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Can Oxaloacetate Be Converted To Glucose?

Gluconeogenesis - An Overview | Sciencedirect Topics

Gluconeogenesis - An Overview | Sciencedirect Topics

Gluconeogenesis is the process that leads to the generation of glucose from a variety of sources such as pyruvate, lactate, glycerol, and certain amino acids. Larry R. Engelking, in Textbook of Veterinary Physiological Chemistry (Third Edition) , 2015 Gluconeogenesis occurs in the liver and kidneys. Gluconeogenesis supplies the needs for plasma glucose between meals. Gluconeogenesis is stimulated by the diabetogenic hormones (glucagon, growth hormone, epinephrine, and cortisol). Gluconeogenic substrates include glycerol, lactate, propionate, and certain amino acids. PEP carboxykinase catalyzes the rate-limiting reaction in gluconeogenesis. The dicarboxylic acid shuttle moves hydrocarbons from pyruvate to PEP in gluconeogenesis. Gluconeogenesis is a continual process in carnivores and ruminant animals, therefore they have little need to store glycogen in their liver cells. Of the amino acids transported to liver from muscle during exercise and starvation, Ala predominates. b-Aminoisobutyrate, generated from pyrimidine degradation, is a (minor) gluconeogenic substrate. N.V. Bhagavan, Chung-Eun Ha, in Essentials of Medical Biochemistry , 2011 Gluconeogenesis refers to synthesis of new glucose from noncarbohydrate precursors, provides glucose when dietary intake is insufficient or absent. It also is essential in the regulation of acid-base balance, amino acid metabolism, and synthesis of carbohydrate derived structural components. Gluconeogenesis occurs in liver and kidneys. The precursors of gluconeogenesis are lactate, glycerol, amino acids, and with propionate making a minor contribution. The gluconeogenesis pathway consumes ATP, which is derived primarily from the oxidation of fatty acids. The pathway uses several enzymes of the glycolysis with the exception of enzymes Continue reading >>

Gluconeogenesis

Gluconeogenesis

Gluconeogenesis is the metabolic process by which organisms produce sugars (namely glucose) for catabolic reactions from non-carbohydrate precursors. Glucose is the only energy source used by the brain (with the exception of ketone bodies during times of fasting), testes, erythrocytes, and kidney medulla. In mammals this process occurs in the liver and kidneys. Introduction The need for energy is important to sustain life. Organisms have evolved ways of producing substrates required for the catabolic reactions necessary to sustain life when desired substrates are unavailable. The main source of energy for eukaryotes is glucose. When glucose is unavailable, organisms are capable of metabolizing glucose from other non-carbohydrate precursors. The process that coverts pyruvate into glucose is called gluconeogenesis. Another way organisms derive glucose is from energy stores like glycogen and starch. Overview Gluconeogenesis is much like glycolysis only the process occurs in reverse. However, there are exceptions. In glycolysis there are three highly exergonic steps (steps 1,3,10). These are also regulatory steps which include the enzymes hexokinase, phosphofructokinase, and pyruvate kinase. Biological reactions can occur in both the forward and reverse direction. If the reaction occurs in the reverse direction the energy normally released in that reaction is now required. If gluconeogenesis were to simply occur in reverse the reaction would require too much energy to be profitable to that particular organism. In order to overcome this problem, nature has evolved three other enzymes to replace the glycolysis enzymes hexokinase, phosphofructokinase, and pyruvate kinase when going through the process of gluconeogenesis: The first step in gluconeogenesis is the conversion of p 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 >>

