WARNING!!!! THIS IS GOING TO LONG AND BORING IN SOME PARTS BUT ALAS IT MUST BE DONE.
Alrighty then folks let us get into the nitty, gritty of this glycolytic pathway.
As you may know, glycolysis is the process of converting glucose (a simple sugar) into pyruvate and producing energy in the form of ATP.
However, you might be asking, why is this important and why do I even need to know about this conversion?
Well the obvious answers are, because you have to know it for exam and the more important one….some cells in your body rely heavily on this pathway for energy generation. Therefore, it is prudent to understand and appreciate the dynamics of this process. I am going to take you through the various stages of glycolysis, mention the fates of pyruvate, and give some inclination about other methods of conducting the glycolytic pathway and then some extra info. That may interest you about the pathway.
Now I touched on the basics of glycolysis in a prior posting, which I have copied and pasted below to jog your memory.
Glycolysis is the first stage of cellular respiration and is involved in the conversion of glucose into a three-carbon compound known as pyruvate. This process is essential for energy generation for the cell and facilitates the control of blood glucose levels by ensuring that there is a steady intake and utilization of glucose from the blood.
As you would know, I went into why high blood glucose levels are hazardous to our tissues and why it must be metabolized quickly and efficiently. (Check out the Highs and Lows of glucose on my blog).
Glycolysis is the most primitive energy producing reaction that occurs in bacteria, fungi and even us humans. It occurs in the absence or presence of oxygen. Glycolysis occurs in the cytosol of the cell and therefore can occur in both prokaryotes as well as eukaryotes since it does not require an organelle to occur.
Of importance, is the fact that erythrocytes or rbcs’ as I call them, depend solely on energy generated from glycolysis to carry out its functions. Now, I hope that you know that red blood cells do not possess organelles; hence, this process is ideal for them. You see rbcs’ transport oxygen via haemoglobin, which if you are still unsure, is the most important job in the body, so in order to become more efficient and effective in their duties, rbcs’ shed most of their organelles to make room for the haemoglobin. Hence, you might derive the fact that inability for glycolysis to occur, will lead to degeneration of function of rbcs’ leading to a little known ailment as anaemia.
Glycolysis involves 10 enzymes that catalyse three irreversible reactions and seven reversible reactions to yield two molecules of pyruvate (3C), four molecules of ATP (net ATP equals two), two molecules of NADH and two molecules of water. All of this results from one glucose molecule.
Now, ATP is a nucleotide that comprises of adenosine and three phosphate groups. These phosphate bonds have high chemical energy stored. This energy is released by the hydrolysis of the phosphate bonds to yield ADP. Therefore, production of one molecule of ATP stores high levels of energy, enough to adequately power the functions of the cell. NADH is also a high-energy compound. It is the reduced form of NAD, which is a co-enzyme that is found in tissue. NADH is able to transport electrons to the electron transport chain in order to yield ATP or energy.
Pyruvate may move on to the Krebs cycle or TCA cycle as the hip people call it, in the mitochondria or to produce lactic acid if there is no oxygen present as seen in muscle cells that undergo the Cori cycle. TCA further metabolizes the pyruvate to yield more energy and produce electron transporters. NADH produced is then transported to the inner mitochondria through the electron transport chain to yield energy/ATP. The ATP produced may be utilized to facilitate the different functions of the cell that require energy such as contraction of actin and myosin fibres.
The initial process of glycolysis involves the conversion of glucose to glucose 6-phosphate which occurs in the cytosol of all cells. But you must be wondering how does glucose enter the cell? Well here is a brief idea of how this occurs.
Glucose from the diet enters the bloodstream from the digestive system, where it is first transported to the liver and then to the rest of the body. Unfortunately, glucose cannot easily diffuse into cells and so require two mechanisms to enter cells. One system involves a sodium-monosaccharide co-transporter system and the other a facilitated diffusion transport system, the latter of which is performed by the use of transporters in cell membranes of cells.
The facilitated diffusion mechanism involves the use of special glucose transporters known as GLUT transporters. There are more than 14 types of these transporters but they exhibit tissue-specificity and hence, one particular type is found on certain cells. These transporters found in the cell membrane are existent in two conformational states. When glucose binds to these transporters, it induces a conformational change that allows for movement of the glucose molecule across the cell membrane. Now, as I mentioned before, GLUT transporters show tissue-specificity and therefore certain isoforms are found on particular cells. Hereunder is a list of the most common isoforms:
GLUT 1: ERYTHROCYTES AND BRAIN
GLUT 2: LIVER, KIDNEY AND PANCREAS
GLUT 3: NEURONES
GLUT 4: ADIPOSE TISSUE AND SKELETAL MUSCLES
GLUT 5: TESTES AND SMALL INTESTINES
GLUT 7: LIVER AND GLUCONEOGENIC TISSUES (KIDNEY/SMALL INTESTINES)
Okay, so you get the idea, but if you want to check out the full list and get some more information, visit this site below where there is an entire paper devoted to reviewing these transporters.
