Carbohydrate metabolism and gluconeogenesis pathway -
Physiological Reviews. The Journal of Clinical Investigation. Vander's Human Physiology. McGraw Hill. The Journal of Biological Chemistry. February Cancer Research. Frontiers in Pharmacology.
Diabetic Medicine. Journal of Animal Science. Fundamentals of Biochemistry. Critical Reviews in Biochemistry and Molecular Biology. May Annals of the New York Academy of Sciences. Bibcode : NYASA January International Journal of Molecular Medicine.
December The Journal of Endocrinology. Hundal RS, Krssak M, Dufour S, Laurent D, Lebon V, Chandramouli V, et al. Nature Communications. Bibcode : NatCo Bibcode : Natur. Chemical Reviews. Proceedings of the National Academy of Sciences of the United States of America.
Bibcode : PNAS.. The discovery of a non-enzymatic metabolism and its role in the origins of life". The Biochemical Journal. ISSN Metabolism , catabolism , anabolism. Metabolic pathway Metabolic network Primary nutritional groups. Purine metabolism Nucleotide salvage Pyrimidine metabolism Purine nucleotide cycle.
Pentose phosphate pathway Fructolysis Polyol pathway Galactolysis Leloir pathway. Glycosylation N-linked O-linked. Photosynthesis Anoxygenic photosynthesis Chemosynthesis Carbon fixation DeLey-Doudoroff pathway Entner-Doudoroff pathway. Xylose metabolism Radiotrophism.
Fatty acid degradation Beta oxidation Fatty acid synthesis. Steroid metabolism Sphingolipid metabolism Eicosanoid metabolism Ketosis Reverse cholesterol transport. Metal metabolism Iron metabolism Ethanol metabolism Phospagen system ATP-PCr. Fructose-bisphosphate aldolase Aldolase A , B , C Triosephosphate isomerase.
Glyceraldehyde 3-phosphate dehydrogenase Phosphoglycerate kinase Phosphoglycerate mutase Enolase Pyruvate kinase PKLR , PKM2. Pyruvate carboxylase Phosphoenolpyruvate carboxykinase.
Lactate dehydrogenase. Alanine transaminase. Glycerol kinase Glycerol dehydrogenase. Fructose 6-P,2-kinase:fructose 2,6-bisphosphatase PFKFB1 , PFKFB2 , PFKFB3 , PFKFB4 Bisphosphoglycerate mutase.
Metabolism map. Carbon fixation. Photo- respiration. Pentose phosphate pathway. Citric acid cycle. Glyoxylate cycle. Urea cycle. Fatty acid synthesis. Fatty acid elongation. Beta oxidation. beta oxidation. Glyco- genolysis.
Glyco- genesis. Glyco- lysis. Gluconeo- genesis. Pyruvate decarb- oxylation. Keto- lysis. Keto- genesis. feeders to gluconeo- genesis. Light reaction. We have limited glycogen storage capacity. Thus, after a high-carbohydrate meal, our glycogen stores will reach capacity.
After glycogen stores are filled, glucose will have to be metabolized in different ways for it to be stored in a different form. The synthesis of glycogen from glucose is a process known as glycogenesis. Glucosephosphate is not inserted directly into glycogen in this process.
There are a couple of steps before it is incorporated. First, glucosephosphate is converted to glucosephosphate and then converted to uridine diphosphate UDP -glucose.
UDP-glucose is inserted into glycogen by either the enzyme, glycogen synthase alpha-1,4 bonds , or the branching enzyme alpha-1,6 bonds at the branch points 1. The process of liberating glucose from glycogen is known as glycogenolysis. This process is essentially the opposite of glycogenesis with two exceptions:.
Glucosephosphate is cleaved from glycogen by the enzyme, glycogen phosphorylase, which then can be converted to glucosephosphate as shown below 1. If a person is in a catabolic state or in need of energy, such as during fasting, most glucosephosphate will be used for glycolysis.
Glycolysis is the breaking down of one glucose molecule 6 carbons into two pyruvate molecules 3 carbons. The figure below shows the stages of glycolysis, as well as the transition reaction, citric acid cycle, and electron transport chain that are utilized by cells to produce energy.
