Glycolysis: 1 glucose → 2 pyruvate, net 2 ATP, 2 NADH. In cytoplasm. No oxygen.
Glycolysis
Ten steps of glycolysis — inputs and outputs
Invest 2 ATP early, gain 4 → net 2 ATP. Also produces 2 NADH. Occurs in cytoplasm, no oxygen needed. With oxygen → pyruvate enters mitochondria. Without → fermentation.
What one complete Krebs cycle produces per glucose
Runs twice per glucose (one turn per pyruvate). Carbon atoms leave as CO₂. NADH and FADH₂ carry electrons to the Electron Transport Chain (ETC) where most ATP is made. Occurs in mitochondrial matrix.
Electron Transport Chain
ETC: electrons flow NADH → Complex I → CoQ → III → Cyt c → IV → O₂. H⁺ pumped out → ATP synthase.
Electron Transport Chain
The electron highway producing most of cellular ATP
Electrons from NADH and FADH₂ move through protein complexes. Energy pumps H⁺ into intermembrane space. H⁺ flows back through ATP synthase → ~32 ATP. O₂ is final electron acceptor → becomes H₂O.
ATP Yield
Total ATP per glucose: ~36-38 (2 glycolysis + 2 Krebs + ~32-34 ETC)
ATP Yield
The total energy harvest from complete glucose oxidation
Glycolysis: 2 net ATP. Krebs: 2 ATP. ETC: ~32-34 ATP. Total theoretical maximum: ~36-38 ATP per glucose. Actual yield slightly lower due to membrane proton leakage.
Gluconeogenesis
Gluconeogenesis: makes glucose from non-carbohydrate sources (amino acids, lactate, glycerol) — liver
Gluconeogenesis
The liver makes new glucose when blood sugar is low
Occurs in fasting, starvation, and prolonged exercise. Substrates: amino acids (from muscle breakdown), lactate (from red blood cells (RBCs) and anaerobic muscle), glycerol (from fat breakdown). Mostly in liver, some in kidney.
Anabolism vs Catabolism
Anabolism: building molecules (requires energy). Catabolism: breaking molecules (releases energy).
Anabolism vs Catabolism
Two directions of metabolism — building and breaking down
Anabolism: synthesis reactions — build complex molecules from simple ones. Requires ATP. Protein synthesis, fatty acid synthesis, gluconeogenesis. Catabolism: degradation reactions — break complex molecules into simple ones. Releases ATP. Glycolysis, beta-oxidation, protein digestion. Metabolism = anabolism + catabolism.
Pyruvate Oxidation
Pyruvate dehydrogenase complex: pyruvate → acetyl-CoA + CO₂ + NADH. Bridge between glycolysis and Krebs.
Pyruvate Oxidation
The link between glycolysis and the Krebs cycle
Pyruvate (3 carbons) enters mitochondria → pyruvate dehydrogenase complex removes one carbon as CO₂ → acetyl-CoA (2 carbons) + NADH. This step is irreversible — acetyl-CoA cannot be converted back to glucose (unlike pyruvate). Why alcohol can't be converted to glucose: ethanol → acetaldehyde → acetyl-CoA (irreversible).
Fatty Acid Synthesis vs Oxidation
Fatty acid synthesis: in cytoplasm. Beta-oxidation: in mitochondria. Opposite processes, opposite compartments.
Fatty Acid Synthesis vs Oxidation
Two opposing pathways in different cellular compartments
Beta-oxidation (catabolism): mitochondria, uses FAD and NAD⁺, produces acetyl-CoA and NADH. Fatty acid synthesis (anabolism): cytoplasm, uses NADPH, uses malonyl-CoA building blocks, requires biotin. They cannot run simultaneously — when one is active, the other is inhibited. Malonyl-CoA inhibits carnitine shuttle (blocks beta-oxidation).
Pentose Phosphate Pathway
Pentose phosphate pathway: produces NADPH (for biosynthesis and antioxidant) and ribose-5-phosphate (for nucleotides)
Pentose Phosphate Pathway
An alternative glucose pathway producing NADPH and nucleotide precursors
Runs parallel to glycolysis. Two products: NADPH (reduced glutathione, fatty acid synthesis, keeps red blood cells (RBCs) from oxidative damage) and ribose-5-phosphate (nucleotide synthesis). G6PD deficiency: can't make NADPH → RBCs vulnerable to oxidative stress → hemolytic anemia triggered by certain foods (fava beans) and drugs.
Glycogen Metabolism
Glycogen synthesis: in liver (blood glucose buffer) and muscle (local energy). Glycogen phosphorylase breaks it down.
Glycogen Metabolism
How the body stores and mobilizes glucose
Glycogen: branched polymer of glucose — rapid glucose storage. Liver glycogen: maintains blood glucose levels during fasting. Muscle glycogen: fuel for muscle contraction only. Glycogen synthase: builds glycogen. Glycogen phosphorylase: breaks it down, regulated by glucagon (liver), epinephrine (muscle and liver).