These GLUT transporters facilitate the diffusion of glucose and other hexoses by following a concentration gradient i.e. diffusion of glucose from a state of high concentration to a state of low concentration. However, these isoforms operate a little different in their uptake. GLUT 1, 3, 4 usually uptake glucose from the blood and does this periodically. However, GLUT 2 transporters uptake glucose primarily in states of hyperglycaemia or release glucose in fasting states of hypoglycaemia. GLUT 4 transporters have also been known to increase in activation in the presence of high insulin levels and therefore are stimulated by increased blood glucose levels.
GLUT 5 is a special case since it usually does not transport glucose but rather another hexose sugar, FRUCTOSE. But can you guess why it does this? Let me put your mind to rest, as I mentioned before, these transporters are mainly found in the testes. And what is the testes responsible for? You guessed it, producing sperm which main source of energy is from fructose. So when it needs to make that long voyage up the vaginal canal and uterus to the fundus of the fallopian tubes for fertilization it possesses fructose around the head of the sperm stored to generate energy. GLUT 7 is also a peculiar case since it actually mediates glucose flux across the endoplasmic reticulum membrane in gluconeogenic cells rather than uptake of glucose from the blood.
The mechanism of action of GLUT transporters
Glucose/hexose sugar present in the extracellular space encounters the transporters in the cell membrane and bind to the transporters. This binding causes the transporter molecule to change in conformation and close off at the extracellular space end and open into the cytosol. This opening into the cytosol allows glucose to move across the cell membrane and into the cell.
The other method mentioned was sodium monosaccharide co-transporter system. As you might figure from the title, it is a process of transportation against the concentration gradient and therefore will require energy in the form of ATP, in order to occur. This is a carrier-mediated process in which glucose transport is coupled with sodium influx from cells. This process is known as SGLT or sodium dependent glucose transport in which one molecule of glucose is pumped into the cell while sodium ions are pumped into cells. This may be jogging your memory of Biology in high school and therefore it is no surprise that this type of transport occurs in the epithelial cells of the intestines, renal tubules and the choroid plexus of the ventricles in the brain.
However, that is enough of that. Here is where the fun begins, with the aid of the mnemonics I created prior; we will dive into this exciting process. Again for a recap, hereunder is the mnemonics for glycolysis:
Triose phosphate isomerase
Glyceraldehyde 3-phosphate dehydrogenase
- H = Helen
- P = Paints
- P = Pictures
- A = Along
- T = The Training
- G = Grounds
- P = Praying
- P = People
- E = Enjoy
- P = Paintings
Glyceraldehyde 3-P + Dihydroxyacetone-P
- G = Gross
- G = Guys
- F = Favour
- B = Big Boobs but
- G = Gorgeous + D = Dreamy
- B = Boys
- P = Prefer
- P = Pretty
- P = Petite
- P = Photogenic girls
Well, we have glucose in our cytosol, so what now?
Here we come to the first phase of glycolysis, THE ENERGY INVESTMENT PHASE. This involves five reactions, two of which are irreversible reactions and there is the consumption of two ATP molecules. Therefore, we are using up some energy to get some energy.
THE ENERGY INVESTMENT STAGE
- GLUCOSE –> GLUCOSE 6-PHOSPHATE
Glucose is converted into glucose 6-phosphate by the enzyme HEXOKINASE. This is the phosphorylation of glucose in which hexokinase facilitates the transfer of a terminal phosphate group from ATP to glucose.
This is performed in order to trap the glucose in the cells. Glucose can readily diffuse out of the cells by use of the aforementioned transporters and thus we have to ensure that they remain in the cell to carry out the reactions. Phosphorylated sugars cannot readily leave cells since they cannot penetrate the cell membrane. This is due to two main reasons. The first is the fact that it cannot diffuse across the cell membrane and there are no transporter molecules that may transport glucose 6-phosphate across the cell membrane. The GLUT transporters cannot transport a phosphorylated compound. Another reason is that the phosphate group is highly negative and therefore will be repelled by the negative polar bi-lipid layer of the cell membrane. This effectively traps the glucose 6-phosphate in the cytosol and hence committing it to undergo reactions.
