty acids – seems also important for health, though definitive experimental demonstration has been elusive. Both of these "omega" long-chain polyunsaturated fatty acids are substrates for a class of eicosanoids known as prostaglandins, which have roles throughout the human body. They are hormones, in some respects. The omega-3 eicosapentaenoic acid (EPA), which can be made in the human body from the omega-3 essential fatty acid

neg: Acute fatty liver of pregnancy an accumulation of medium and long chain fatty acids. When this occurs in the foetus, the unmetabolized fatty acids will re-enter the maternal circulation through the placenta, and overwhelm the beta-oxidation enzymes of the mother. The gene responsible for LCHAD has been isolated, and the most common mutation found in acute fatty liver of pregnancy is the E474Q missense mutation. LCHAD deficiency is autosomal recessive in inheritance and mothers are often found to be heterozygous for the affected mutation. The diagnosis of acute fatty liver of pregnancy is usually made on clinical grounds by the treating physician or midwife, but

neg: Glyoxysome Glyoxysome Glyoxysomes are specialized peroxisomes found in plants (particularly in the fat storage tissues of germinating seeds) and also in filamentous fungi. Seeds that contain fats and oils include corn, soybean, sunflower, peanut and pumpkin. As in all peroxisomes, in glyoxysomes the fatty acids are oxidized to acetyl-CoA by peroxisomal β-oxidation enzymes. When the fatty acids are oxidized hydrogen peroxide (HO) is produced as oxygen (O) is consumed. Thus the seeds need oxygen to germinate. Besides peroxisomal functions, glyoxysomes possess additionally the key enzymes of glyoxylate cycle (isocitrate lyase and malate synthase) which accomplish the glyoxylate cycle bypass. Thus, glyoxysomes

neg: Fatty acid synthesis carboxylic acids as primers instead of alpha-keto acids. In general, this method is used by bacteria that do not have the ability to perform the branch-chain fatty acid system using alpha-keto primers. Typical short-chain primers include isovalerate, isobutyrate, and 2-methyl butyrate. In general, the acids needed for these primers are taken up from the environment; this is often seen in ruminal bacteria. The overall reaction is: The difference between (straight-chain) fatty acid synthase and branch-chain fatty acid synthase is substrate specificity of the enzyme that catalyzes the reaction of acyl-CoA to acyl-ACP. Omega-alicyclic fatty acids typically contain an omega-terminal propyl

neg: Reverse Krebs cycle Reverse Krebs cycle The reverse Krebs cycle (also known as the reverse tricarboxylic acid cycle, the reverse TCA cycle, or the reverse citric acid cycle) is a sequence of chemical reactions that are used by some bacteria to produce carbon compounds from carbon dioxide and water. The reaction is the citric acid cycle run in reverse: Where the Krebs cycle takes complex carbon molecules in the form of sugars and oxidizes them to CO and water, the reverse cycle takes CO and water to make carbon compounds. This process is used by some bacteria to synthesise carbon compounds, sometimes using

neg: Reverse Krebs cycle Reverse Krebs cycle The reverse Krebs cycle (also known as the reverse tricarboxylic acid cycle, the reverse TCA cycle, or the reverse citric acid cycle) is a sequence of chemical reactions that are used by some bacteria to produce carbon compounds from carbon dioxide and water. The reaction is the citric acid cycle run in reverse: Where the Krebs cycle takes complex carbon molecules in the form of sugars and oxidizes them to CO and water, the reverse cycle takes CO and water to make carbon compounds. This process is used by some bacteria to synthesise carbon compounds, sometimes using

neg: Beta oxidation until the entire chain is cleaved into acetyl CoA units. The final cycle produces two separate acetyl CoAs, instead of one acyl CoA and one acetyl CoA. For every cycle, the Acyl CoA unit is shortened by two carbon atoms. Concomitantly, one molecule of FADH, NADH and acetyl CoA are formed. In general, fatty acids with an odd number of carbons are found in the lipids of plants and some marine organisms. Many ruminant animals form a large amount of 3-carbon propionate during the fermentation of carbohydrates in the rumen. Long-chain fatty acids with an odd number of carbon atoms

neg: History of biochemistry he took in was lost through what he called "insensible perspiration". One of the most prolific of these modern biochemists was Hans Krebs who made huge contributions to the study of metabolism. Krebs was a student of extremely important Otto Warburg, and wrote a biography of Warburg by that title in which he presents Warburg as being educated to do for biological chemistry what Fischer did for organic chemistry. Which he did. Krebs discovered the urea cycle and later, working with Hans Kornberg, the citric acid cycle and the glyoxylate cycle. These discoveries led to Krebs being awarded the Nobel