They are also the focus of the next 3 sections. If a person is in a catabolic state, or needs energy, how pyruvate will be used depends on whether adequate oxygen levels are present. If there are adequate oxygen levels aerobic conditions , pyruvate moves from the cytoplasm, into the mitochondria, and then undergoes the transition reaction.
If there are not adequate oxygen levels anaerobic conditions , pyruvate will instead be used to produce lactate in the cytoplasm. We are going to focus on the aerobic pathway to begin with, then we will address what happens under anaerobic conditions in the anaerobic respiration section.
The transition reaction is the transition between glycolysis and the citric acid cycle. We are going to continue to consider its use in an aerobic, catabolic state need energy.
The following figure shows the citric acid cycle. This leaves alpha-ketoglutarate 5 carbons. GTP is readily converted to ATP, thus this step is essentially the generation of 1 ATP. The first video does a good job of explaining and illustrating how the cycle works.
The second video is an entertaining rap about the cycle. Under aerobic conditions, these molecules will enter the electron transport chain to be used to generate energy through oxidative phosphorylation as described in the next section. The electron transport chain is located on the inner membrane of mitochondria.
The electron transport chain contains a number of electron carriers. This creates a proton gradient between the intermembrane space high and the matrix low of the mitochondria.
ATP synthase uses the energy from this gradient to synthesize ATP. We live in an environment that produces a large amount of oxidation in our tissues.
These oxidation reactions can damage our cells. The reducing power of NADPH makes it ideal as a co-factor for many of our anti-oxidant defense systems.
This is very important in RBCs which have to maintain the iron in hemoglobin in the reduced state. Note that lesions in the pentose phosphate pathway in RBCs can cause serious reactions to certain medications.
The liver's job is to make sure that levels of blood glucose are sufficiently maintained to support brain and RBC function. The actual levels of glucose can be regulated by the hormones insulin and glucagon. Gluconeogenesis is almost like glycolysis run in reverse.
A coenzyme is a small molecule that participates in an enzymatic reaction without really getting used up. It may get oxidized or reduced but that is easily reversible. Often the structure of coenzymes is somewhat complex which means that our bodies do not have the enzymes to put them together and hence we consume the complex part of the coenzyme as a vitamin.
Then we often add something to the vitamin, sometimes a nucleotide, and it becomes a coenzyme. Many of the enzymatic reactions discussed above use coenzymes derived from vitamins.
The table below summarizes this information:. GTP is energetically equivalent to ATP, so why doesn't the TCA cycle just produce ATP in the succinyl CoA synthetase reaction instead of GTP, since ATP is produced in all the other energetic reactions in glycolysis and electron transport?
The GTP produced in the TCA cycle may actually be a very ancient molecular "fossil".
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Charilaos Chourpiliadis ; Shamim S. Carbohdyrate Charilaos Chourpiliadis 1 ; Glucomeogenesis S. Mohiuddin 2.
Gluconeogenesis metabolizm to a group gluconeogenesiis metabolic reactions in cytosol and Apple cider vinegar for joint pain to maintain the blood glucose level constant throughout Carbohydrate metabolism and gluconeogenesis pathway fasting state.
Reactions in the gluconeogenesis pathway vluconeogenesis regulated locally and globally by insulin, glucagon, and cortisoland some of them are highly Carbohgdrate and irreversible. Carbohydrate metabolism and gluconeogenesis pathway liver and, Carbohydrate metabolism and gluconeogenesis pathway, the kidney are the organs that supply glucconeogenesis blood glucose to various Carbohydrate metabolism and gluconeogenesis pathway.
Different tissues have multiple mechanisms to generate metabo,ism during pathwaj, maintaining adequate energy levels for their proper mrtabolism. Several tissues require continuous Body fat calipers types supply, including the brain, erythrocytes, gluconeogenessis medulla, the lens and cornea, testes, Techniques for better memory skeletal muscles during exercise.
The brain Carbohydarte glucose patbway in Cafbohydrate the fed gluconepgenesis fasting states except for Cadbohydrate fasting, which gluconegoenesis ketones. Initially, during the first hours Caebohydrate fasting, hepatic glycogenolysis gluconeogenesiis the primary source of Carboydrate.