This phosphorylation of glucose is referred to as the first priming reaction of the cell. This means that essentially, the addition of the phosphate group to glucose causes an increase in the reactivity of glucose and fosters the forward movement of the pathway. This reaction is conveniently enough, the first IRREVERSIBLE REACTION. This reaction is irreversible since it has a very negative ΔG value that means that it is a highly energetically feasible reaction and will occur spontaneously. However, the conversion of glucose 6-phosphate to glucose will require a very high positive activation energy and hence will not be energetically feasible. Therefore, conversion of glucose 6-phosphate to glucose will not occur spontaneously. Thus, the conversion of glucose to glucose 6-phosphate is IRREVERSIBLE.
A bit about hexokinase.
Hexokinase is an isozyme, meaning that it belongs to a family of enzymes that catalyse the same reaction but possess different enzymatic kinetics such as km and Vmax. Hexokinase is not absolutely specific to glucose and may act on other hexose sugar such as fructose but does possess a high affinity for glucose. Hexokinase is one of the three regulatory enzymes found in the glycolytic pathway and found in most cells of the human body. However, in certain cells such as hepatocytes and beta islet cells of the pancreas, another isoform of hexokinase is present, GLUCOKINASE. Glucokinase aka hexokinase D, is responsible for the phosphorylation of glucose in the liver and islet cells of the pancreas. Glucokinase in the pancreas acts as a glucose sensor that aids in glucose homeostasis by aiding in the regulation of release of insulin from the beta cells of the pancreas. Glucokinase has a higher km than other hexokinases.
Whether hexokinase or glucokinase, the mechanism of action involves transfer of a high-energy terminal phosphate group from ATP and adding it to the glucose molecule. Hexokinase requires magnesium ions as a co-factor to ensure its efficacy and efficiency. When ATP molecule binds to hexokinase, it causes slight conformation to induce a complimentary fit that facilitates better binding of glucose to the active site of hexokinase. However, ATP is highly unstable since it possesses a large negative charge from its three phosphate groups. Therefore, the positively charged magnesium ions must be present in order to stabilize the ATP molecule and hence allow for the phosphorylation to occur. In this reaction, when the high-energy phosphate group is removed from ATP, there is the formation of ADP.
Hexokinase is inhibited allosterically by glucose 6-phosphate and therefore build up in glucose 6-phosphate prevents the phosphorylation of glucose. Glucokinase is however, not inhibited by glucose 6-phosphate but may be inhibited indirectly by fructose 6-phosphate which is produced in the next step.
Summary of stage: glucose + ATP + Mg2+ –> glucose 6-phosphate + ADP by hexokinase/glucokinase.
2. GLUCOSE 6-PHOSPHATE –> FRUCTOSE 6-PHOSPHATE
Glucose 6-phosphate is then converted to fructose 6-phosphate via an isomerization reaction. This is a reversible reaction and is catalysed by the enzyme PHOSPHOHEXOSE ISOMERASE. This reaction involves the conversion of an aldose sugar to a ketose sugar.
Something to note however, this reaction is not the only reaction that occurs with glucose 6-phosphate. Glucose 6-phosphate may be utilized in other reactions and its fate is not only in the glycolytic pathway. Glucose 6-phosphate may be utilized as a precursor molecule in many pathways that involve glucose such as the pentose phosphate pathway and glycogenesis. Glucose 6-phosphate may also be fed into the glycolytic pathway through other pathways such as glycogenolysis, gluconeogenesis from non-carbohydrate sources as well as from the pentose phosphate pathway.
Summary of step: glucose 6-phosphate –> fructose 6-phosphate by phosphohexose isomerase
3. FRUCTOSE 6-PHOSPHATE –> FRUCTOSE 1,6-BISPHOSPHATE
This reaction is another IRREVERSIBLE REACTION. It is also known as the 2nd priming reaction in glycolysis. Fructose 6-phosphate is converted to fructose 1, 6 bisphosphate by the enzyme PHOSPHOFRUCTOKINASE-1 (PFK-1). PFK-1 performs a phosphorylation of fructose 6 phosphate by transferring a high-energy terminal phosphate group from ATP to fructose 6-phosphate to form fructose 1, 6-bisphosphate. This is a similar reaction to hexokinase. PFK-1 is the MOST REGULATED enzyme in the glycolytic pathway. It is considered the rate-limiting reaction and is the committed step in the pathway.
