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The Interactive Metabolic Map

Chapter 13: The Interactive Metabolic Map

9 min read Updated Aug 2, 2026

Metabolism is the part of MCAT biochemistry that punishes memorizing pathways one at a time. The exam rarely asks you to recite the ten steps of glycolysis. It asks what happens to fat when oxaloacetate runs low, or why a liver enzyme defect raises blood lactate, or which molecule connects a pathway you know well to one you have not thought about since you learned it. Those questions are about the joins between pathways, and the joins are exactly what you lose when each pathway lives on its own page.

This chapter is one map instead of twenty. Every pathway in the metabolism chapters is drawn on a single canvas, positioned where it belongs relative to everything else: digestion across the top where fuel enters, storage and outlets on the left, NADPH and lipids on the right, and the carbon trunk running straight down the middle through pyruvate, acetyl-CoA, the TCA cycle, and the electron transport chain.

Opening a pathway moves the view rather than replacing it. Click β-oxidation and you travel to β-oxidation, which is drawn out past the right edge of the master map, next to the fatty acids it burns. You arrive knowing which direction you came from. That is the point: the spatial memory you build is the same structure the exam tests.

The whole of metabolism, one chart

Interactive chart

The whole of metabolism

Cytosol Mitochondrion · intermembrane space Mitochondrion · matrix Lactose metabolism Glycogen Fructose metabolism Pentose phosphate pathway Ketone bodies GlycolysisGluconeogenesisAnaerobic fermentationFatty acid synthesisFatty acid transportβ-oxidationKrebs cycleOxidative phosphorylation Aconitase Citrate Isocitrate dehydrogenase NADH · CO₂ Isocitrate α-KG dehydrogenase NADH · CO₂ α-Ketoglutarate Succinyl-CoA synthetase GTP Succinyl-CoA Succinate dehydrogenase FADH₂ Succinate Fumarase Fumarate Malate dehydrogenase NADH Malate Citrate synthase Oxaloacetate turns twice per glucose 3 NADH · 1 FADH₂ · 1 GTP · 2 CO₂ per turn Complex I NADH-CoQ reductase 4 H⁺ NADH → NAD⁺ + H⁺ Fe-S centres · FMN Complex II succinate-CoQ FADH₂ → FAD Fe-S centres · no pumping Complex III CoQH₂-cyt c 4 H⁺ CoQH₂ → CoQ cytochromes b and c₁ · Fe-S Complex IV cytochrome c oxidase 2 H⁺ O₂ + 4 H⁺ → 2 H₂O cytochromes a and a₃ · Cu CoQ lipid-soluble, moves in the membrane Cyt c water-soluble, on the outer face Oxygen is the only thing at the end of this chain. Without it nothing above can hand off its electrons, so every pathway on the chart stalls. ATP synthase about 30-32 ATP per glucose H⁺ back in ATP ADP ATP ADP NAD⁺ NADH ADP ATP ADP ATP NADP⁺ NADPH NADP⁺ NADPH NADH NAD⁺ GTP GDP ATP ADP NADPH NADP⁺ NAD⁺ NADH FAD FADH₂ NAD⁺ NADH CO₂ CO₂ H₂O H₂O CoA-SH Glucose Glucose-6-phosphate Fructose-6-phosphate Fructose-1,6-bisphosphate Dihydroxyacetone phosphate Glyceraldehyde-3-phosphate 1,3-Bisphosphoglycerate 2,3-BPG 3-Phosphoglycerate 2-Phosphoglycerate Phosphoenolpyruvate Pyruvate Lactate Alanine Oxaloacetate Malate Glycerol-3-phosphate Glucose-1-phosphate UDP-glucose Glycogen Lactose Galactose Glucose Galactose-1-P 6-Phosphogluconate Ribulose-5-phosphate Ribose-5-phosphate Nucleotide