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Metabolism-boosting herbal extracts several Carbohydrate metabolism and gluconeogenesis pathway of starvation, gluconeogenesis and glycogenolysis contribute equally to blood glucose.
The amount of glucose supplied by glycogen decreases rapidly while the Carbohyerate in the glucose fraction contributed by gluconeogenesis results in keeping constant the total ajd of glucose gluconeogenesks. Alanine, produced in skeletal muscles by protein catabolism and subsequent transamination reactions, is shuttled out in blood and ;athway up by the liver.
Inside hepatocytes, alanine undergoes transamination into pyruvate, gluocneogenesis for gluconeogenesis. Glucose produced in the liver is shuttled gluconeogeneesis in circulation and taken up by muscle cells gluconeogenesi use in ATP production Cahill glucneogenesis. Other gluconeogenic gluconeoggenesis acids e.
In red blood cells pthway other tissues lens that lack mitochondria and the exercising muscle tissue pathwy favors anaerobic metabolism, metabloism is converted amd pyruvate and subsequently metaboliem lactate. Lactate is secreted into plasma and metaboliwm up by the liver for conversion into glucose Cori Cadbohydrate via a Carbohydrzte reaction catalyzed by lactate dehydrogenase.
Pathwayy contrast to the ketogenic even-chain fatty acids, Pathwxy fatty acids are converted Crbohydrate propionyl Gluconeogejesis during beta-oxidation.
After Carbohudrate steps, propionyl CoA is converted into methylmalonyl CoA. Succinyl-CoA is an intermediate of the TCA cycle that is eventually converted into gluconegoenesis acid and enters Caebohydrate gluconeogenesis pathway.
Even-chain fatty acids and purely ketogenic amino acids leucine, lysine converted to acetyl-CoA cannot enter gluconeogenesis because the step is pahway by pyruvate dehydrogenase PDH is irreversible.
In Carbohydrate metabolism and gluconeogenesis pathway conditions, such as ischemic strokes and brain tumor development, astrocytes have increased activity of gluconeogenic enzymes, and they use lactate, alanine, aspartate, and glutamate as substrates.
Multiple factors contribute to the regulation of substrates, enzymes, and reactions involved in gluconeogenesis, including:.
Acetyl-CoA is the indicator of the cells' metabolic activity and functions as a gluconeogenesis regulator at a local level. Acetyl-CoA levels back up and allosterically activate pyruvate carboxylase. This prevents the simultaneous occurrence of gluconeogenesis and the TCA cycle in the cells. Pyruvate generation from phosphoenolpyruvate is the last irreversible step of glycolysis.
Once cells are committed to the gluconeogenesis pathway, sequential reverse reactions convert pyruvate to oxaloacetate and phosphoenolpyruvate PEP.
Glycogen storage disease type 1 is a group of inherited complex metabolic disorders which share poor fasting tolerance. This disease affects both glycogenolysis and gluconeogenesis since the missing enzyme is common in both pathways resulting in the accumulation of glucose-6 phosphate in liver cells.
Symptoms include:. Hyperuricemia results from increased uric acid production and decreased uric acid excretion uric acid competes with lactate for excretion via the same organic acid transporter in proximal renal tubules. Pyruvate carboxylase deficiency is due to the lack of pyruvate carboxylase or altered enzyme activity.
It causes lactic acidosis, hyperammonemia, and hypoglycemia. Hyperammonemia is due to pyruvate not being converted into oxaloacetic acid. Oxaloacetic acid gets transaminated into aspartate; reducing aspartate levels results in the reduced introduction of ammonia into the urea cycle.
Glucogenic Amino Acids. This illustration shows how the glucogenic amino acids enter the Krebs cycle. Image courtesy Dr Chaigasame.
Disclosure: Charilaos Chourpiliadis declares no relevant financial relationships with ineligible companies. Disclosure: Shamim Mohiuddin declares no relevant financial relationships with ineligible companies.
This book is distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives 4. You are not required to obtain permission to distribute this article, provided that you credit the author and journal.