neg: Fatty acid synthesis g is locked inside the skeletal muscles and is unavailable to the body as a whole. The 100 g or so of glycogen stored in the liver is depleted within one day of starvation. Thereafter the glucose that is released into the blood by the liver for general use by the body tissues, has to be synthesized from the glucogenic amino acids and a few other gluconeogenic substrates, which do not include fatty acids. Fatty acids are broken down to acetyl-CoA by means of beta oxidation inside the mitochondria, whereas fatty acids are synthesized from acetyl-CoA outside the mitochondrion, in

neg: Long-chain-alcohol oxidase oxidized by long-chain fatty alcohol oxidase in yeast. The long-chain alcohol is then oxidized by long-chain fatty aldehyde dehydrogenase to a carboxylic acid, also producing NADH from NAD+. Fatty acids can be oxidized again to make dicarboxylic species that join with coenzyme A and enter the beta oxidation pathway in the peroxisome. Long-chain alcohol oxidase is also used in germinating seedlings of jojoba ("Simmondsia chinensis") to degrade esterified long-chain fatty alcohols stored as wax. This enzyme has been found in the following species: Yeast Other Fungi Plants This enzyme is required for production of dicarboxylic acids by industrial Candida yeast,

neg: Randle cycle glucose fatty acid cycle is also observed in the fed state after a high-fat meal or during exercise. This is when plasma concentrations of fatty acids or ketone bodies are increased. The glucose that is not oxidized is then rerouted to glycogen. This rerouting to glycogen explains the rapid resynthesis of muscle glycogen after exercise as well as the increased glycogen content in muscles found in starvation or diabetes. This mechanism replenishes the intermediates of the citric acid cycle. The impairment of glucose metabolism by fatty acid oxidation is mediated by the short-term inhibition of several glycolytic processes. The extent

neg: Melanoplus bivittatus shortage, this species has been known to cannibalize one another. During times of colder weather (below 25 °C) "Melanoplus bivittatus" will not feed since fecal production is low and excrete can not be expelled. This species of Orthoptera require a diet with linoleic acid or unsaturated fatty acids, since these acids keep the organism's wings from crumpling. Orthoptera are known pests to agricultural environments. Some species can completely ruin crops and have detrimental economic effects on farmers. "Melanoplus bivittatus" can cause crop damage all through their life cycle. Not only do "M. bivittatus" damage crops, but they tend to eat

neg: Methylmalonyl-CoA mutase deficiency described for propanoyl-CoA. Odd chain fatty acids are also metabolized through the methylmalonyl pathway. The degradation of odd chain fatty acids releases Acetyl-CoA and propionyl-CoA. Propionyl-CoA is then converted to succinyl-CoA, and both succinyl-CoA and propionyl-CoA are interjected into the tricarboxylic acid cycle for continued production of reductant. The final product of methylmalonyl-CoA mutase activity is succinyl-CoA which is a tricarboxylic acid cycle substrate. A side effect of excess methylmalonyl-CoA is an interruption of the enzymes responsible for other transformations earlier in the metabolism of propionyl-CoA, leading to propanoic acidemia as well. This, along with an excess of methylmalonyl-CoA leads

neg: Calanus hyperboreus year of development, indicating a likely life cycle of two to three years. Compared to the congeneric "C. finmarchicus", "C. hyperboreus" has a higher concentration of lipids as a percentage of dry mass. Additionally, its lipid stores have a higher concentration of wax esters than "C. finmarchicus" and "C. glacialis". "C. hyperboreus" also has longer chained fatty alcohols and (albeit to a lesser extent) fatty acids than the two other species. This is likely due to the higher concentration of energy per unit mass of longer chained fatty alcohols and acids. Finally, this species also has higher concentrations of polyunsaturated

neg: Amphibolic converge into the following pathway, viz, Glycolysis , Krebs cycle and electron transport chain ,exist as amphibolic pathway meaning that they can function anabolically as well as catabolically. Other important amphibolic pathway are :Embden – Meyerhof pathway , Pentose phosphate pathway and Entner -Doudoroff pathway The Embeden – Meyerhof pathway along with Krebs cycle are the centre of metabolism in nearly all bacteria and eukaryotes, they do not only provide energy they also provide precursors for biosynthesis of macromolecules that make up living system The citric acid cycle (The Krebs Cycle) is a good example of "amphibolic pathway", because it