PFK-1 is inhibited allosterically by elevated levels of ATP meaning that in high-energy states there is a decrease in this reaction to conserve cell resources. This inhibition may also occur with high levels of citrate, which is formed in the TCA cycle by the combination of acetyl-CoA and oxaloacetate. This negative feedback is an indicator that there is a high-energy state in the cell and therefore, there is a decrease demand for energy production and pyruvate by extension.
However, PFK-1 may also be activated in low energy states in the cell by AMP, which signals that there is low energy available in cells. The most potent activator of PFK-1 is fructose 2, 6-bisphosphate. This substance is formed by phosphofructokinase-2 which converts fructose 6-phosphate to fructose 2, 6-bisphosphate.
This phosphorylation involves the addition of a high-energy phosphate group to the C-1 atom on fructose 6-phosphate, thus there is a phosphate group on two different C atoms and hence is a bisphosphate compound and not a diphosphate compound which possesses two phosphate groups on the same atom.
Summary of the step: fructose 6-phosphate + ATP –> fructose 1, 6-bisphosphate + ADP by phosphofructokinase-1
4. FRUCTOSE 1,6-BISPHOSPHATE –> GLYCERALDEHYDE 3-PHOSPHATE + DIHYDROXYACETONE PHOSPHATE
This is referred to as the splitting reaction. In all the other steps prior, the products were 6C sugar molecules but in this step, there is the splitting of the 6C sugar to form two 3C sugar molecules. Fructose 1, 6-bisphosphate is converted into glyceraldehyde 3-phosphate and dihydroxyacetone phosphate by the enzyme ALDOLASE. This is not a regulated step and is reversible.
Thing to note is that there is an isoform of aldolase enzyme known as Aldolase B which is responsible for cleaving fructose 1-phosphate in the liver and facilitating the feeding of glyceraldehyde 3-phosphate and dihydroxyacetone phosphate into the glycolytic pathway (will touch on this later).
Summary of step: fructose 1, 6-bisphosphate –> glyceraldehyde 3-phosphate + dihydroxyacetone phosphate by aldolase.
5. DIHYDROXYACETONE PHOSPHATE –> GLYCERALDEHYDE 3-PHOSPHATE.
This is the final step in the energy investment phase and involves the conversion of dihydroxyacetone phosphate to glyceraldehyde 3-phosphate by the enzyme, TRIOSE PHOSPHATE ISOMERASE. This is also a reversible reaction and is not regulated involving isomerization of dihydroxyacetone phosphate to glyceraldehyde 3-phosphate.
A thing to note with triose phosphate isomerase is that this enzyme is kinetically perfect. It gains this characteristic since as the substrate binds to the active site, there is an immediate reaction. This occurs since the intermediates formed in this reaction are quite labile and unstable and therefore to avoid the formation of these intermediates, there is the quick formation of the product.
Summary of the step: dihydroxyacetone phosphate –> glyceraldehyde 3-phosphate by triose phosphate isomerase
This is the end of the energy investment phase and thus far, one molecule of glucose is converted into two molecules of glyceraldehyde 3-phosphate. Two ATP molecules were consumed during this phase and there were two irreversible reactions catalysed by hexokinase and PFK-1 respectively. These enzymes catalysed a phosphorylation reaction in which a high-energy terminal phosphate group from ATP is transferred to a hexose sugar molecule. There were also three reversible reactions within this phase, two of which were isomerization reactions and one was a splitting reaction.
Let us now proceed to the next phase in the glycolytic pathway, the ENERGY GENERATION PHASE. This phase also involves five reactions, with one of them being irreversible. This phase involves the generation of four ATP molecules, two NADH molecules and two molecules of pyruvate. This stage involves the conversion of two molecules of glyceraldehyde 3-phosphate to two molecules of pyruvate.
ENERGY GENERATION PHASE
6. 2 GLYCERALDEHYDE 3-PHOSPHATE –> 2 1,3 BISPHOSPHOGLYCERATE
This reaction is the only OXIDATION REACTION in the glycolytic pathway. 2 molecules glyceraldehyde 3-phosphate are converted to 2 molecules of 1, 3 bisphosphoglycerate by the enzyme, GLYCERALDEHYDE 3-PHOSPHATE DEHYDROGENASE. In this reaction, glyceraldehyde 3-phosphate dehydrogenase, first utilizes NAD+ to perform the oxidation of glyceraldehyde 3-phosphate. NAD+ is reduced and gains an H+ ion from glyceraldehyde 3-phosphate to form NADH + H+. This redox reaction causes a release of energy. This release of energy is then utilized by glyceraldehyde 3-phosphate dehydrogenase to drive a PHOSPHORYLATION REACTION using an inorganic phosphate group. As you might realize, this phosphorylation does not involve ATP but rather an inorganic phosphate group. Thus, the conversion of glyceraldehyde 3-phosphate to 1, 3 bisphosphoglycerate involves an oxidation as well as a phosphorylation reaction. This reaction is a reversible reaction however and does not regulate the pathway.