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Search term. Biochemistry, Gluconeogenesis Charilaos Chourpiliadis ; Shamim S. Author Information and Affiliations Authors Charilaos Chourpiliadis 1 ; Shamim S. Affiliations 1 General Hospital of Patras, Pathology Department.
Introduction Gluconeogenesis refers to a group of metabolic reactions in cytosol and mitochondria to maintain the blood glucose level constant throughout the fasting state. Fundamentals Several tissues require continuous glucose supply, including the brain, erythrocytes, renal medulla, the lens and cornea, testes, and skeletal muscles during exercise.
Covalent modification of enzyme activity phosphorylation of pyruvate kinase results in its inactivation. Induction of enzymes gene expression glucagon via CRE response elements increases the expression of PEPCK. Acetyl CoA activates pyruvate carboxylase allosterically [11]. AMP inhibits fructose-1,6 bisphosphatase allosterically [12].
Mechanism Pyruvate generation from phosphoenolpyruvate is the last irreversible step of glycolysis. The enzyme consumes one ATP molecule, uses biotin vitamin B7 as a cofactor, and uses a CO2 molecule as a carbon source.
Biotin is bound to a lysine residue of PC. After ATP hydrolysis, an intermediate molecule PC-biotin-CO2 is formed, which carboxylates pyruvate to produce oxaloacetate. Apart from forming an intermediate for gluconeogenesis, this reaction provides oxaloacetic acid to the TCA cycle anaplerotic reaction.
The enzyme also requires magnesium. Pyruvate carboxylation happens in mitochondria; then, via malate shuttle, oxaloacetate is being shuttled into the cytosol to be phosphorylated.
Malate can cross the inner mitochondrial membrane while oxaloacetic acid cannot. The produced NADH is used in a subsequent step when 1,3 bisphosphoglycerate converts into glyceraldehyde-3 phosphate. The following exergonic reaction catalyzed by PEP carboxykinase PEPCKa lyase, uses GTP as a phosphate donor to phosphorylate oxaloacetate and form PEP.
Glucocorticoids induce PEPCK gene expression; cortisol, after binding to its steroid receptor intracellularly, moves inside the cell nucleus. Then, the zinc finger domain in cortisol binds to the glucocorticoid response element GRE on DNA.
The rest of the reactions are reversible and common with gluconeogenesis. Enolase, a lyase, cleaves carbon-oxygen bonds and catalyzes the conversion of PEP into 2-phosphoglycerate. Phosphoglycerate mutase, an isomerase, catalyzes the conversion of 2-phosphoglycerate to 3-phosphoglycerate by transferring a phosphate from carbon-2 to carbon Glyceraldehyde 3-phosphate dehydrogenase catalyzes the reduction of 1,3-bisphosphoglycerate to glyceraldehyde 3-phosphate.
NADH is oxidized as it donates its electrons for the reaction. As described earlier, glycerol phosphate from triglyceride catabolism is converted eventually into DHAP. Triosephosphate isomerase converts DHAP into glyceraldehyde 3-phosphate. Aldolase A converts glyceraldehyde 3-phosphate into fructose-1,6 bisphosphate.
The following irreversible step involves the conversion of fructose 1,6 bisphosphate into fructose-6 phosphate.
This step is important as it is the rate-limiting step of gluconeogenesis. Locally, increased ATP levels and increased citrate levels the first intermediate of the TCA cycle activate fructose-1,6 bisphosphatase.
However, increased AMP and increased fructose-2,6 bisphosphate F2,6BP inactivate this enzyme. Glucagon binds to its receptor, a GPCR, and activates adenylate cyclase.
The subsequent increase in cyclic AMP cAMP levels leads to the activation of protein kinase A PKA. PKA phosphorylates fructose 2,6 bisphosphatase F2,6BPase and phosphofructokinase-2 PFK Phosphorylated PFK-2 is inactive, while F2,6BPase is active and catalyzes the dephosphorylation of fructose 2,6 bisphosphate.