synthesis F6P + G3P, back to glycolysis Fructose-2,6-bisphosphate Sucrose Fructose Glucose Fructose-1-phosphate DHAP Glyceraldehyde Malate Oxaloacetate Citrate Acetyl-CoA Malonyl-CoA Palmitate Fatty acid Fatty acyl-CoA Acyl-carnitine Pyruvate Acetyl-CoA Oxaloacetate Acyl-carnitine Fatty acyl-CoA trans-Δ²-Enoyl-CoA L-3-Hydroxyacyl-CoA 3-Ketoacyl-CoA Acetoacetyl-CoA HMG-CoA Acetoacetate β-hydroxybutyrate Hexokinase glucokinase in liver ⊖ glucose-6-P Phosphoglucose isomerase PFK-1 committed, rate-limiting ⊖ ATP, citrate ⊕ AMP, fructose-2,6-bisP Aldolase Glyceraldehyde-3-P dehydrogenase Phosphoglycerate kinase Phosphoglycerate mutase Enolase Pyruvate kinase ⊖ ATP, alanine ⊕ fructose-1,6-bisP Triose phosphate isomerase Lactate dehydrogenase Alanine aminotransferase PEP carboxykinase ⊕ glucagon, cortisol Pyruvate carboxylase in the matrix · needs CO₂, ATP and biotin ⊕ acetyl-CoA Glycerol-3-P dehydrogenase Fructose-1,6-bisphosphatase ⊖ AMP, fructose-2,6-bisP Glucose-6-phosphatase liver and kidney only Phosphoglucomutase UDP-glucose pyrophosphorylase synthesis direction only Glycogen synthase ⊕ insulin Glycogen phosphorylase straight to glucose-1-P, not back through UDP ⊕ glucagon, epinephrine Lactase Galactokinase costs one ATP GALT and epimerase Glucose-6-P dehydrogenase rate-limiting ⊖ NADPH ⊕ insulin, NADP⁺ Isomerase Transketolase and transaldolase Red blood cells only 2,3-BPG lowers haemoglobin’s oxygen affinity PFK-2 ⊖ glucagon ⊕ insulin Sucrase Fructokinase Aldolase B ATP-citrate lyase Acetyl-CoA carboxylase committed, needs biotin ⊖ glucagon ⊕ insulin, citrate Fatty acid synthase uses NADPH, not NADH Acyl-CoA synthetase costs 2 ATP equivalents Carnitine acyltransferase I rate-limiting for burning fat ⊖ malonyl-CoA Carnitine acyltransferase II Acyl-CoA dehydrogenase FAD, not NAD⁺ Enoyl-CoA hydratase 3-Hydroxyacyl-CoA dehydrogenase β-Ketothiolase cuts the last two carbons off as acetyl-CoA Pyruvate dehydrogenase irreversible: fat can never become glucose ⊖ acetyl-CoA, NADH, ATP ⊕ ADP, NAD⁺, Ca²⁺ HMG-CoA synthase and lyase the same four steps, over and over each turn leaves the chain two carbons shorter pyruvate carrier citrate shuttle carnitine transporter malate-aspartate shuttle

Tap a pathway to travel to it, drag to look around, double-click or use + and − to zoom. For the whole chart at readable size, open it fullscreen.

The whole chart

The whole of metabolism

One continuous chart. Pick a pathway to travel to it; the drawing never changes, only where you are looking.

Pathways

Junction metabolites

How to use it

Start at the whole map and read it top to bottom. That direction is catabolism: fuels come in at the top, carbon funnels down through the junction metabolites, and the electron carriers cash out at the bottom. Read it bottom to top and you are reading anabolism, which is why gluconeogenesis is drawn as a climb back up the same trunk rather than as a separate picture.

When a block on the master map is one you want to see properly, click it. You will land on the full pathway, drawn in the same visual language: the same navy pills for junction metabolites, the same colour for ATP, NADH, and FADH2, the same red for a step that cannot run backwards. Nothing has to be relearned when you move between pathways.

