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Dear students, This manuscript is by no means intended to replace any textbook of. Biochemistry or your lecture notes While you will start reading it you will. realize that you will not understand everything simply because. Biochemistry is a very coherent subject and the information data that it. contains cannot be just dissected away from each other The purpose of this. manuscript is not more than to give you a brief reference to each question. required to be known by the student at the exam and also to provide some. information on the field of Biochemistry that are not readily apparent after. reading the book, After having read Biochemistry and being fed up with the hundreds of. regulations metabolic intermediates and enzymes you must realize that the. most important enzyme which is not mentioned in any textbook of. Biochemistry is the biochemase in order for you to digest this huge. material which can only be done by PPP Pen Paper and Patience by. writing the pathways again and again,Christos Chinopoulos M D Ph D. BIOENERGETICS, For bioenergetics only the answers 16 and 17 will be provided as the rest of the questions rely. on material of the First Year Second Semester under the title Descriptive Biochemistry and. Bioenergetics, 16 What is the mechanism of development of lactic acidosis in the.
absence of pyruvate dehydrogenase activity What further symptoms. can be observed if pyruvate dehydrogenase deficiency is caused by. the lack of lipoamide dehydrogenase subunit,Theoretical Background. The lactic acid that circulates in the human body is the product of anaerobic metabolism of. glucose that takes place primarily in RBC s skin kidney medulla and white skeletal muscle. Some of it is oxidized by red muscle and kidney cortex but the bulk of it is taken up by the. liver and converted into glucose, Some tissues such as blood have either very few white blood cells or no red blood cells. mitochondria and thus a glycolytic mode of metabolism is obligatory Other tissues have such. a high glycolytic capacity that oxidative metabolism is suppressed a phenomenon known as. the Crabtree effect, In case of pyruvate dehydrogenase deficiency lactic acidosis develops because of pile up of. pyruvate that it will convert to lactate in order to regenerate NAD as the citric acid cycle. TCA is nonfunctional, Further symptoms if PDH deficiency is caused by the lack of lipoamide dehydrogenase. subunit As this subunit participates in other enzymes too namely the Kg DHase the. Branched Chain Keto Acid DHase and the glycine cleavage system the symptoms will be the. following Slowing down of the TCA inability of catabolism of BCAA which are preferred by. the muscle and the brain and hyperglycinemia, 17 What is the mechanism of brain damage detected in pyruvate.
carboxylase deficiency Explain the development of, hyperammonemia Which metabolic pathways can be associated. with the pyruvate carboxylase function,The reasons for brain damage are. a Absence of TCA, b Hyperammonemia resulting to cerebral edema due to absence of OAA that would give. Aspartate Asp would give a Nitrogen to combine with ammonia and give urea see Harper. c No Glutamate No GABA formation,d No Acetylcholine formation. e No myelin synthesis because of low citrate levels. Metabolic pathways associated with PC function See question 22. CARBOHYDRATES,1 Sequence of reactions in Glycolysis I.
Harper Fig 19 2, Glycolysis is found in the cytosol of the cell along with the Pentose Phosphate Pathway. PPP and the Fatty Acid synthesis plus others It was the first pathway discovered by. researchers and the first pathway on earth simply because it does not require oxygen which. was not available in the atmosphere when life started to evolve. Although the enzymes of glycolysis are usually described as soluble components of the. cytosol it seems that they form large multienzyme complexes for the effective shuttling of the. metabolic intermediates and for minimizing the diffusion factor that could limit the speed of. the reactions Furthermore certain glycolytic enzymes form specific noncovalent complexes. with structural components of the cell which may serve to organize reaction sequences and. assure efficient transfer of intermediates between cellular compartments e g though not a. glycolytic enzyme Glucose 6 Phosphatase is found in the luminal side of the ER Certain. glycolytic enzymes bind to microtubules or to actin microfilaments bringing these enzymes. into close association and holding them in a specific region of the cytoplasm e g hexokinase. HK is bound to the outer membrane of the mitochondria allowing ATP produced in the. mitochondrion to move directly to the catalytic site of the HK without entering and being. diluted by the cytosol, In malignant cells glycolysis proceeds at much higher rates than normal more than the citric. acid cycle can take Thus an excess of pyruvate is formed that it can only be metabolized to. lactate for the provision of NAD Therefore lactate builds up favoring an acidic. environment for the tumor The pathway from the glycolysis until the formation of lactate is. also known as Embden Meyerhof pathway, Certain tissues and cell types retina brain RBC s convert glucose to lactate even under. aerobic conditions, Glycolysis is also the pathway for the oxidation of Fructose bypassing the. Phosphofructokinase PFK 1 step Galactose see question 6 and Mannose. Glucose enters cells through the action of glucose transporters These are. i GLUT 1 RBC s brain muscle adipocytes, ii GLUT 2 liver beta pancreatic cells kidney intestinal epithelial cells It has a high KM.