neg: ELFV dehydrogenase and the NAD-dependent enzyme, which catalyses the reverse reaction - this form links the L-amino acids with the Krebs cycle, which provides a major pathway for metabolic interconversion of alpha-amino acids and alpha-keto acids. Leucine dehydrogenase (LeuDH) is a NAD-dependent enzyme that catalyses the reversible deamination of leucine and several other aliphatic amino acids to their keto analogues. Each subunit of this octameric enzyme from "Bacillus sphaericus" contains 364 amino acids and folds into two domains, separated by a deep cleft. The nicotinamide ring of the NAD+ cofactor binds deep in this cleft, which is thought to close during the

neg: Keto acid Keto acid Keto acids or ketoacids (also called oxo acids or oxoacids) are organic compounds that contain a carboxylic acid group and a ketone group. In several cases, the keto group is hydrated. The alpha-keto acids are especially important in biology as they are involved in the Krebs citric acid cycle and in glycolysis. Common types of keto acids include: Keto acids appear in a wide variety of anabolic pathways in metabolism, across living organisms. For instance, in plants (specifically, in hemlock, pitcher plants, and fool's parsley), 5-oxo-octanoic acid is converted in enzymatic and non-enzymatic steps into the cyclic class

neg: Citric acid cycle source of carbon for the TCA cycle. Citric acid cycle The citric acid cycle (CAC) – also known as the" TCA cycle (tricarboxylic acid cycle) " or the" Krebs cycle "– is a series of chemical reactions used by all aerobic organisms to release stored energy through the oxidation of acetyl-CoA derived from carbohydrates, fats, and proteins into adenosine triphosphate (ATP) and carbon dioxide. In addition, the cycle provides precursors of certain amino acids, as well as the reducing agent NADH, that are used in numerous other reactions. Its central importance to many biochemical pathways suggests that it was one

neg: Butterfat in dairy products. Commercial products generally contain the minimum legal amount of fat with any excess being removed to make cream, a valuable commodity. Butterfat Butterfat or milkfat is the fatty portion of milk. Milk and cream are often sold according to the amount of butterfat they contain. The fatty acids of butterfat are typically composed as follows (by mass fraction): As shown above, the composition of fats in milk is usually discussed in terms of the fatty acids. Fatty acids do not occur as such in milk (and rarely in any food). Instead, they are incorporated into compounds called

neg: Butterfat Butterfat Butterfat or milkfat is the fatty portion of milk. Milk and cream are often sold according to the amount of butterfat they contain. The fatty acids of butterfat are typically composed as follows (by mass fraction): As shown above, the composition of fats in milk is usually discussed in terms of the fatty acids. Fatty acids do not occur as such in milk (and rarely in any food). Instead, they are incorporated into compounds called triglycerides. In the U.S., there are federal standards for butterfat content of dairy products. Many other countries also have standards for minimum fat levels

neg: Aquaculture carnivorous species like salmon and shrimp leads to a high demand for forage fish to match the nutrition they get in the wild. Fish do not actually produce omega-3 fatty acids, but instead accumulate them from either consuming microalgae that produce these fatty acids, as is the case with forage fish like herring and sardines, or, as is the case with fatty predatory fish, like salmon, by eating prey fish that have accumulated omega-3 fatty acids from microalgae. To satisfy this requirement, more than 50 percent of the world fish oil production is fed to farmed salmon. Farmed salmon consume

neg: Perilipin-5 enter the complex SIRT1/PGC-1α, involved in fatty acid oxidation. PLIN5 removes SIRT1 inhibitor DBC1, therefore increasing its activity. As a consequence, PGC-1α boost activity levels activating certain types of genes that enhances mitochondrial function. Higher levels of perilipin 5 are closely related to the association between lipid droplet and mitochondria. This is useful in case of starvation (energy shortage). When energy is needed and no glucose is available, the cell uses lipids to feed itself. In order to do that, lipid droplets move towards the mitochondria to transfer the stored fatty acids. The perilipin family opens the channel, giving way

neg: Hans Adolf Krebs energy in the cells of humans and other oxygen-respiring organisms, often eponymously known as the "Krebs cycle", earned him a Nobel Prize in Physiology or Medicine in 1953. With Hans Kornberg, he also discovered the glyoxylate cycle, which is a slight variation of the citric acid cycle found in plants, bacteria, protists, and fungi. Krebs died in 1981 in Oxford, where he had spent 13 years of his career from 1954 until his retirement in 1967 at the University of Oxford. Krebs was born in Hildesheim, Germany, to Georg Krebs, an ear, nose, and throat surgeon, and Alma Krebs (née

