Fatty Acid β-Oxidation Tournament
Two onboarding diagrams place β-oxidation inside fatty-acid metabolism. Then eight MCAT-DoK rounds: the four-step cycle, the carnitine shuttle, MCAD deficiency, the canonical 106 ATP per palmitate, propionyl-CoA's gluconeogenic exception, and the liver-only ketogenesis spillover.
Where the Mitochondrial fatty acid β-oxidation fits in Fatty acid metabolism
Mitochondrial β-oxidation chops long-chain fatty acids into 2-carbon acetyl-CoA fragments, generating FADH2 + NADH for the ETC and feeding the TCA cycle (or, in fasting liver, ketogenesis). To enter the tournament, click the highlighted Mitochondrial fatty acid β-oxidation box.
Click the highlighted Mitochondrial fatty acid β-oxidation box to continue.
What this tournament tests
Each task maps to a distinct MCAT cognitive demand. The first two orient you in the broader topology; the next eight test the high-yield mechanism, regulation, sequence and quantitative reasoning that consistently appear on test day.
The Bigger Picture
Locate β-oxidation inside Reactome's Fatty Acid Metabolism overview.
Whole-Pathway Overview
Pan and zoom the WikiPathways β-oxidation figure before you play.
Fill in the Blank
Recall acetyl-CoA as the 2-carbon output of each β-oxidation cycle.
Disruptor
Diagnose MCAD deficiency from hypoketotic hypoglycemia + medium-chain acylcarnitines.
Sequence Ordering
Walk the four enzymatic steps of one cycle: oxidize, hydrate, oxidize, cleave.
Match the Pairs
Pair each carnitine-shuttle component (synthetase, CPT-I, translocase, CPT-II) to its function.
Numeric Input
Compute the 106 ATP from complete palmitate oxidation.
Select All That Apply
Sort true β-oxidation facts from common MCAT confusions.
Odd One Out
Spot malonyl-CoA - the regulator of β-oxidation that is NOT a product.
Liver-Only Ketogenesis
Recognize ketone bodies as the brain-friendly spillover when OAA runs out in fasting liver.
Public leaderboard
Your score posts to a global, persistent leaderboard scored by points first, time as tiebreaker.
Fatty acid β-oxidation in 60 seconds
Activation: acyl-CoA synthetase tags the fatty acid with CoA on the OUTER mitochondrial membrane (cost: 2 ATP equivalents). Carnitine shuttle: CPT-I swaps CoA for carnitine; carnitine-acylcarnitine translocase carries it across the inner membrane; CPT-II swaps carnitine back for CoA in the matrix. CPT-I is the rate-limiting step and is INHIBITED by malonyl-CoA - the first committed FA-synthesis intermediate. That inhibition is how the cell prevents simultaneous synthesis and oxidation.
Each cycle = oxidation (FAD), hydration, oxidation (NAD+), thiolytic cleavage. Output: 1 acetyl-CoA + 1 FADH2 + 1 NADH per turn, and the chain is now 2 carbons shorter. Palmitate (C16) goes through 7 cycles -> 8 acetyl-CoA + 7 FADH2 + 7 NADH. Plug into ETC stoichiometry: roughly 106 ATP after the activation cost.
Odd-chain FAs end with propionyl-CoA -> methylmalonyl-CoA (B12) -> succinyl-CoA - the only FA-derived carbons that can become net glucose. Even-chain FAs cannot net glucose because acetyl-CoA carbons are lost as CO2 in the TCA.
In fasting liver, OAA gets siphoned into gluconeogenesis -> acetyl-CoA piles up -> HMG-CoA synthase makes ketone bodies (acetoacetate, β-OH-butyrate). Brain and heart re-convert ketones to acetyl-CoA via thiophorase - an enzyme liver lacks, which is why liver makes ketones but cannot use them.
FAQ
Why is hypoketotic hypoglycemia the signature of MCAD deficiency?
Without medium-chain acyl-CoA dehydrogenase, β-oxidation stalls. Acetyl-CoA is not produced -> two consequences: (1) no substrate for ketogenesis (hypoKETOTIC), and (2) no allosteric activator for pyruvate carboxylase, so gluconeogenesis fails (hypoglycemic). Both deficits at once is uniquely diagnostic.
Where do very long chain fatty acids get oxidized?
VLCFAs (>C20) are oxidized in PEROXISOMES until they reach a medium-chain length, then transferred to mitochondria for completion. Peroxisomal β-oxidation uses a different acyl-CoA oxidase (donates electrons to O2 -> H2O2, no ATP captured), which is why X-ALD (defective ABCD1 transporter) accumulates VLCFAs and damages myelin.
Do I need an account to play?
No. The tournament is fully public. You get a randomized handle and your score posts to the public leaderboard at the bottom of this page.
Keep going
Mirror chemistry, opposite direction, opposite hormonal control. Learn both to bulletproof MCAT lipid questions.
Where the acetyl-CoA from β-oxidation goes - and why fasting OAA depletion forces ketogenesis instead.
Overview diagram: Reactome Pathway R-HSA-8978868, licensed CC BY 4.0.