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Can Acetyl Coa Be Converted To Glucose?

Evolving Health: Why Can't We Convert Fat To Glucose?

Evolving Health: Why Can't We Convert Fat To Glucose?

As evident by many sugar-laden soda pop "potbellies" of North America, lipogenesis can obviously occur from drinking and eating too much sugar (1). Wouldnt it be just grand to reverse the process and be able to lose all that fat via gluconeogenesis? Unfortunately mammals do not have the ability to synthesize glucose from fats (1). The fact is that once glucose is converted to acetyl coA there is no method of getting back to glucose. The pyruvate dehydrogenase reaction that converts pyruvate to acetyl CoA is not reversible (1p252). Because lipid metabolism produces acetyl CoA via beta-oxidation, there can be no conversion to pyruvate or oxaloacetate that may have been used for gluconeogenesis (1p252). Further, the two carbons in the acetyl CoA molecule are lost upon entering the citric acid cycle (1p252). Thus, the acetyl CoA is used for energy (1p252). There are some fatty acids that have an odd number of carbon atoms that can be converted to glucose, but these are not common in the diet (1p253). Maybe they should be made more common. Do they taste good? 1. Gropper SS, Smith JL, Groff JL. Advanced Nutrition and Human Metabolism. Belmont, CA: Thomson Wadsworth, 2009. Continue reading >>

Why Can Fatty Acids Not Be Converted Into Glucose? : Mcat

Why Can Fatty Acids Not Be Converted Into Glucose? : Mcat

Rudeness or trolling will not be tolerated. Be nice to each other, hating on other users won't help you get extra points on the MCAT, so why do it? Do not post any question information from any resource in the title of your post. These are considered spoilers and should be marked as such. For an example format for submitting pictures of questions from practice material click here Do not link to content that infringes on copyright laws (MCAT torrents, third party resources, etc). Do not post repeat "GOOD LUCK", "TEST SCORE", or test reaction posts. We have one "stickied" post for each exam and score release day, contain all test day discussion/reactions to that thread only. Do not discuss any specific information from your actual MCAT exam. You have signed an examinee agreement, and it will be enforced on this subreddit. Do not intentionally advertise paid products or services of any sort. These posts will be removed and the user banned without warning, subject to the discretion of the mod team Learn More All of the above rules are subject to moderator discretion C/P = Chemical and Physical Foundations of Biological Systems CARS = Critical Analysis and Reasoning Skills B/B = Biological and Biochemical Foundations of Living Systems P/S = Psychological, Social, and Biological Foundations of Behavior Continue reading >>

Gluconeogenesis: Endogenous Glucose Synthesis

Gluconeogenesis: Endogenous Glucose Synthesis

Reactions of Gluconeogenesis: Gluconeogenesis from two moles of pyruvate to two moles of 1,3-bisphosphoglycerate consumes six moles of ATP. This makes the process of gluconeogenesis very costly from an energy standpoint considering that glucose oxidation to two moles of pyruvate yields two moles of ATP. The major hepatic substrates for gluconeogenesis (glycerol, lactate, alanine, and pyruvate) are enclosed in red boxes for highlighting. The reactions that take place in the mitochondria are pyruvate to OAA and OAA to malate. Pyruvate from the cytosol is transported across the inner mitochondrial membrane by the pyruvate transporter. Transport of pyruvate across the plasma membrane is catalyzed by the SLC16A1 protein (also called the monocarboxylic acid transporter 1, MCT1) and transport across the outer mitochondrial membrane involves a voltage-dependent porin transporter. Transport across the inner mitochondrial membrane requires a heterotetrameric transport complex (mitochondrial pyruvate carrier) consisting of the MPC1 gene and MPC2 gene encoded proteins. Following reduction of OAA to malate the malate is transported to the cytosol by the malate transporter (SLC25A11). In the cytosol the malate is oxidized to OAA and the OOA then feeds into the gluconeogenic pathway via conversion to PEP via PEPCK. The PEPCK reaction is another site for consumption of an ATP equivalent (GTP is utilized in the PEPCK reaction). The reversal of the glyceraldehyde-3-phosphate dehydrogenase (GAPDH) reaction requires a supply of NADH. When lactate is the gluconeogenic substrate the NADH is supplied by the lactate dehydrogenase (LDH) reaction (indicated by the dashes lines), and it is supplied by the malate dehydrogenase reaction when pyruvate and alanine are the substrates. Secondly, one mo Continue reading >>