: Carbohydrate metabolism and gluconeogenesis pathway| Carbohydrate Metabolism | This results in a positive-feedback system where the reduced physical activity leads to even more muscle loss, further reducing metabolism. Studies have shown that the absence of hepatic glucose production has no major effect on the control of fasting plasma glucose concentration. Glucogenic amino acids have this ability Ketogenic amino acids do not. In this reaction, lactic acid replaces oxygen as the final electron acceptor. Under the action of phosphofructokinase, glucosephosphate is converted into fructosephosphate. They depend on glycolysis and lactic acid production for rapid ATP production. |
| We have a new app! | The second video is an entertaining rap about the cycle. Under aerobic conditions, these molecules will enter the electron transport chain to be used to generate energy through oxidative phosphorylation as described in the next section. The electron transport chain is located on the inner membrane of mitochondria. The electron transport chain contains a number of electron carriers. This creates a proton gradient between the intermembrane space high and the matrix low of the mitochondria. ATP synthase uses the energy from this gradient to synthesize ATP. Oxygen is required for this process because it serves as the final electron acceptor, forming water. Collectively this process is known as oxidative phosphorylation. The following figure does a nice job of illustrating how the electron transport chain functions. The first video does a nice job of illustrating and reviewing the electron transport chain. The second video is a great rap video explaining the steps of glucose oxidation. The table below shows the ATP generated from one molecule of glucose in the different metabolic pathways. Notice that the vast majority of ATP is generated by the electron transport chain. Remember that this is aerobic and requires oxygen to be the final electron acceptor. But the takeaway message remains the same. The electron transport chain by far produces the most ATP from one molecule of glucose. Conditions without oxygen are referred to as anaerobic. In this case, the pyruvate will be converted to lactate in the cytoplasm of the cell as shown below. What happens if oxygen isn't available to serve as the final electron acceptor? However, anaerobic respiration only produces 2 ATP per molecule of glucose, compared to 32 ATP for aerobic respiration. The biggest producer of lactate is the muscle. Through what is known as the Cori cycle, lactate produced in the muscle can be sent to the liver. In the liver, through a process known as gluconeogenesis, glucose can be regenerated and sent back to the muscle to be used again for anaerobic respiration forming a cycle as shown below. It is worth noting that the Cori cycle also functions during times of limited glucose like fasting to spare glucose by not completely oxidizing it. Search site Search Search. Go back to previous article. Sign in. Monosaccharide Metabolism Galactose and fructose metabolism is a logical place to begin looking at carbohydrate metabolism, before shifting focus to the preferred monosaccharide glucose. Fructose Unlike galactose, fructose cannot be used to form phosphorylated glucose. GlucosePhosphate Within hepatocytes or myocytes muscle cells , glucosephosphate can be used either for glycogenesis glycogen synthesis or glycolysis breakdown of glucose for energy production. Glycogenesis The synthesis of glycogen from glucose is a process known as glycogenesis. Please note the structuring into the three stages: a Priming stage; b Splitting stage; c Oxidoreduction—phosphorylation stage. Phosphorylation of glucose and conversion to phosphorylated fructose. This stage requires energy in the form of ATP. If oxygen is present , the 2 NADHs can donate a pair of electrons to the electron transport pathway in mitochondria and generate up to , making 7 ATPs total. The acetyl-CoA thus produced can go into the TCA cycle or be converted into fatty acids, ketone bodies, or steroids. NADH can be used to generate energy via electron transport: 2. Bottom Line : In this mitochondrial pathway, the 2-carbon acetyl group derived via glycolysis from glucose or by oxidation of fatty acids, disappears and is replaced by two CO 2 's. The