To note, NAD+ is a scarce commodity in the cell and therefore found in small quantities. Thus, this must be replenished in order to ensure that glycolysis continues as well as other reactions in the cells. Also, arsenate (pentavalent arsenic) may prevent production of ATP and NADH by glycolysis by competing with inorganic phosphate to bind to the active site of glyceraldehyde 3-phosphate dehydrogenase. In effect, it acts as a competitive inhibitor of glyceraldehyde 3-phosphate dehydrogenase, causing the formation of a complex that is spontaneously hydrolysed to 3-phosphoglycerate. This skipping or bypassing of the 1, 3-bisphosphoglycerate causes the prevention of NADH formation as well as the generation of ATP.
Additionally, 1, 3-bisphosphoglycerate does not only proceed through glycolysis but may be converted to 2, 3-bisphosphoglycerate via the bisphosphoglycerate shunt utilizing the enzyme bisphosphoglycerate mutase. This occurs in red blood cells in order to regulate oxygen binding to heme. 2, 3-bisphosphoglycerate serves as an inhibitor of allosteric binding of Oxygen to heme on red blood cells. 2, 3 bisphosphoglycerate may be dephosphorylated by a phosphatase to 3-phosphoglycerate that enables feeding into the glycolytic pathway again.
Summary of the step: 2 glyceraldehyde 3-phosphate + NAD+ + Inorganic phosphate –> 2 NADH + H+ + 2 1, 3-bisphosphosphoglycerate by glyceraldehyde 3-phosphate dehydrogenase
7. 2 1,3-BISPHOSPHOGLYCERATE –> 2 3-PHOSPHOGLYCERATE
This reaction is the first SUBSTRATE-LEVEL PHOSPHORYLATION. 1, 3-bisphosphoglycerate is converted to 3-phosphoglycerate by the enzyme, PHOSPHOGLYCERATE KINASE. Phosphoglycerate kinase transfers a high energy phosphate group from the C-1 atom of 1, 3-BPG to ADP and forms ATP. The energy released from the removal of the phosphate group is utilized to drive the formation of ATP. This reaction is also a reversible reaction.
Summary of the step: 2 1, 3-BPG + 2 ADP –> 2 3-phosphoglycerate + 2 ATP by phosphoglycerate kinase.
8. 2 3-PHOSPHOGLYCERATE –> 2 2-PHOSPHOGLYCERATE
2 molecules of 3 phosphoglycerate are converted to 2 molecules of 2 phosphoglycerate by the enzyme PHOSPHOGLYCERATE MUTASE. This involves the shift of the high energy phosphate group from the C-3 atom to the C-2 atom. This reaction is freely reversible as well and enables an isomerization reaction.
Summary of the step: 2 3-phosphoglycerate –> 2 2-phosphoglycerate by phosphoglycerate mutase
9. 2 2-PHOSPHOGLYCERATE –> PHOSPHOENOLPYRUVATE
The conversion of 2 phosphoglycerate to phosphoenolpyruvate is catalysed by ENOLASE. This is the hydrolysis of 2-phosphoglycerate to form a very high energy enol phosphate compound by removal of a water molecule. This reaction is however reversible even though phosphoenolpyruvate is a high energy compound.
Summary of the step: 2 2-phosphoglycerate –> 2 phosphoenolpyruvate + 2 molecules water by enolase
10. 2 PHOSPHOENOLPYRUVATE –> 2 PYRUVATE
This is the final step in the glycolytic pathway and also a regulated step. It is the final IRREVERSIBLE REACTION in the pathway and involves the 2nd SUBSTRATE-LEVEL PHOSPHORYLATION. 2 molecules of phosphoenolpyruvate are converted to 2 molecules of pyruvate by the enzyme, PYRUVATE KINASE. As in the other substrate-level phosphorylation, there is the transfer of a high energy phosphate group from phosphoenolpyruvate to ADP to produce ATP. This step allows for a net gain in ATP in the glycolytic pathway.