low affinity great capacity It works both ways in and out. iii GLUT 3 brain, iv GLUT 4 muscle adipocytes It is the only insulin dependent glucose transporter. v GLUT 5 fructose transporter,vi GLUT 6 similar to GLUT 3. vii GLUT 7 found within the ER of liver and kidney cells It translocates glucose molecules. to the exterior of the cell after the action of Glc 6 Phosphatase. Hexokinase the first step in glycolysis is found in all extrahepatic tissues except the beta. cells of the pancreas In liver and beta pancreatic cells there is glucokinase GK Hexokinase. and glucokinase are isoenzymes they differ in their kinetic properties Harper Fig 21 5 and. in the way they are regulated the other name of glucokinase is hexokinase D. Hexokinase or glucokinase phosphorylates glucose to Glc 6 P as it enters the cell for the. following reasons, a To maintain the gradient between the extracellular and intracellular compartment in. order for glucose to have always a tendency towards the interior of the cell. b All phosphorylated molecules cannot exit the cell therefore Glc 6 P is trapped in the. interior of the cell of course a gradient is formed for the Glc 6 P towards the. extracellular milieu but now Glc 6 P cannot even approach the inner side of the. plasma membrane because both Glc 6 P and the inner plasma membrane are. negatively charged, c The phosphorylation of glucose by hexokinase or glucokinase serves as an. activation for the provision of energy from glucose as a substrate at the substrate. d It serves also for the facilitation of the glycolytic reactions due to the fact that. binding of phosphate groups to the active sites of enzymes provides binding energy. that contributes to lowering the activation energy and increasing the specificity of. enzyme catalyzed reactions,2 Sequence of reactions in Glycolysis II.
Harper Fig 19 2, In red blood cells the 6th step of glycolysis which is the Phosphoglycerate kinase PGK step. the only reversible kinase of glycolysis Harper Fig 19 4 can be bypassed in order for the. RBC s to form 2 3 BPG The latter molecule binds to hemoglobin and decreases its affinity. for oxygen with a concomitant displacement of the oxyhemoglobin dissociation curve to the. right therefore promoting the release of oxygen to the tissues However if it is 2 3 BPG to be. formed PGK is bypassed and therefore there will be no net formation of 2 ATP s as PGK. generates 1 ATP two times This bypass happens only in the arterial blood when there is a need. for oxygen release to the tissues in venous blood 2 3 BPG is not formed and PGK is not. bypassed The two enzymes participating in the bypass of PGK are Bisphosphoglycerate. mutase and 2 3 Bisphosphoglycerate phosphatase which are both parts of a tandem enzyme. tandem enzyme means that both enzymes are found on the same polypeptide chain. Glycolysis in RBC s always terminates in lactate formation RBC s posses no mitochondria. In mitochondria containing cells as pyruvate is formed it enters the mitochondria either with. a cotransport of a proton or the antiport of a hydroxyl group Note that pyruvate possesses a. negative charge and this proton cotransport or hydroxyl antiport system contributes to the. maintenance of the charge balance between the two sides of the mitochondria moreover the. inner membrane space of mitochondria is very negatively charged and it would be very. unlikely for a negative molecule such as pyruvate to enter this space without the expenditure of. energy or the usage of a transport system, 3 Regulation and energetics of glycolysis The Pasteur effect. Harper Fig 21 1 Table 19 1, Nonequilibrium reactions monodromic are potential targets for regulation A. nonequilibrium reaction is identified as a reaction in which the KM of the enzyme is. considerably lower than the normal substrate concentration In glycolysis there are three such. a At the level of the phosphorylation of glucose immediately as it enters the cell namely the. HK or GK step,b At the level of PFK 1,c At the level of Pyruvate Kinase PK. a Hexokinase is subject to allosteric inhibition by its own product negative feedback Glc. 6 P and this is the only regulation of hexokinase, Glucokinase is subject to the following regulations Induced by insulin and repressed by.