acetyl groups are fully oxidized to generate NADH and FADH 2 and a great deal of energy is generated. The TCA cycle only occurs under aerobic conditions; it generates energy in the form of GTP equivalent to ATP , NADH, and FADH 2. For a picture of the TCA cycle, see Devlin, Figure Bottom Line: This simple, yet complicated, pathway serves four very different purposes. It connects with glycolysis in several places. For a picture of the pentose phosphate pathway, see Devlin, Figure We live in an environment that produces a large amount of oxidation in our tissues. These oxidation reactions can damage our cells. The reducing power of NADPH makes it ideal as a co-factor for many of our anti-oxidant defense systems. Oregon State University. Endocrinology: Adult and Pediatric. A review". The Canadian Veterinary Journal. Bibcode : Natur. Journal of General Microbiology. Metabolism , catabolism , anabolism. Metabolic pathway Metabolic network Primary nutritional groups. Purine metabolism Nucleotide salvage Pyrimidine metabolism Purine nucleotide cycle. Pentose phosphate pathway Fructolysis Polyol pathway Galactolysis Leloir pathway. Glycosylation N-linked O-linked. Photosynthesis Anoxygenic photosynthesis Chemosynthesis Carbon fixation DeLey-Doudoroff pathway Entner-Doudoroff pathway. Xylose metabolism Radiotrophism. Fatty acid degradation Beta oxidation Fatty acid synthesis. Steroid metabolism Sphingolipid metabolism Eicosanoid metabolism Ketosis Reverse cholesterol transport. Metal metabolism Iron metabolism Ethanol metabolism Phospagen system ATP-PCr. Metabolism map. Carbon fixation. Photo- respiration. Pentose phosphate pathway. Citric acid cycle. Glyoxylate cycle. Urea cycle. Fatty acid synthesis. Fatty acid elongation. Beta oxidation. beta oxidation. Glyco- genolysis. Glyco- genesis. Glyco- lysis. Gluconeo- genesis. Pyruvate decarb- oxylation. Keto- lysis. Keto- genesis. feeders to gluconeo- genesis. Light reaction. Oxidative phosphorylation. Amino acid deamination. Citrate shuttle. MVA pathway. MEP pathway. Shikimate pathway. Glycosyl- ation. Sugar acids. Simple sugars. Nucleotide sugars. Propionyl -CoA. Acetyl -CoA. Oxalo- acetate. Succinyl -CoA. α-Keto- glutarate. Ketone bodies. Respiratory chain. Serine group. Branched-chain amino acids. Aspartate group. Amino acids. Ascorbate vitamin C. Bile pigments. Cobalamins vitamin B Various vitamin Bs. Calciferols vitamin D. Retinoids vitamin A. Nucleic acids. Terpenoid backbones. |
| Gluconeogenesis | Amino Acid Degradation and Synthesis". Lippincott's Illustrated Reviews. Diabetes Care. Principles of Biochemistry with a Human Focus. Nutritional Ecology of the Ruminant 2nd ed. Harper's Illustrated Biochemistry 31st ed. McGraw-Hill Publishing Company. Medical Biochemistry 4th ed. The American Journal of Physiology. A test case for pathway analysis tools". Developmental Biology. Biology Direct. Physiological Reviews. The Journal of Clinical Investigation. Vander's Human Physiology. McGraw Hill. The Journal of Biological Chemistry. February Cancer Research. Frontiers in Pharmacology. Diabetic Medicine. Journal of Animal Science. Fundamentals of Biochemistry. Critical Reviews in Biochemistry and Molecular Biology. May Annals of the New York Academy of Sciences. Bibcode : NYASA January International Journal of Molecular Medicine. December The Journal of Endocrinology. Hundal RS, Krssak M, Dufour S, Laurent D, Lebon V, Chandramouli V, et al. Nature Communications. Bibcode : NatCo Bibcode : Natur. Chemical Reviews. Proceedings of the National Academy of Sciences of the United States of America. Bibcode : PNAS.. The discovery of a non-enzymatic metabolism and its role in the origins of life". The Biochemical Journal. ISSN Metabolism , catabolism , anabolism. Metabolic pathway Metabolic network Primary nutritional groups. Purine metabolism Nucleotide salvage Pyrimidine metabolism Purine nucleotide cycle. Pentose phosphate pathway Fructolysis Polyol pathway Galactolysis Leloir pathway. Glycosylation N-linked O-linked. Photosynthesis Anoxygenic photosynthesis Chemosynthesis Carbon fixation DeLey-Doudoroff pathway Entner-Doudoroff pathway. Xylose metabolism Radiotrophism. Fatty acid degradation Beta oxidation Fatty acid synthesis. Steroid metabolism Sphingolipid metabolism Eicosanoid metabolism Ketosis Reverse cholesterol