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 >>

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 >>

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 >>

Gluconeogenesis Flashcards | Quizlet

Gluconeogenesis Flashcards | Quizlet

How are these steps bypassed in gluconeogenesis? Name the enzymes. F-1,6-BisP --> F-6-P + Pi (fructose-1,6-Bisphosphatase) 1. Pyr + CO2 + ATP --> oxaloacetate + ADP (occurs in mitochondria; pyruvate carboxylase - contains biotin & requires acetyl CoA as positive modulator) oxaloacetate + NADH --> malate + NAD+ (in mitochondria; malate dehydrogenase) malate + NAD+ --> NADH + oxaloacetate (in cytoplasm; malate dehydrogenase) (goal: moving oxaloacetate out to cytoplasm) 3. oxaloactetate + GTP --> PEP + CO2 + GDP (phosphoenolpyruvate carboxykinase - PEPCK) What is the role of pyruvate carboxylase in gluconeogenesis & anaplerosis? How is it regulated? gluconeogenesis: pyruvate carboxylase adds CO2 to pyruvate --> oxaloacetate in mitochondria anaplerosis: forms catalytic amounts of oxaloactetate in ALL mitochondria - produces oxaloacetate (when lacking) when stimulated by acetyl CoA, also requires ATP. Pyruvate carboxylase = regulatory enzyme (requires biotin as coenzyme) Key regulator: acetyl CoA = positive modulator (EXAM) Write the sequence of steps involved in the conversion of pyruvate to phosphoenol pyruvate. 1. Pyr + CO2 + ATP --> oxaloacetate + ADP (occurs in mitochondria; pyruvate carboxylase - contains biotin & requires acetyl CoA as positive modulator) oxaloacetate + NADH --> malate + NAD+ (in mitochondria; malate dehydrogenase) malate + NAD+ --> NADH + oxaloacetate (in cytoplasm; malate dehydrogenase) (goal: moving oxaloacetate out to cytoplasm) 3. oxaloactetate + GTP --> PEP + CO2 + GDP (phosphoenolpyruvate carboxykinase - PEPCK) Explain why acetyl CoA cannot serve as a precursor for gluconeogenesis. acetyl CoA comes from beta-oxidation & from pyruvate (pyruvate dehydrogenase) pyr + CoA + NAD+ --> Acetyl CoA + NADH + CO2 (pyruvate dehydrogenase) What key role do Continue reading >>

Gluconeogenesis

Gluconeogenesis

What is gluconeogenesis? Gluconeogenesis is a metabolic pathway that leads to the synthesis of glucose from pyruvate and other non-carbohydrate precursors, even in non-photosynthetic organisms. It occurs in all microorganisms, fungi, plants and animals, and the reactions are essentially the same, leading to the synthesis of one glucose molecule from two pyruvate molecules. Therefore, it is in essence glycolysis in reverse, which instead goes from glucose to pyruvate, and shares seven enzymes with it. Glycogenolysis is quite distinct from gluconeogenesis: it does not lead to de novo production of glucose from non-carbohydrate precursors, as shown by its overall reaction: Glycogen or (glucose)n → n glucose molecules The following discussion will focus on gluconeogenesis that occurs in higher animals, and in particular in the liver of mammals. Why is gluconeogenesis important? Gluconeogenesis is an essential metabolic pathway for at least two reasons. It ensures the maintenance of appropriate blood glucose levels when the liver glycogen is almost depleted and no carbohydrates are ingested. Maintaining blood glucose within the normal range, 3.3 to 5.5 mmol/L (60 and 99 mg/dL), is essential because many cells and tissues depend, largely or entirely, on glucose to meet their ATP demands; examples are red blood cells, neurons, skeletal muscle working under low oxygen conditions, the medulla of the kidney, the testes, the lens and the cornea of the eye, and embryonic tissues. For example, glucose requirement of the brain is about 120 g/die that is equal to: over 50% of the total body stores of the monosaccharide, about 210 g, of which 190 g are stored as muscle and liver glycogen, and 20 g are found in free form in body fluids; about 75% of the daily glucose requirement, abou Continue reading >>

Substrates Of Gluconeogenesis (lecture -2)

Substrates Of Gluconeogenesis (lecture -2)

Substrates of Gluconeogenesis (Lecture -2) The major substrates are lactate, glycerol, propionate and the glucogenic amino acids . (For lactate, glycerol and propionate check lecture-1) Glucogenic amino acids- Amino acids are derived from the dietary proteins, tissue proteins or from the breakdown of skeletal muscle proteins during starvation. After transamination or deamination, glucogenic amino acids yield either pyruvate or intermediates of the citric acid cycle. Amino acids that are degraded to acetyl CoA or Acetoacetyl CoA are termed ketogenic amino acids because they can give rise to ketone bodies or fatty acids. Acetyl co A cannot be termed glucogenic, since the conversion back to pyruvate is not possible due to irreversible nature of the reaction and in TCA cycle Acetyl co A loses both of its carbons as carbon dioxide, hence there is nothing left to contribute to glucose production. Amino acids that are degraded to pyruvate, -ketoglutarate, succinyl CoA, fumarate, or oxaloacetate are termed glucogenic amino acids. The net synthesis of glucose from these amino acids is feasible because these citric acid cycle intermediates and pyruvate can be converted into phosphoenolpyruvate. The entry point of these glucogenic amino acids in to the pathway of gluconeogenesis is as follows- 1) Pyruvate is the point of entry for alanine, serine, cysteine, glycine, threonine, and tryptophan (Figure-1). The transamination of alanine directly yields pyruvate. The glucose-alanine cycle is used primarily as a mechanism for skeletal muscle to eliminate nitrogen while replenishing its energy supply. Glucose oxidation produces pyruvate which can undergo transamination to alanine. This reaction is catalyzed by alanine transaminase, ALT (ALT used to be referred to a serum glutamate-pyruv 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 >>