Acetyl-coa - An Overview | Sciencedirect Topics

Acetyl-coa - An Overview | Sciencedirect Topics

Acetyl-CoA is a thioester between the acyl group carrier, acetic acid and a thiol, coenzyme A. Acetyl-CoA, as a carrier of acyl groups, is an essential cofactor in the posttranslational acetylation reactions of histone and nonhistone proteins catalyzed by HATs. N.V. Bhagavan, Chung-Eun Ha, in Essentials of Medical Biochemistry , 2011 Acetyl-CoA is synthesized in mitochondria by a number of reactions: oxidative decarboxylation of pyruvate; catabolism of some amino acids (e.g., phenylalanine, tyrosine, leucine, lysine, and tryptophan); and -oxidation of fatty acids (see above). Since acetyl-CoA cannot be transported directly across the inner mitochondrial membrane to the cytosol, its carbon atoms are transferred by two transport mechanisms. Transport dependent upon carnitine: Carnitine participates in the transport of long-chain acyl-CoA into the mitochondria and plays a similar role in the transport of acetyl-CoA out of mitochondria. However, carnitine acetyl transferases have a minor role in acetyl-CoA transport. Cytosolic generation of acetyl-CoA (citrate shuttle): This pathway is shown in Figure 16-8. Citrate synthesized from oxaloacetate and acetyl-CoA is transported from mitochondria to the cytosol via the tricarboxylate anion carrier system and cleaved to yield acetyl-CoA and oxaloacetate. Thus, citrate not only modulates the rate of fatty acid synthesis but also provides carbon atoms for the synthesis. The oxaloacetate formed from pyruvate may eventually be converted (via malate) to glucose by the gluconeogenic pathway. The glucose oxidized via the pentose phosphate pathway augments fatty acid synthesis by providing NADPH. Pyruvate generated from oxaloacetate can enter mitochondria and be converted to oxaloacetate, which is required for the formation of citrate. Continue reading >>

We Really Can Make Glucose From Fatty Acids After All! O Textbook, How Thy Biochemistry Hast Deceived Me!

We Really Can Make Glucose From Fatty Acids After All! O Textbook, How Thy Biochemistry Hast Deceived Me!

Biochemistry textbooks generally tell us that we can’t turn fatty acids into glucose. For example, on page 634 of the 2006 and 2008 editions of Biochemistry by Berg, Tymoczko, and Stryer, we find the following: Animals Cannot Convert Fatty Acids to Glucose It is important to note that animals are unable to effect the net synthesis of glucose from fatty acids. Specficially, acetyl CoA cannot be converted into pyruvate or oxaloacetate in animals. In fact this is so important that it should be written in italics and have its own bold heading! But it’s not quite right. Making glucose from fatty acids is low-paying work. It’s not the type of alchemy that would allow us to build imperial palaces out of sugar cubes or offer hourly sweet sacrifices upon the altar of the glorious god of glucose (God forbid!). But it can be done, and it’ll help pay the bills when times are tight. All Aboard the Acetyl CoA! When we’re running primarily on fatty acids, our livers break the bulk of these fatty acids down into two-carbon units called acetate. When acetate hangs out all by its lonesome like it does in a bottle of vinegar, it’s called acetic acid and it gives vinegar its characteristic smell. Our livers aren’t bottles of vinegar, however, and they do things a bit differently. They have a little shuttle called coenzyme A, or “CoA” for short, that carries acetate wherever it needs to go. When the acetate passenger is loaded onto the CoA shuttle, we refer to the whole shebang as acetyl CoA. As acetyl CoA moves its caboose along the biochemical railway, it eventually reaches a crossroads where it has to decide whether to enter the Land of Ketogenesis or traverse the TCA cycle. The Land of Ketogenesis is a quite magical place to which we’ll return in a few moments, but n Continue reading >>

Biochemistry - Why Isn't Acetyl-coa An Entry Point For Gluconeogenesis? - Biology Stack Exchange

Biochemistry - Why Isn't Acetyl-coa An Entry Point For Gluconeogenesis? - Biology Stack Exchange