neg: Metabolism reactive sugar-phosphate donor such as uridine diphosphate glucose (UDP-glucose) to an acceptor hydroxyl group on the growing polysaccharide. As any of the hydroxyl groups on the ring of the substrate can be acceptors, the polysaccharides produced can have straight or branched structures. The polysaccharides produced can have structural or metabolic functions themselves, or be transferred to lipids and proteins by enzymes called oligosaccharyltransferases. Fatty acids are made by fatty acid synthases that polymerize and then reduce acetyl-CoA units. The acyl chains in the fatty acids are extended by a cycle of reactions that add the acyl group, reduce it to

neg: Citric acid cycle cytosol. There it is cleaved by ATP citrate lyase into acetyl-CoA and oxaloacetate. The oxaloacetate is returned to mitochondrion as "malate" (and then converted back into "oxaloacetate" to transfer more "acetyl-CoA" out of the mitochondrion). The cytosolic acetyl-CoA is used for fatty acid synthesis and the production of cholesterol. Cholesterol can, in turn, be used to synthesize the steroid hormones, bile salts, and vitamin D. The carbon skeletons of many non-essential amino acids are made from citric acid cycle intermediates. To turn them into amino acids the alpha keto-acids formed from the citric acid cycle intermediates have to acquire their

neg: Fatty acid which merges into larger lymphatic vessels. It is transported via the lymphatic system and the thoracic duct up to a location near the heart (where the arteries and veins are larger). The thoracic duct empties the chylomicrons into the bloodstream via the left subclavian vein. At this point the chylomicrons can transport the triglycerides to tissues where they are stored or metabolized for energy. When metabolized, fatty acids yield large quantities of ATP. Many cell types can use either glucose or fatty acids for this purpose. Fatty acids (provided either by ingestion or by drawing on triglycerides stored in fatty

neg: Citric acid cycle Citric acid cycle The citric acid cycle (CAC) – also known as the" TCA cycle (tricarboxylic acid cycle) " or the" Krebs cycle "– is a series of chemical reactions used by all aerobic organisms to release stored energy through the oxidation of acetyl-CoA derived from carbohydrates, fats, and proteins into adenosine triphosphate (ATP) and carbon dioxide. In addition, the cycle provides precursors of certain amino acids, as well as the reducing agent NADH, that are used in numerous other reactions. Its central importance to many biochemical pathways suggests that it was one of the earliest established components of cellular

neg: Fish oil do not actually produce omega-3 fatty acids, but instead accumulate them by consuming either microalgae or prey fish that have accumulated omega-3 fatty acids. Fatty predatory fish like sharks, swordfish, tilefish, and albacore tuna may be high in omega-3 fatty acids, but due to their position at the top of the food chain, these species may also accumulate toxic substances through biomagnification. For this reason, the United States Environmental Protection Agency recommends limiting consumption (especially for women of childbearing age) of certain (predatory) fish species (e.g. albacore tuna, shark, king mackerel, tilefish and swordfish) due to high levels of the

neg: Aquaculture of salmonids for fish meal implies that the development of salmon aquaculture had no impact on forage fish harvest rates. Fish do not actually produce omega-3 fatty acids, but instead accumulate them from either consuming microalgae that produce these fatty acids, as is the case with forage fish like herring and sardines, or as is the case with fatty predatory fish, like salmon, by eating prey fish that have accumulated omega-3 fatty acids from microalgae. To satisfy this requirement, more than 50% of the world fish oil production is fed to farmed salmon. In addition, salmon require nutritional intakes of protein, which

neg: Fatty acid desaturase desaturating stearic acid, a saturated fatty acid either synthesized in the body from palmitic acid or ingested directly. Δ and Δ desaturases are required for the synthesis of highly unsaturated fatty acids such as eicosopentaenoic and docosahexaenoic acids (synthesized from α-linolenic acid); arachidonic acid and adrenic acid (synthesized from linoleic acid). This is a multi-stage process requiring successive actions by elongase and desaturase enzymes. The genes coding for Δ and Δ desaturase production have been located on human chromosome 11. DEGS1; DEGS2; FADS1; FADS2; FADS3; FADS6; SCD4; SCD5 Vertebrates are unable to synthesize polyunsaturated fatty acids because they do not

neg: Saturated fat and cardiovascular disease reduction of dietary saturated fat and partial replacement by unsaturated fats." A 2014 systematic review looking at observational studies of dietary intake of fatty acids, observational studies of measured fatty acid levels in the blood, and intervention studies of polyunsaturated fat supplementation concluded that the findings ″do not support cardiovascular guidelines that promote high consumption of long-chain omega-3 and omega-6 and polyunsaturated fatty acids and suggest reduced consumption of total saturated fatty acids.″ Researchers acknowledged that despite their results, further research is necessary, especially in people who are initially healthy. Until the picture becomes clearer, experts recommend people stick to