A bit about pyruvate kinase. Pyruvate kinase may be activated by fructose 1, 6-bisphosphate in a feed forward regulation. Therefore, activation of PFK-1 leads to the increase in fructose 1, 6-bisphosphate and this then leads to increased activation of pyruvate kinase leading to increased production of pyruvate and ATP. Hence, regulation of glycolysis occurs at this point. This feed forward regulation is observed in hepatocytes of the liver.
Another key aspect of pyruvate kinase involves RBC. In erythrocytes, there is the absence of mitochondria and therefore cannot undergo TCA Cycle or ETC like other cells of the human body. Therefore, erythrocytes depend heavily on glycolysis for energy generation in the form of ATP. ATP is utilized to fulfil all the metabolic requirements of rbcs including maintenance of its biconcave shape and flexibility in blood vessels. However, mutations to the structure of pyruvate kinase enzyme may occur leading to altered kinetics and function of the enzyme progressing to a deficiency of pyruvate kinase. This deficiency leads to decreased gain in ATP from glycolysis and hence will result in alterations to the metabolism of erythrocytes. This alteration to the metabolic activities of the red blood cells also causes alterations to the cell membrane and morphological features of the RBC. This results in sickling or loss of biconcavity and prone to be destroyed by phagocytes in the blood. The increased phagocytosis of RBC is referred to as haemolytic anaemia. Decreased RBC count means that there is decrease oxygen transportation in the blood and therefore affects the metabolism of other aerobic tissues of the body.
Pyruvate kinase deficiency is the 2nd most common cause of enzyme-related haemolytic anaemia and usually requires blood transfusions to rectify the loss of RBC. When RBC are lost, there is a compensation by the remaining RBC to increase the production of 2, 3-BPG. 2, 3-BPG binds to deoxyhaemoglobin molecules on RBC and decreases the affinity of haemoglobin for oxygen. This facilitates the increased release of oxygen from Haemoglobin into tissues.
Summary of the step: 2 phosphoenolpyruvate + 2 ADP –> 2 pyruvate + 2 ATP
At the end of the Energy Generation phase, 2 molecules of glyceraldehyde 3-phosphate was converted to two molecules of pyruvate. During this phase, 4 molecules of ATP were generated as well as 2 molecules of NADH. This involved 4 reversible reactions and one irreversible reaction. The irreversible reaction was catalysed by pyruvate kinase, which converted phosphoenolpyruvate to pyruvate via a substrate-level phosphorylation. This was the last reaction in the glycolytic pathway and was the last of the three regulated reactions of glycolysis. Another phosphorylation reaction was catalysed by phosphoglycerate kinase in the conversion of 1, 3-BPG to 3-phosphoglycerate. However, this reaction was reversible. Glyceraldehyde 3-phosphate dehydrogenase also performed the only oxidation reaction in glycolysis. As well as enolase catalysed the hydrolysis of 2-phosphoglycerate to phosphoenolpyruvate which resulted in the release of water molecule.
Glycolytic pathway resulted in the conversion of one glucose molecule into two pyruvate molecules. In this process, 2 molecules of NADH and 4 molecules of ATP are produced. However, two molecules of ATP were also consumed in the energy investment phase. Therefore, there was a net gain of 2 molecules of ATP.
Okay, then folks…. That was an obscene amount of information that I just threw at you. But this is just the surface and I hope that the explanation of each stage of the pathway, will aid in better conceptualizing and understanding of the functioning of this important pathway. I suggest that you take a read through and apply the mnemonics I created in the previous postings and then summarize the key points to note. Look out for subsequent postings on the feeder pathways as well as the fates of pyruvate.
Peace out peeps and happy studying.
Kumar, Vinay, Abul K. Abbas, Nelson Fausto and Richard N. Mitchell. 2007. Robbins Basic Pathology. 8th ed. Pennsylvania, PA: Saunders Elsevier.
Rhoades, Rodney A. and David R. Bell. 2009. Medical Physiology: Principles for Clinical Medicine. 3rd ed. Baltimore, MD: Wolters Kluwer.
Champe, Pamela C., 4th ed. 2008. Lippincott’s Illustrated Reviews: Biochemistry. Baltimore: Wolters Kluwer.
Marks, Allan D., Michael Lieberman and Colleen Smith. 2007. Marks’ Essentials of Medical Biochemistry: A Clinical Approach. 3rd ed. Baltimore, MD: Wolters Kluwer.