The two opposing hormones that regulate blood glucose
Fed state (glucose high): insulin released from beta cells. Promotes: GLUT4 (glucose transporter type 4) insertion (glucose uptake in muscle/fat), glycolysis, glycogen synthesis, fatty acid synthesis. Inhibits gluconeogenesis. Fasting (glucose low): glucagon released from alpha cells. Promotes glycogenolysis and gluconeogenesis in liver.
Insulin
Fed state — store glucose, build glycogen
Glucagon
Fasting — release glucose, gluconeogenesis
Mnemonic
What it means
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🎓 Common Exam Questions
Q: Walk through glycolysis — key steps, products, and regulation.
A: Glycolysis (cytoplasm, 10 steps): converts 1 glucose (6C) to 2 pyruvate (3C). Investment phase (steps 1-5): uses 2 ATP to phosphorylate glucose and fructose-6-phosphate; splits into 2 triose phosphates. Payoff phase (steps 6-10): generates 4 ATP and 2 NADH. Net: 2 ATP, 2 NADH, 2 pyruvate. Key regulated enzymes: hexokinase (step 1, inhibited by glucose-6-phosphate), phosphofructokinase-1/PFK-1 (step 3, rate-limiting — inhibited by ATP and citrate, activated by AMP; the main control point), pyruvate kinase (step 10, inhibited by ATP and alanine). Under anaerobic conditions, pyruvate → lactate (regenerates NAD+ for continued glycolysis).
Q: Describe the Krebs cycle and explain why it is central to metabolism.
A: The Krebs (citric acid) cycle occurs in the mitochondrial matrix. Per turn (per acetyl-CoA): 1 acetyl-CoA (2C) + oxaloacetate (4C) → citrate (6C) → 2 CO2 released; generates 1 ATP, 3 NADH, 1 FADH2; regenerates oxaloacetate. Per glucose (2 turns): 2 ATP, 6 NADH, 2 FADH2, 6 CO2. Centrality: it is amphibolic — both catabolic (oxidizes acetyl-CoA from carbs, fats, amino acids) and anabolic (intermediates are precursors for amino acids, nucleotides, heme, glucose). Regulated by: substrate availability, NADH/NAD+ ratio, ATP/ADP ratio. Isocitrate dehydrogenase and alpha-ketoglutarate dehydrogenase are key regulated steps.
Q: How does the electron transport chain generate ATP?
A: The ETC (inner mitochondrial membrane) uses NADH and FADH2 (from glycolysis, pyruvate oxidation, Krebs) as electron donors. Electrons flow: NADH → Complex I → CoQ → Complex III → Cytochrome c → Complex IV → O2 (forming water). FADH2 → Complex II → CoQ. Complexes I, III, and IV pump H+ from matrix to intermembrane space, creating the proton gradient (chemiosmosis). H+ flows back through ATP synthase (Complex V) — the rotary motor — driving ATP synthesis. Each NADH yields ~2.5 ATP; each FADH2 yields ~1.5 ATP. O2 is the terminal electron acceptor — absence causes ETC shutdown (anaerobic conditions).
Q: What is gluconeogenesis and when does it occur?
A: Gluconeogenesis synthesizes glucose from non-carbohydrate precursors — primarily in the liver (and kidney during prolonged fasting). Substrates: lactate (from muscle and RBCs via Cori cycle), alanine and other glucogenic amino acids (from muscle protein breakdown), glycerol (from fat breakdown). It is essentially the reverse of glycolysis except at three irreversible steps, which require distinct bypass enzymes: pyruvate carboxylase + PEPCK (bypass pyruvate kinase), fructose-1,6-bisphosphatase (bypass PFK-1), glucose-6-phosphatase (liver only — allows glucose export). Activated by: glucagon, cortisol, fasting. Inhibited by: insulin, high glucose. Essential for maintaining blood glucose during fasting, exercise, and starvation.
Q: How do insulin and glucagon oppositely regulate blood glucose?
A: Insulin (beta cells, released when blood glucose rises): promotes glucose uptake (GLUT4 translocation in muscle/fat), glycolysis, glycogen synthesis (glycogen synthase activation), fatty acid synthesis, and protein synthesis. Inhibits gluconeogenesis and glycogenolysis. Net effect: lowers blood glucose, promotes anabolic state. Glucagon (alpha cells, released when blood glucose falls): promotes glycogenolysis (glycogen phosphorylase activation), gluconeogenesis, and fatty acid oxidation. Inhibits glycogen synthesis and glycolysis. Net effect: raises blood glucose, promotes catabolic state. Both work via second messengers — insulin activates PI3K/Akt; glucagon activates adenylate cyclase/cAMP/PKA. In Type 1 diabetes: no insulin → uncontrolled glucagon effects → hyperglycemia and ketoacidosis.