The list underneath the map reaches every pathway directly, including the ones that have no block of their own on the master map: cholesterol synthesis, the fed and fasted states, the fuel hormones, and the bioenergetics that sit underneath all of it. Under each pathway you will also find two or three connected pathways, which is the fastest way to study a join: open β-oxidation, then jump straight to ketone bodies and see why one turns into the other when fasting goes on long enough.

Four regions exist mainly to answer questions the individual pathway chapters leave open. Digestion and absorption sits above the map because it is where the three fuels actually come from, and it is the only place the chylomicron route is visible next to the portal vein route. Fructose and galactose shows why the two dietary sugars that are not glucose behave so differently, since one joins the trunk above PFK-1 and the other joins below it. The fuel hormones is a grid rather than a pathway, because the exam question is almost always “this hormone rises, what happens to that process?”. Oxidative stress hangs off the electron transport chain and closes the loop back to the pentose phosphate pathway, which is the only reason a pathway that makes no ATP is essential.

The four molecules that hold it together

Four metabolites appear as navy pills because they are where pathways meet. If you know what arrives at each one and what leaves it, you can rebuild most of the map without having memorized it.

Glucose-6-phosphate is the first fork. Glucose is phosphorylated the moment it enters a cell, which traps it inside, and from there it can be stored as glycogen, burned through glycolysis, or diverted into the pentose phosphate pathway for NADPH and ribose-5-phosphate. Only liver and kidney carry glucose-6-phosphatase, so only those two organs can reverse the trap and release free glucose back into the blood. That single enzyme is why muscle glycogen cannot raise your blood sugar.

Pyruvate is the last fork in the cytosol, and which branch it takes is a question about oxygen and tissue. With oxygen it crosses into the mitochondrion. Without oxygen it becomes lactate, which regenerates the NAD+ that glycolysis needs to keep running. In muscle it can be transaminated to alanine and shipped to the liver. In the fasting liver it is carboxylated to oxaloacetate to begin the climb back to glucose.

Acetyl-CoA is the great convergence. Carbohydrate, fat, and the ketogenic amino acids all arrive here, which is what makes it the busiest molecule on the map. It burns in the TCA cycle, leaves the mitochondrion as citrate to build fatty acids and cholesterol, or condenses into ketone bodies. What it can never do is become glucose, because pyruvate dehydrogenase runs one way only. Every exam question about why fat cannot be turned into sugar is this one fact wearing a costume.

Oxaloacetate is the gatekeeper. Acetyl-CoA cannot enter the TCA cycle without it, so anything that drains oxaloacetate stalls the cycle. During a long fast the liver pulls oxaloacetate away for gluconeogenesis, acetyl-CoA from fat backs up with nowhere to go, and the overflow is condensed into ketone bodies. That is the whole mechanism behind fasting ketosis, and it is visible on the map as two arrows competing for the same molecule.

What the map is good for

Use it when you are studying a pathway, not instead of studying one. Open the pathway you are working on, learn it properly from the chapter, then come back to the whole map and find it in place. The pathway sticks better when it has neighbours.

It is also the fastest way to answer the question the exam actually likes, which is some version of “this pathway is blocked, now what?” Block pyruvate dehydrogenase and pyruvate has nowhere to go except lactate, so blood lactate climbs. Block the carnitine shuttle and long-chain fatty acids never reach the matrix, so the cell falls back on glucose and runs out early. On a single map these are one step of tracing rather than a memory test.

Finally, use it in the last week before the exam. Being able to redraw the trunk from glucose to the electron transport chain, hang the four junction metabolites on it, and say what enters and leaves each one is a better use of an hour than rereading any individual pathway.

Where each pathway is covered in full

The map is a way of seeing the connections. The reasoning, the regulation, and the exam traps for each pathway live in the chapters:

Four things the chart cannot show

A pathway chart maps molecules onto molecules. Four topics the exam tests are not shaped like that, so they get their own figures here rather than being forced onto the map.