Why isn't acetyl-coA an entry point for gluconeogenesis? The process of gluconeogenesis starts from various possible precursors - plausible entry points like, Pyruvate, OAA, Fumarate, Propionate (as succinate) and alpha-KG. It is important to note that, acetyl-coA is not an entry point for Gluconeogenesis. The most common reason cited for this is the irreversibility of the enzyme, pyruvate dehydrogenase. Since it is irreversible, Acetyl coA can't get back to pyruvate to go on forming glucose. But, Acetyl CoA naturally enters the Kreb's cycle, so why can't it go ahead and form glucose via gluconeogenesis using one of the Kreb's intermediates? I have had this doubt for very long and tried to come up with an explanation to satisfy myself but I still don't know if it is valid. So here it goes. All the entry points to gluconeogenesis (mentioned before) are an addition to the Kreb's cycle. They get on the boat, sail along, get off at oxaloacetate and leave. They don't bother the boat in any other way. Even Pyruvate, forms oxaloacetate via pyruvate carboxylase and then gets on the boat for gluconeogenesis. On the other hand, Acetyl coA would be a part of the Kreb's cycle itself. It is not adding anything to it (2 carbons that are added are lost as CO2). So an Acetyl CoA added, can't leave as OAA. It would be analogous not sailing on the boat but eating it down itself. Slowly, it would lead to a decay and loss of the intermediates Kreb's cycle and it would come to a standstill (?) Is this explanation right? Are there any other ways to explain why irreversibility of PDH results in this? Although acetyl-coA can enter gluconeogenesis via pathways like glyoxylate cycle (not in humans) and pathways to make pyruvate from acetone (not economical) to form glucose, the question is why Continue reading >>

Gluconeogenesis

Gluconeogenesis

Not to be confused with Glycogenesis or Glyceroneogenesis. Simplified Gluconeogenesis Pathway Gluconeogenesis (GNG) is a metabolic pathway that results in the generation of glucose from certain non-carbohydrate carbon substrates. From breakdown of proteins, these substrates include glucogenic amino acids (although not ketogenic amino acids); from breakdown of lipids (such as triglycerides), they include glycerol (although not fatty acids); and from other steps in metabolism they include pyruvate and lactate. Gluconeogenesis is one of several main mechanisms used by humans and many other animals to maintain blood glucose levels, avoiding low levels (hypoglycemia). Other means include the degradation of glycogen (glycogenolysis)[1] and fatty acid catabolism. Gluconeogenesis is a ubiquitous process, present in plants, animals, fungi, bacteria, and other microorganisms.[2] In vertebrates, gluconeogenesis takes place mainly in the liver and, to a lesser extent, in the cortex of the kidneys. In ruminants, this tends to be a continuous process.[3] In many other animals, the process occurs during periods of fasting, starvation, low-carbohydrate diets, or intense exercise. The process is highly endergonic until it is coupled to the hydrolysis of ATP or GTP, effectively making the process exergonic. For example, the pathway leading from pyruvate to glucose-6-phosphate requires 4 molecules of ATP and 2 molecules of GTP to proceed spontaneously. Gluconeogenesis is often associated with ketosis. Gluconeogenesis is also a target of therapy for type 2 diabetes, such as the antidiabetic drug, metformin, which inhibits glucose formation and stimulates glucose uptake by cells.[4] In ruminants, because dietary carbohydrates tend to be metabolized by rumen organisms, gluconeogenesis occurs Continue reading >>

Chapter 19 : Carbohydrate Biosynthesis

Chapter 19 : Carbohydrate Biosynthesis

Thus the synthesis of glucose from pyruvate is a relativelycostly process. Much of this high energy cost is necessary toensure that gluconeogenesis is irreversible. Under intracellularconditions, the overall free-energy change of glycolysis is atleast -63 kJ/mol. Under the same conditions the overallfree-energy change of gluconeogenesis from pyruvate is alsohighly negative. Thus glycolysis and gluconeogenesis are bothessentially irreversible processes under intracellularconditions. Citric Acid Cycle Intermediates and Many Amino Acids AreGlucogenic The biosynthetic pathway to glucose described above allows thenet synthesis of glucose not only from pyruvate but also from thecitric acid cycle intermediates citrate, isocitrate,-ketoglutarate, succinate, fumarate, and malate. All may undergooxidation in the citric acid cycle to yield oxaloacetate.However, only three carbon atoms of oxaloacetate are convertedinto glucose; the fourth is released as CO in the conversion ofoxaloacetate to phosphoenolpyruvate by PEP carboxykinase (Fig.19-3). In Chapter 17 we showed that some or all of thecarbon atoms of many of the amino acids derived from proteins areultimately converted by mammals into either pyruvate or certainintermediates of the citric acid cycle. Such amino acids cantherefore undergo net conversion into glucose and are calledglucogenic amino acids (Table 19-3). Alanine and glutamine makeespecially important contributions in that they are the principalmolecules used to transport amino groups from extrahepatictissues to the liver. After removal of their amino groups inliver mitochondria, the carbon skeletons remaining (pyruvate anda-ketoglutarate, respectively) are readily funneled intogluconeogenesis. In contrast, there is no net conversion of even-carbon fattyacids into gl Continue reading >>