glucagon glucagon action mediated by cAMP high carbohydrate feeding upregulates the GK. gene expression while starvation and diabetes have opposite effects GK is also inhibited by. Frc 6 P This partial inhibition of GK by Frc 6 P is mediated by an additional protein the. regulatory protein This regulatory protein has also affinity for Frc 1 P which competes with. Frc 6 P and cancels its inhibitory effect on GK Frc 1 P displaces Frc 6 P from the regulator. protein so the latter cannot inhibit GK Because Frc 1 P is present in the liver only when. there is fructose in the blood this property of the regulator protein explains the observation that. ingested fructose stimulates the phosphorylation of glucose in the liver The beta pancreatic. cells also contain this regulator protein, PFK 1 is the committed step of glycolysis That means that x inhibition of PFK 1 would. give an x inhibition of the final glycolytic product that is pyruvate PFK 1 is allosterically. activated by,a Frc 6 P positive feedforward, c Frc 2 6 BP2 Frc 2 6 BP2 is formed by PFK 2 which is inhibited by glucagon acting. through cAMP see Harper Fig 21 3 Frc 2 6 BP2 is the most potent allosteric effector on. PFK 1 than any other signal,PFK 1 is allosterically inhibited by. b Citrate it is a metabolic index in the mitochondria. PFK 1 gene is subject to induction by insulin and high carbohydrate feeding while starvation. and diabetes have opposite effects,PK is allosterically inhibited by. a Alanine gluconeogenic signal,c Acetyl CoA and Long Chain Fatty Acids LCFA.
while PK is allosterically activated by, a Frc 1 6 BP2 it is a metabolic index in the cytosol. PK is very tightly regulated in the liver by the aforementioned mechanisms and this serves to. prevent the leak down of pyruvate formed by phosphoenolpyruvate carboxykinase PEPCK. in case of gluconeogenesis that would convert to oxaloacetate OAA and then to. phosphoenolpyruvate PEP and that would be a futile cycle. PK is also subject to covalent modification by phosphorylation de phosphorylation. mechanisms, The Pasteur effect Originally Pasteur observed that in the presence of oxygen yeast. consume more than 10 times less their carbohydrate supplies than when they are incubated in. the absence of oxygen The explanation of this phenomenon is the following The aerobic. oxidation via citric acid cycle TCA inhibits the anaerobic degradation of glucose This is. because in the presence of oxygen the NADH NAD ration would be low and therefore PDH. would be uninhibited to form Acetyl CoA and this would give citrate and a lot of ATP. through the TCA Citrate and ATP would inhibit PFK 1 and therefore glycolysis would cease. In the absence of oxygen the NADH NAD ratio would be high as there would be no final. reducing equivalent acceptors PDH would be inhibited to give Acetyl CoA and therefore. citrate and ATP So PFK 1 would not be inhibited and glucose would be consumed at a much. higher rate in order to compensate for the loss of TCA and its product ATP. 4 Digestion and absorption of carbohydrates, Dietary carbohydrates provide a major portion of the daily caloric requirement They consist of. mono di and polysaccharides Monosaccharides need not be hydrolyzed for absorption. Disaccharides require the intestinal surface enzymes for hydrolysis into monosaccharides. while polysaccharides depend on pancreatic amylase for degradation amylase of the saliva. plays a very minor role Exceptionally trisaccharides cannot be hydrolyzed by humans Starch. ANSWERS FOR THE BIOCHEMISTRY FINAL EXAM by CHRISTOS CHINOPOULOS M D Ph D Semmelweis University of Medicine Department of Medical Biochemistry Budapest 1998 Dear students This manuscript is by no means intended to replace any textbook of Biochemistry or your lecture notes While you will start reading it you will realize that you will not understand everything simply because

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