πŸ§ͺ Biochemistry · Metabolism

Metabolism tricks that make pathways click

Glycolysis, Krebs cycle, and oxidative phosphorylation β€” memorized.

πŸ”₯ Metabolism

Memory tricks

Proven mnemonics — fast to learn, hard to forget.

Krebs Cycle
Krebs cycle (per glucose): 2 acetyl-CoA β†’ 6 COβ‚‚, 2 ATP, 6 NADH, 2 FADHβ‚‚
Krebs Cycle
What one complete Krebs cycle produces per glucose
Runs twice per glucose (one turn per pyruvate). Carbon atoms leave as COβ‚‚. NADH and FADHβ‚‚ carry electrons to ETC where most ATP is made. Occurs in mitochondrial matrix.
Electron Transport Chain
ETC: electrons flow NADH β†’ Complex I β†’ CoQ β†’ III β†’ Cyt c β†’ IV β†’ Oβ‚‚. H⁺ pumped out β†’ ATP synthase.
Electron Transport Chain
The electron highway producing most of cellular ATP
Electrons from NADH and FADHβ‚‚ move through protein complexes. Energy pumps H⁺ into intermembrane space. H⁺ flows back through ATP synthase β†’ ~32 ATP. Oβ‚‚ is final electron acceptor β†’ becomes Hβ‚‚O.
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) β€” 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 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 β€” building and breaking down
Anabolism: synthesis reactions β€” build complex molecules from simple ones. Requires ATP. Protein synthesis, fatty acid synthesis, gluconeogenesis. Catabolism: degradation reactions β€” break complex molecules into simple ones. Releases ATP. Glycolysis, beta-oxidation, protein digestion. Metabolism = anabolism + catabolism.
Pyruvate Oxidation
Pyruvate dehydrogenase complex: pyruvate β†’ acetyl-CoA + COβ‚‚ + NADH. Bridge between glycolysis and Krebs.
Pyruvate Oxidation
The link between glycolysis and the Krebs cycle
Pyruvate (3 carbons) enters mitochondria β†’ pyruvate dehydrogenase complex removes one carbon as COβ‚‚ β†’ acetyl-CoA (2 carbons) + NADH. This step is irreversible β€” acetyl-CoA cannot be converted back to glucose (unlike pyruvate). Why alcohol can't be converted to glucose: ethanol β†’ acetaldehyde β†’ 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 β€” 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 RBCs from oxidative damage) and ribose-5-phosphate (nucleotide synthesis). G6PD deficiency: can't make NADPH β†’ RBCs vulnerable to oxidative stress β†’ 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 β€” 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).
Levels of Metabolic Regulation
Metabolic regulation: allosteric control (fast), covalent modification (phosphorylation/dephosphorylation), gene expression (slow)
Levels of Metabolic Regulation
Three ways cells control metabolic flux at different speeds
Allosteric: immediate β€” effector molecules change enzyme shape. ATP inhibits many catabolic enzymes (enough energy). AMP activates them (need more energy). Covalent modification: phosphorylation (usually activates or inhibits), minutes. Gene expression: changes enzyme amounts over hours to days.
Allosteric
Immediate β€” feedback molecules
Covalent modification
Minutes β€” phosphorylation
Gene expression
Hours/days β€” change enzyme amounts
Insulin and Glucagon
Insulin lowers blood glucose: promotes glucose uptake, glycolysis, glycogen synthesis, fat storage. Glucagon raises it: promotes gluconeogenesis, glycogenolysis.
Insulin and Glucagon
The two opposing hormones that regulate blood glucose
Fed state (glucose high): insulin released from beta cells. Promotes: GLUT4 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 β€” store glucose, build glycogen
Glucagon
Fasting β€” release glucose, gluconeogenesis