Gluconeogenesis Flashcards | Quizlet

Gluconeogenesis Flashcards | Quizlet

What is the definition of gluconeogensis? the synthesis of glucose from noncarbohydrate precursors how many days do the direct glucose reserves sufficient for the needs of the body? how many grams of glucose does the brain need daily? how many grams of glucose does the entire body need daily? how many grams of glucose are in body fluids to use for the body? how mans grams of readily mobilized glucose are there in glycogen stores? What is the major site of gluconeogenesis? mostly by the liver, and a smaller amount in the kidney 1. decreased insulin/glucagon ratio as in an overnight fast 3. high protein-low carb diet (need minimum of 50 g carb for insulin secretion) 4. stress; due to the hormones cortisol and epinephrine which are elevated under these conditions What are the 4 major non-carbohydrate presursors used as substrates for gluconeogenesis? 2. amino acids (muscle protein degradation in skeletal muscle) 3. glycerol (triglyceride breakdown in adipose tissue) what is lactate's role in the gluconeogenic pathway? 1. during vigorous exercise, lactate buildup and NADH 2. NADH can be reoxidized during the reduction of pyruvate to lactate 3. lactate is then returned to the liver, where it can be reoxidized to pyruvate by liver LDH the liver provides glucose to muscle for exercise and then reprocesses lactate into new glucose in the liver, what is the reaction when lactate enters from the blood? Lactate + LDH -> pyruvate + 6 phosphoryl groups -> glucose to the muscle what compound does muscle protein degradation give to gluconeogenesis? what is the process of alanine for conversion to glucose? alanine + alanine aminotransferase -> pyruvate what compound does triglyceride breakdown in adipose tissue give to gluconeogenesis? what is the process of glycerol for conversion to Continue reading >>

Why Can't Fat Produce Glucose?

Why Can't Fat Produce Glucose?

Tousief Irshad Ahmed Sirwal Author has 77 answers and 106.2k answer views Acetyl CoA is NOT a substrate for gluconeogenesis in animals 1. Pyruvate dehydrogenase reaction is irreversible. So, acetyl CoA cannot be converted back to pyruvate. 2. 2C Acetyl CoA enters the TCA cycle by condensing with 4C oxaloacetate. 2 molecules of CO2 are released & the oxaloacetate is regenerated. There is no NET production of oxaloacetate. Animals cannot convert fat into glucose with minimal exceptions 1. Propionyl CoA derived from odd chain fatty acids are converted to Succinyl CoA Glucogenic 2. Glycerol derived from triglycerides are glucogenic. Answered Mar 26, 2017 Author has 942 answers and 259.1k answer views Yijia Xiong pointed out that the glycerol portion of triglycerides (fats) can indeed be converted to glucose. It is not so energy-inefficient that it is avoided by our bodies. If nutritionally, we are in a gluconeogenesis mode (building up glucose stores rather than consuming them), glycerol would be a perfectly acceptable precursor. However, I think the original question had more to do with the vast bulk of the triglycerides that are not glycerol, but are fatty acids. And it is true that we cant produce glucose from fatty acids. The reason is that the catabolic reactions of fatty acids break off two carbon atoms at a time as Acetyl-CoA. But our metabolic suite of pathways has no way to convert a two-carbon fragment to glucose. The end product of glycolysis is pyruvate, a three-carbon compound. Pyruvate can be back-synthesized into glucose. But the committing reaction for the Krebs cycle is the pyruvate dehydrogenase step, forming acetyl-CoA. That reaction is not reversible. Once pyruvate loses a carbon atom, it cant go back. The three main macronutrients are carbohydrates, pr Continue reading >>