Where the fuel comes from. The chart begins at glucose, fatty acids, and amino acids. Getting there is digestion, and the exam asks about it: which enzyme cuts what, where, and which route each fuel takes into the body. Fat is the odd one out, leaving in chylomicrons through the lymph while everything else goes to the liver by the portal vein.

From food to fuel: digestion and absorption

Pathway map
What you eat Cut up by, and where Crosses the wall as Travels by Starch, sucrose and lactose salivary amylase mouth pancreatic amylase small intestine · leaves short chains brush border: maltase, sucrase, lactase, isomaltase lactase is the one people lose Glucose · galactose SGLT1, pulled in with Na⁺ Fructose GLUT5, no energy needed. All leave on GLUT2 Portal vein liver first Triacylglycerol bile salts emulsify it made in liver, stored in gallbladder pancreatic lipase + colipase cuts positions 1 and 3 emulsifying first is what gives the enzyme enough surface to work on 2-monoacylglycerol Free fatty acids ferried to the cell in micelles, then rebuilt inside the enterocyte Lymph Chylomicron skips the liver Protein pepsin stomach, needs the acid trypsin · chymotrypsin · carboxypeptidase pancreas, released as inactive zymogens aminopeptidase brush border Amino acids and short di- and tripeptides Portal vein Ethanol: a fourth fuel, and the NADH it leaves behind Ethanol Acetaldehyde Acetate Acetyl-CoA alcohol dehydrogenase aldehyde dehydrogenase NADH NADH All that NADH pushes pyruvate to lactate and oxaloacetate to malate, so gluconeogenesis stalls and fat accumulates: hypoglycemia and fatty liver. In yeast the anaerobic route runs the other way: pyruvate becomes acetaldehyde and then ethanol. Human muscle makes lactate instead, but the purpose is the same, to regenerate NAD⁺ so glycolysis can keep running. Glucose, fatty acids, and amino acids are the three doors into the master map. Everything above is how food gets through them.
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Fuel that reaches the master map Lumen and enterocyte Rate-setting or clinically tested step Intermediate

Only fat skips the liver firstSugars and amino acids go straight into the portal vein, so the liver sees them before anyone else and can buffer the load. Dietary fat leaves in chylomicrons through the lymphatics and enters the bloodstream at the thoracic duct, which means muscle and adipose get first refusal on it. That is why a fatty meal raises plasma triglyceride for hours while a sugary one is cleared much faster.

The two lipases students confusePancreatic lipase works in the gut lumen on food you have just eaten. Lipoprotein lipase sits on the capillary wall of muscle and adipose and unloads triglyceride out of circulating chylomicrons and VLDL. Hormone-sensitive lipase is different again: it is inside the fat cell and releases stored fat during fasting, which is the arrow that feeds β-oxidation.

Lactose intolerance in one lineLactase is a brush border enzyme and the first one to be lost with age. Undigested lactose stays in the lumen, pulls in water osmotically, and is fermented by colonic bacteria into gas and short-chain acids. Nothing is wrong with absorption itself, which is why the symptoms are bloating and diarrhea rather than malnutrition.

Three fuels, three routes, one destination. Carbohydrate and protein are broken to their monomers and go to the liver by the portal vein. Fat is emulsified, cut, ferried in micelles, rebuilt inside the enterocyte, and shipped out in chylomicrons through the lymph. Everything here arrives at the top of the master map as glucose, fatty acids, or amino acids.

The two dietary sugars that are not glucose. The chart shows where fructose and galactose join the trunk. This shows what happens when the enzymes are missing, which is where the named diseases live.

