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MCAT - Biochemistry - Lipid MetabolismLive tournament10 tasks

Fatty Acid Synthesis Tournament

Two onboarding diagrams place fatty-acid synthesis inside fatty-acid metabolism. Then eight MCAT-DoK rounds: FAS as the 7-active-site polyfunctional enzyme, why high-carb feeding flips lipogenesis ON and β-oxidation OFF, the four-step elongation cycle, NADPH stoichiometry (14 per palmitate), and ACC's biotin-citrate regulatory hub.

Step 1 of 3 - The bigger pictureFatty Acid Synthesis Tournament

Where the Fatty acyl-CoA biosynthesis fits in Fatty acid metabolism

Fatty acid synthesis is the cytosolic, NADPH-driven, citrate-fueled construction of palmitate (C16). It runs full-throttle in the fed state under insulin / SREBP-1c control. To enter the tournament, click the highlighted Fatty acyl-CoA biosynthesis box.

FFAs FFAs SLC25A20 beta-oxidation ABCD1 PEROXISOME PLASMA MEMBRANE CYTOSOL beta-oxidation ENDOPLASMIC RETICULUM SLC22A5 SLC25A1 PALMITIC ACID MITOCHONDRION FADH2 Prop-CoA FFAs Fatty acyl-CoA Ac-CoA NADH Succinyl-CoA XXX/YYY MITOCHONDRIAL FATTY ACID BETA-OXIDATION Fatty acyl-CoA ACYLCARNITINE ACYLCARNITINE CAR CAR CAR CAR Mal-CoA XXX/YYY CARNITINE METABOLISM ALA ALA LA LA DPA DHA LA-CoA ALA-CoA XXX/YYY ALPHA-LINOLENIC (OMEGA3) AND LINOLEIC (OMEGA6) ACID METABOLISM VLCFA-CoA Mal-CoA CITRATE CITRATE Ac-CoA XXX/YYY FATTY ACYL-CoA BIOSYNTHESIS VLCFA-CoA FADH2 NADH Ac-CoA PEROXISOMAL LIPID METABOLISM XXX/YYY MEMBRANE PHOSPHOLIPIDS AA EICOSANOIDS XXX/YYY ARACHIDONIC ACID METABOLISM

Click the highlighted Fatty acyl-CoA biosynthesis 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.

1

The Bigger Picture

Locate fatty-acid synthesis inside Reactome's Fatty Acid Metabolism overview.

2

Whole-Pathway Overview

Pan and zoom the WikiPathways FAS figure before you play.

3

Fill in the Blank

Recall FAS as the 7-active-site polyfunctional enzyme that builds palmitate.

4

Disruptor

Walk the high-carb-feeding cascade: insulin -> SREBP-1c -> high malonyl-CoA -> FAS up + β-ox down.

5

Sequence Ordering

Walk the four-step elongation cycle: condense, reduce, dehydrate, reduce.

6

Match the Pairs

Pair each cytosolic-feeder enzyme (ACL, ACC, FAS, malic enzyme, PPP) with its role.

7

Numeric Input

Compute the 14 NADPH cost per palmitate (C16).

8

Select All That Apply

Discriminate true ACC activators from inhibitors and from no-effect distractors.

9

Odd One Out

Spot the β-oxidation cofactor (FADH2) hiding among the synthesis molecules.

10

Biotin Cofactor

Recall ACC as the rate-limiting biotin-dependent carboxylase activated by citrate.

Public leaderboard

Your score posts to a global, persistent leaderboard scored by points first, time as tiebreaker.

Fatty acid synthesis in 60 seconds

Where: cytosol of liver, adipose, lactating mammary, adrenal cortex. Carbon source: mitochondrial citrate exported and cleaved by ATP-citrate lyase (ACL) -> cytosolic acetyl-CoA + OAA. Reductant: NADPH from PPP and from malic enzyme. ACC then puts CO2 on acetyl-CoA -> malonyl-CoA, the activated 2-carbon donor.

FAS is a homodimer with 7 catalytic domains plus an ACP arm. Each cycle: condensation (loses CO2), reduction (NADPH), dehydration, reduction (NADPH). After 7 cycles -> palmitate (C16), the only mammalian FAS product. Total: 1 acetyl-CoA + 7 malonyl-CoA + 14 NADPH -> palmitate.

ACC is the regulatory hub. Allosterically: citrate ACTIVATES (drives polymerization into long active filaments); long-chain acyl-CoA INHIBITS (product feedback). Covalently: insulin -> PP2A dephosphorylates -> ACTIVE; AMPK / glucagon / stress kinases phosphorylate -> INACTIVE.

Reciprocity with β-oxidation: malonyl-CoA INHIBITS CPT-I, so when ACC is cranking, the cell physically cannot import fatty acids into the mitochondrion for oxidation. One molecule, one switch, two opposite outcomes.

FAQ

Why does mammalian FAS only make palmitate?

FAS's KS (β-ketoacyl synthase) domain has a steric pocket sized for ~C14-C16 chains. Once the chain reaches C16, the thioesterase domain hydrolyzes it off as palmitate. Longer chains (stearate, etc.) require separate microsomal elongases.

What is SREBP-1c and why does it matter for FA synthesis?

SREBP-1c is the master lipogenic transcription factor. Insulin (or high-carb feeding) cleaves the ER-tethered SREBP precursor, releasing the active transcription factor that turns on the entire lipogenic gene set: FAS, ACC, ATP-citrate lyase, stearoyl-CoA desaturase. Statins target SREBP-2 (cholesterol synthesis); SREBP-1c is the FA branch.

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.