Lipid Metabolism

Lipid Metabolism

on on Fats (or triglycerides) within the body are ingested as food or synthesized by adipocytes or hepatocytes from carbohydrate precursors ([link]). Lipid metabolism entails the oxidation of fatty acids to either generate energy or synthesize new lipids from smaller constituent molecules. Lipid metabolism is associated with carbohydrate metabolism, as products of glucose (such as acetyl CoA) can be converted into lipids. Lipid metabolism begins in the intestine where ingested triglycerides are broken down into smaller chain fatty acids and subsequently into monoglyceride molecules (see [link]b) by pancreatic lipases, enzymes that break down fats after they are emulsified by bile salts. When food reaches the small intestine in the form of chyme, a digestive hormone called cholecystokinin (CCK) is released by intestinal cells in the intestinal mucosa. CCK stimulates the release of pancreatic lipase from the pancreas and stimulates the contraction of the gallbladder to release stored bile salts into the intestine. CCK also travels to the brain, where it can act as a hunger suppressant. Together, the pancreatic lipases and bile salts break down triglycerides into free fatty acids. These fatty acids can be transported across the intestinal membrane. However, once they cross the membrane, they are recombined to again form triglyceride molecules. Within the intestinal cells, these triglycerides are packaged along with cholesterol molecules in phospholipid vesicles called chylomicrons ([link]). The chylomicrons enable fats and cholesterol to move within the aqueous environment of your lymphatic and circulatory systems. Chylomicrons leave the enterocytes by exocytosis and enter the lymphatic system via lacteals in the villi of the intestine. From the lymphatic system, the chylo Continue reading >>

Connections Of Carbohydrate, Protein, And Lipid Metabolic Pathways

Connections Of Carbohydrate, Protein, And Lipid Metabolic Pathways

Connecting Other Sugars to Glucose Metabolism Sugars, such as galactose, fructose, and glycogen, are catabolized into new products in order to enter the glycolytic pathway. Learning Objectives Identify the types of sugars involved in glucose metabolism Key Takeaways When blood sugar levels drop, glycogen is broken down into glucose -1-phosphate, which is then converted to glucose-6-phosphate and enters glycolysis for ATP production. In the liver, galactose is converted to glucose-6-phosphate in order to enter the glycolytic pathway. Fructose is converted into glycogen in the liver and then follows the same pathway as glycogen to enter glycolysis. Sucrose is broken down into glucose and fructose; glucose enters the pathway directly while fructose is converted to glycogen. disaccharide: A sugar, such as sucrose, maltose, or lactose, consisting of two monosaccharides combined together. glycogen: A polysaccharide that is the main form of carbohydrate storage in animals; converted to glucose as needed. monosaccharide: A simple sugar such as glucose, fructose, or deoxyribose that has a single ring. You have learned about the catabolism of glucose, which provides energy to living cells. But living things consume more than glucose for food. How does a turkey sandwich end up as ATP in your cells? This happens because all of the catabolic pathways for carbohydrates, proteins, and lipids eventually connect into glycolysis and the citric acid cycle pathways. Metabolic pathways should be thought of as porous; that is, substances enter from other pathways, and intermediates leave for other pathways. These pathways are not closed systems. Many of the substrates, intermediates, and products in a particular pathway are reactants in other pathways. Like sugars and amino acids, the catabo Continue reading >>

When Does Glucose Convert To Fat?

When Does Glucose Convert To Fat?

Despite the fact that eating a jelly doughnut seems to deposit fat directly on your hips, converting sugar to fat is actually a relatively complex chemical process. Sugar conversion to fat storage depends not only upon the type of foods you eat, but how much energy your body needs at the time you eat it. Video of the Day Your body converts excess dietary glucose into fat through the process of fatty acid synthesis. Fatty acids are required in order for your body to function properly, playing particularly important roles in proper brain functioning. There are two kinds of fatty acids; essential fatty acids and nonessential fatty acids. Essential fatty acids refer to fatty acids you must eat from your diet, as your body cannot make them. Nonessential fatty acids are made through the process of fatty acid synthesis. Fatty Acid Synthesis Fatty acids are long organic compounds having an acid group at one end and a methyl group at the other end. The location of their first double bond dictates whether they are in the omega 3, 6, or 9 fatty acid family. Fatty acid synthesis takes place in the cytoplasm of cells and requires some energy input. In other words, your body actually has to expend some energy in order to store fat. Glucose is a six-carbon sugar molecule. Your body first converts this molecule into two three-carbon pyruvate molecules through the process of glycolysis and then into acetyl CoA. When your body requires immediate energy, acetyl CoA enters the Citric Acid Cycle creating energy molecules in the form of ATP. When glucose intake exceeds your body's energy needs--for example, you eat an ice-cream sundae and then go relax on the sofa for five hours--your body has no need to create more energy molecules. Therefore, acetyl CoA begins the process of fatty acid syn Continue reading >>