Fructose and galactose: the side doors into glycolysis

Pathway map
Galactose · joins early Fructose · joins late Lactose lactase brush border Galactose galactokinase missing: cataracts ! Galactose-1-P GALT missing: galactosemia ! UDP-galactose epimerase UDP-glucose or straight to glycogen Glucose-1-P joins at glucose-6-phosphate Sucrose sucrase brush border Fructose fructokinase missing: harmless ! Fructose-1-P aldolase B missing: intolerance ! DHAP Glyceraldehyde triose kinase G3P both are triose phosphates joins after PFK-1, past the gate Where each one joins the glycolysis trunk Glucose Glucose-6-P Fructose-6-P F-1,6-BP DHAP + G3P ! PFK-1 galactose queues at the regulated step fructose is already past it A large fructose load therefore reaches pyruvate, acetyl-CoA, and fatty acid synthesis without ever waiting for PFK-1 to allow it.
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Junction metabolite Step that causes disease when missing Cytosol of the liver cell Intermediate

Why fructose is not just another sugarGalactose joins the trunk at glucose-6-phosphate, upstream of PFK-1, so it is subject to the same brake as glucose. Fructose in the liver joins as DHAP and glyceraldehyde-3-phosphate, downstream of PFK-1, so it pours in past the gate. That is why a large fructose load feeds straight into pyruvate, acetyl-CoA, and fatty acid synthesis without waiting for permission.

The enzyme deficienciesEssential fructosuria (fructokinase) is harmless: fructose simply appears in urine. Hereditary fructose intolerance (aldolase B) is not: fructose-1-phosphate piles up and traps the cell's phosphate, which stalls glycogenolysis and gluconeogenesis and causes hypoglycemia after fruit or sucrose. The same pattern holds for galactose: galactokinase deficiency gives cataracts from galactitol, while GALT deficiency is classic galactosemia, which is severe.

Where the cataracts come fromWhen galactose backs up, aldose reductase converts it to galactitol, which cannot leave the lens and pulls in water osmotically. The same enzyme makes sorbitol from glucose, which is the mechanism behind diabetic cataracts and neuropathy.

Two side doors into glycolysis. Galactose enters above PFK-1 and is regulated like glucose. Liver fructose enters below PFK-1 and is not, which is why fructose is handled so much faster and pushes so readily toward fat. Every enzyme marked in red causes a named disease when it is missing.

Who gives the orders. Every arrow on the chart can run in one direction or the other depending on hormonal state. This is a grid rather than a pathway, because the exam question is almost always “this hormone rises, what happens to that process?”.

Who gives the orders: the fuel hormones

Regulation map
The hormone where it comes from and what triggers it Insulin β cells, pancreas when blood glucose high Glucagon α cells, pancreas when blood glucose low Epinephrine adrenal medulla when stress, exercise Cortisol adrenal cortex when long stress, fasting Glycogen synthesis ↑↓↓↑ Glycogen breakdown ↓↑↑· Gluconeogenesis ↓↑↑↑ Glycolysis in the liver ↑↓·↓ Fatty acid synthesis ↑↓↓· Fat release from adipose ↓↑↑↑ Ketone body production ↓↑↑↑ Muscle protein breakdown ↓··↑ GLUT4 at the membrane ↑··↓ ↑ increases the process · ↓ decreases it · a dot means no important direct effect And the one rule that makes the grid stick TAKES THE PHOSPHATES OFF Insulin, via a receptor tyrosine kinase and GLUT4 vesicles fuse with the membrane PUT THE PHOSPHATES ON Glucagon and epinephrine: GPCR → cAMP → PKA synthase off, phosphorylase on, in seconds MAKES MORE ENZYME Cortisol: steroid → nuclear receptor → DNA hours, not seconds, and it lasts Whether you eat at all is a separate pair of signals Leptin comes from adipose in proportion to fat mass and tells the hypothalamus to stop eating; obesity is usually resistance to it, not a shortage. Ghrelin comes from the stomach, rises before a meal, and says eat now.
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Hormone increases this process Hormone decreases it Little direct effect The enzyme each one acts through

Phosphorylated or notGlucagon and epinephrine both work through cAMP and PKA, so both end up phosphorylating the same enzymes. Insulin activates phosphatases, so it strips those phosphates off. This is why one rule covers most of metabolism: phosphorylation switches glycogen synthase off and glycogen phosphorylase on, and dephosphorylation does the reverse. Learn the rule once and you no longer have to memorize each enzyme.

