Master the pathways that power your cells — and what happens when they go wrong
Catabolic = breaking down for energy = starvation state
Sympathetic nervous system controls catabolic pathways. Enzymes work hardest when PHOSPHORYLATED.
Starvation signals these hormones to wake up:
These hormones activate adenylyl cyclase → cAMP increases → Phosphorylates catabolic enzymes to turn them ON.
Mitochondria is catabolic HQ (TCA, oxidative phosphorylation, β-oxidation). Exception: Glycolysis happens in cytoplasm.
GLUCOSE
40% of diet
4 kcal/g
FATS
30% of diet
9 kcal/g
PROTEINS
30% of diet
4 kcal/g
KETONES
Last resort
> 36 hours starvation
Click a stress level to see what changes:
| Organ | Normal: Preferred Fuel | Why This Matters (Board Alert!) |
|---|---|---|
| Brain | Glucose | Hypoglycemia destroys the brain first. Seizures, coma, death. |
| Heart | FFAs (60% of ATP) | In stress, heart DEMANDS glucose. Explains why acute MI + cardiogenic shock = give dextrose IV. |
| Muscles | Glucose + FFAs | During long fasts, muscles break down → FFAs, but also catabolized for gluconeogenesis (loss of mass). |
| RBCs | ALWAYS Glucose | RBCs have NO mitochondria. Only pathway = glycolysis (+ pentose phosphate for NADPH). Hypoglycemia → hemolytic anemia in 36h. |
When glucose runs out, your body runs this playbook:
Plasma Glucose: 2–4 hours
Fed state → normal blood glucose
Liver Glycogen: 24–28 hours
Glycogenolysis maxed out, then depleted
Lipolysis: > 36 hours
Break down fat → FFAs → gluconeogenesis, ketogenesis
Ketogenesis: > 36 hours
Brain shifts to ketones, muscle finally spares glucose
RBCs only eat glucose via glycolysis. They have NO mitochondria → can't use FFAs, ketones, amino acids.
RBCs need NADPH to protect themselves from oxidative damage. Only source: pentose phosphate pathway (happens in cytoplasm, requires glucose as substrate).
Severe hypoglycemia (< 36h starvation) → RBCs lose NADPH protection → oxidative stress → hemolytic anemia. This is why treating hypoglycemia ASAP is life-saving.
Click each step to reveal the enzyme, substrate, product, and ATP cost/gain.
ATP Counter
4 ATP created − 2 ATP invested = +2 ATP net
⚠️ Also produces 2 NADH per glucose (crucial for energy in the electron transport chain).
Every NADH contains Niacin (Vitamin B3). Glycolysis makes 2 NADH per glucose.
Niacin deficiency → Pellagra → The 4 Ds:
Defective renal transport of tryptophan (can't reabsorb from urine) → tryptophan not available to make niacin → presents like pellagra.
A branch off glycolysis (at G1,3DP) makes an RBC secret weapon:
2,3-DPG binds hemoglobin → lowers its O₂ affinity → hemoglobin more likely to DROP oxygen in tissues → tissues get MORE oxygen when they need it most.
Stored blood loses its 2,3-DPG over time → hemoglobin grips O₂ too tightly → tissues get less O₂ → why transfusions can paradoxically worsen hypoxia if you give old blood.
Additive inosine to stored blood → helps RBCs regenerate 2,3-DPG → shelf life extends from 21 days → 45 days.
Making glucose from non-glucose sources during starvation. Only liver (90%) and adrenal cortex (10%) can do this.
Triggered by epinephrine + glucagon → second messenger cAMP ↑ → activates Pyruvate Carboxylase (the rate-limiting enzyme).
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⚠️ OAA can't cross membrane from mitochondria to cytoplasm.
↓ Solution: AST shuttle (OAA → Aspartate → shuttle out → back to OAA)
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* Bypass enzymes — unique to gluconeogenesis, not found in glycolysis.
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