Principles Of Biochemistry/gluconeogenesis And Glycogenesis

Principles Of Biochemistry/gluconeogenesis And Glycogenesis

Gluconeogenesis (abbreviated GNG) is a metabolic pathway that results in the generation of glucose from non-carbohydrate carbon substrates such as lactate, glycerol, and glucogenic amino acids. It is one of the two main mechanisms humans and many other animals use to keep blood glucose levels from dropping too low (hypoglycemia). The other means of maintaining blood glucose levels is through the degradation of glycogen (glycogenolysis). Gluconeogenesis is a ubiquitous process, present in plants, animals, fungi, bacteria, and other microorganisms. In animals, gluconeogenesis takes place mainly in the liver and, to a lesser extent, in the cortex of kidneys. This process occurs during periods of fasting, starvation, low-carbohydrate diets, or intense exercise and is highly endergonic. For example, the pathway leading from phosphoenolpyruvate to glucose-6-phosphate requires 6 molecules of ATP. Gluconeogenesis is often associated with ketosis. Gluconeogenesis is also a target of therapy for type II diabetes, such as metformin, which inhibits glucose formation and stimulates glucose uptake by cells. Lactate is transported back to the liver where it is converted into pyruvate by the Cori cycle using the enzyme lactate dehydrogenase. Pyruvate, the first designated substrate of the gluconeogenic pathway, can then be used to generate glucose. All citric acid cycle intermediates, through conversion to oxaloacetate, amino acids other than lysine or leucine, and glycerol can also function as substrates for gluconeogenesis.Transamination or deamination of amino acids facilitates entering of their carbon skeleton into the cycle directly (as pyruvate or oxaloacetate), or indirectly via the citric acid cycle. Whether fatty acids can be converted into glucose in animals has been a longst Continue reading >>

Can Sugars Be Produced From Fatty Acids? A Test Case For Pathway Analysis Tools

Can Sugars Be Produced From Fatty Acids? A Test Case For Pathway Analysis Tools

Can sugars be produced from fatty acids? A test case for pathway analysis tools Department of Bioinformatics, 2Bio Systems Analysis Group, Friedrich-Schiller-Universitt Jena, Ernst-Abbe-Platz 2, 07743 Jena, Germany and 3School of Life Sciences, Oxford Brookes University, Headington, Oxford, OX3 0BP, UK *To whom correspondence should be addressed. Search for other works by this author on: Department of Bioinformatics, 2Bio Systems Analysis Group, Friedrich-Schiller-Universitt Jena, Ernst-Abbe-Platz 2, 07743 Jena, Germany and 3School of Life Sciences, Oxford Brookes University, Headington, Oxford, OX3 0BP, UK *To whom correspondence should be addressed. Search for other works by this author on: Department of Bioinformatics, 2Bio Systems Analysis Group, Friedrich-Schiller-Universitt Jena, Ernst-Abbe-Platz 2, 07743 Jena, Germany and 3School of Life Sciences, Oxford Brookes University, Headington, Oxford, OX3 0BP, UK Search for other works by this author on: Department of Bioinformatics, 2Bio Systems Analysis Group, Friedrich-Schiller-Universitt Jena, Ernst-Abbe-Platz 2, 07743 Jena, Germany and 3School of Life Sciences, Oxford Brookes University, Headington, Oxford, OX3 0BP, UK Search for other works by this author on: Bioinformatics, Volume 25, Issue 1, 1 January 2009, Pages 152158, Luis F. de Figueiredo, Stefan Schuster, Christoph Kaleta, David A. Fell; Can sugars be produced from fatty acids? A test case for pathway analysis tools, Bioinformatics, Volume 25, Issue 1, 1 January 2009, Pages 152158, Motivation: In recent years, several methods have been proposed for determining metabolic pathways in an automated way based on network topology. The aim of this work is to analyse these methods by tackling a concrete example relevant in biochemistry. It concerns the question wh Continue reading >>

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