Why cortisol looks slowCortisol is a steroid, so it crosses the membrane, binds a nuclear receptor, and changes transcription. Its effects take hours and work by changing how much enzyme exists rather than how active it is. That is why cortisol dominates prolonged fasting and chronic stress while epinephrine dominates the first minute of a sprint.

Epinephrine is tissue-specificIn the liver it drives glycogenolysis and the glucose leaves the cell, because the liver has glucose-6-phosphatase. In muscle the same signal drives glycogenolysis but the glucose-6-phosphate is trapped, so it can only be burned locally. Muscle glycogen never raises anyone else's blood sugar.

Four hormones, one grid. Insulin is the only one that says store; the other three all say release, for different reasons and on different timescales. Read a column to learn one hormone, read a row to answer the usual exam question, which is what happens to a single process when the hormonal state changes.

The cost of using oxygen. A small share of the electrons in the transport chain escape early and make superoxide. This closes the loop back to the pentose phosphate pathway, whose NADPH is the only way to reset glutathione.

Oxidative stress: the cost of breathing

Pathway map
Inner mitochondrial membrane Complexes I and III leak about 1 to 2 percent of their electrons straight onto O₂ instead of passing them along the chain. Complex I Complex II Complex III Complex IV ATP synthase Superoxide O₂•⁻ superoxide dismutase Mn in matrix · Cu-Zn in cytosol H₂O₂ catalase in the peroxisome H₂O + O₂ glutathione peroxidase spends two reduced glutathione 2 H₂O 2 GSH GSSG glutathione reductase needs NADPH FROM THE PENTOSE PHOSPHATE PATHWAY the only way to reset glutathione Fe²⁺ · Fenton Hydroxyl radical •OH Nothing defuses this one. It reacts with whatever it touches first: lipid peroxidation in membranes strand breaks in DNA carbonyl damage to proteins Mitochondrial DNA sits closest to the leak and has no histones, so it takes the worst of it. When the damage wins, the mitochondrion starts the cell's own demolition Damaged mitochondrion Cytochrome c out Apoptosome Caspase 3 Apoptosis plus caspase 9 BCL-2 holds the membrane shut BAX opens it. Too much BCL-2 and the cell refuses to die, which is how it acts as an oncogene. G6PD deficiency. A red cell has no mitochondria and no nucleus, so the pentose phosphate pathway is its only NADPH source. Without it glutathione cannot be reset, so fava beans, sulfa drugs, or an infection denature hemoglobin into Heinz bodies: bite cells and hemolysis.
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Inner mitochondrial membrane Damaging species The enzymes that defuse it NADPH, from the pentose phosphate pathway

Why the pentose phosphate pathway matters hereGlutathione is the cell's reusable antioxidant, but it only works in its reduced form. Glutathione reductase resets it and the reducing power comes from NADPH, which for most cells means the pentose phosphate pathway. That is the whole reason a pathway that makes no ATP is still essential.

G6PD deficiency in one lineA red blood cell has no mitochondria and no nucleus, so the pentose phosphate pathway is its only source of NADPH. Lose glucose-6-phosphate dehydrogenase and glutathione cannot be reset, so an oxidative challenge (fava beans, sulfa drugs, infection) denatures hemoglobin into Heinz bodies, and the spleen bites them out, leaving bite cells and hemolysis.

The same organelle kills the cellCytochrome c is a normal carrier between complexes III and IV. If the mitochondrion is damaged badly enough it leaks into the cytosol, where it assembles the apoptosome and activates caspase 9 and then caspase 3. BCL-2 holds the membrane shut and BAX opens it, which is why BCL-2 behaves as an oncogene when overexpressed: the cell simply refuses to die.

Oxygen is a superb electron acceptor and a dangerous one. A small fraction of electrons escape complexes I and III early and make superoxide. Everything on the top row exists to defuse that, everything on the left is what happens when it is not defused, and the bottom row is the cell's decision to give up.
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