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 >>

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 >>

Oxaloacetic Acid - An Overview | Sciencedirect Topics

Oxaloacetic Acid - An Overview | Sciencedirect Topics

D.A. Bender, in Encyclopedia of Food Sciences and Nutrition (Second Edition) , 2003 Anaplerotic Reactions Replenishing the Supply of Tricarboxylic Acid Cycle Intermediates If oxaloacetate is removed from the cycle for glucose synthesis, it must be replaced, since if there is not enough oxaloacetate available to form citrate, the rate of acetyl CoA metabolism, and hence the rate of formation of ATP, will slow down. Similarly, under conditions of hyperammonemia, the reaction of glutamate dehydrogenase leads to withdrawal of a considerable amount of -ketoglutarate, to the extent that ATP formation is impaired, leading to coma and convulsions. As shown in Figure 4, a variety of amino acids give rise to tricarboxylic cycle intermediates, so permitting removal of oxaloacetate for gluconeogenesis. In addition, the reaction of pyruvate carboxylase is a major source of oxaloacetate to maintain tricarboxylic acid cycle activity. The metabolic fate of pyruvate, oxidative decarboxylation to yield acetyl CoA or carboxylation to yield oxaloacetate, is determined by the relative availability of acetyl CoA (which also arises from -oxidation of fatty acids and metabolism of ketone bodies) and the need for oxaloacetate to maintain tricarboxylic acid cycle activity. Pyruvate dehydrogenase is inhibited by both NADH and acetyl CoA, whereas pyruvate carboxylase has an absolute requirement for acetyl CoA for activity. Thus, at times when there is an abundance of acetyl CoA, pyruvate will not undergo decarboxylation and oxidation in the tricarboxylic acid cycle, but rather will be carboxylated to oxaloacetate. Once the pool of tricarboxylic acid cycle intermediates is adequate, further oxaloacetate formed by carboxylation of pyruvate can be used for gluconeogenesis. Alan Radford, in Advances Continue reading >>

Chapter 13: Glucogenesis

Chapter 13: Glucogenesis

In gluconeogenesis, what is pyruvate converted to? True or False: the carbon units from fatty acids can be used as precursors for the net synthesis of new glucose in mammals. False: the carbon units from fatty acids CANNOT be used as precursors for the new synthesis of new glucose in mammals Why can't the carbon units from fatty acids be used as precursors for the net synthesis? Their oxidation yields acetyl-SCoA and the pyruvate dehydrogenase (and pyruvate kinase) reactions are irreversible, preventing the net formation of glucose from acetyl-SCoA The carbon atoms of acetyl-SCoA that enter the citric acid cycle and two carbon atoms leave the citric acid cycle as CO2 thus Glycerol from stored triacyglycerides and is mobilized by what? It can also be converted to glucose via the glycolytic intermediate, dihydroxyacetone phosphate. - Requires glycerol kinase and glycerol 3-phosphate dehydrogenase - Produces DHAP (glycolytic intermediate) The Pathway of Gluconeogenesis is NOT a reversal of What are the 3 irreversible steps in glycolysis that MUST be bypassed? Primarily in the Liver (which is the major site of glucogeneogenesis) Cytosolic alcohol dehydrogenase metabolizes ethanol to Mitochondrial Acetaldehyde dehydrogenase converts acetaldehye to acetate, that is converted to acetyl-SCoA and eventually metabolized to What does alcohol metabolism require, what does it produce? -Shifts the equilibrium of the cytosolic lactate dehydrogenase from pyruvate formation to lactate synthesis - Favors reduction of oxaloacetate -> malate by cytosolic MDH (reducing OAA availability for Gluconeogenesis) What does the use of NAD+ by alcohol metabolism impair? The metabolism of pyrvate, urates and fatty acids, and reduces Gluconeogenesis. What does the use of NAD+ by alcohol metabolism le 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 >>

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