transport. Metal metabolism Iron metabolism Ethanol metabolism Phospagen system ATP-PCr. Fructose-bisphosphate aldolase Aldolase A , B , C Triosephosphate isomerase. Glyceraldehyde 3-phosphate dehydrogenase Phosphoglycerate kinase Phosphoglycerate mutase Enolase Pyruvate kinase PKLR , PKM2. Pyruvate carboxylase Phosphoenolpyruvate carboxykinase. Lactate dehydrogenase. Alanine transaminase. Glycerol kinase Glycerol dehydrogenase. Fructose 6-P,2-kinase:fructose 2,6-bisphosphatase PFKFB1 , PFKFB2 , PFKFB3 , PFKFB4 Bisphosphoglycerate mutase. Metabolism map. Carbon fixation. Photo- respiration. Pentose phosphate pathway. Citric acid cycle. Glyoxylate cycle. Urea cycle. Fatty acid synthesis. Fatty acid elongation. Beta oxidation. beta oxidation. Glyco- genolysis. Glyco- genesis. Glyco- lysis. Gluconeo- genesis. Pyruvate decarb- oxylation. Keto- lysis. Keto- genesis. feeders to gluconeo- genesis. Light reaction. Oxidative phosphorylation. Amino acid deamination. Citrate shuttle. MVA pathway. MEP pathway. Shikimate pathway. Glycosyl- ation. Sugar acids. Simple sugars. Nucleotide sugars. Propionyl -CoA. Acetyl -CoA. Oxalo- acetate. Succinyl -CoA. α-Keto- glutarate. Ketone bodies. Respiratory chain. Serine group. Branched-chain amino acids. Aspartate group. Amino acids. When there is an excess of energy available, gluconeogenesis is inhibited. When energy is required, gluconeogenesis is activated. Search site Search Search. Go back to previous article. Sign in. Introduction The need for energy is important to sustain life. Overview Gluconeogenesis is much like glycolysis only the process occurs in reverse. 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 pyruvate to phosphoenolpyruvic acid PEP. In order to convert pyruvate to PEP there are several steps and several enzymes required. Pyruvate carboxylase, PEP carboxykinase and malate dehydrogenase are the three enzymes responsible for this conversion. Pyruvate carboxylase is found on the mitochondria and converts pyruvate into oxaloacetate. Because oxaloacetate cannot pass through the mitochondria membranes it must be first converted into malate by malate dehydrogenase. Malate can then cross the mitochondria membrane into the cytoplasm where it is then converted back into oxaloacetate with another malate dehydrogenase. Lastly, oxaloacetate is converted into PEP via PEP carboxykinase. The next several steps are exactly the same as glycolysis only the process is in reverse. The second step that differs from glycolysis is the conversion of fructose-1,6-bP to fructoseP with the use of the enzyme fructose-1,6-phosphatase. The conversion of fructoseP to glucoseP uses the same enzyme as glycolysis, phosphoglucoisomerase. The last step that differs from glycolysis is the conversion of glucoseP to glucose with the enzyme glucosephosphatase. This enzyme is located in the endoplasmic reticulum. Regulation Because it is important for organisms to conserve energy, they have derived ways to regulate those metabolic pathways that require and release the most energy. The conversion of pyruvate to PEP is regulated by acetyl-CoA. More specifically pyruvate carboxylase is activated by acetyl-CoA. Because acetyl-CoA is an important metabolite in the TCA cycle which produces a lot of energy, when concentrations of acetyl-CoA are high organisms use pyruvate carboxylase to channel pyruvate away from the TCA cycle. If the organism does not need more energy, then it is best to divert those metabolites towards storage or other necessary processes. The conversion of fructose-1,6-bP to fructoseP with the use of fructose-1,6-phosphatase is negatively regulated and inhibited by the molecules AMP and fructose-2,6-bP. These are reciprocal regulators to glycolysis' phosphofructokinase. Phosphofructosekinase is positively regulated by AMP and fructose-2,6-bP. Once again, when the energy levels produced are higher than needed, i. a large ATP to AMP ratio, the organism increases gluconeogenesis and decreases glycolysis. The opposite also applies when energy levels are lower than needed, i. a low ATP to AMP ratio, the organism increases glycolysis and decreases gluconeogenesis. The conversion of glucoseP to glucose with use of glucosephosphatase is controlled by substrate level regulation. |
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