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MCAT - Biochemistry - Lipid metabolismLive tournament10 tasks

Ketone Body Metabolism Tournament

Two onboarding diagrams orient you in lipid metabolism + ketogenesis. Then eight MCAT-DoK quiz rounds: HMG-CoA synthase as rate-limiting, β-OH-butyrate vs. acetoacetate, why liver makes but cannot use ketones, DKA biochemistry in T1DM, the energetic cost of thiophorase, and MCAD's paradoxical hypoketotic hypoglycemia.

Step 1 of 3 - The bigger pictureKetone Body Metabolism Tournament

Where the Ketone body metabolism fits in Metabolism of lipids

Ketone bodies are the liver's overflow product when fasting / starvation / DKA flood mitochondria with acetyl-CoA. They feed brain, heart, and skeletal muscle when glucose runs short. Click the highlighted Ketone body metabolism box to enter the tournament.

FFAs MITOCHONDRION beta-oxidation beta-oxidation PEROXISOME LIPID DROPLET SREBP CYTOSOL PLASMA MEMBRANE DAG PUFAs SPMs PRO-RESOLVING OF INFLAMMATION XXX/YYY BIOSYNTHESIS OF SPECIALIZED PRORESOLVING MEDIATORS (SPMS) PIs GPLs PHOSPHOLIPIDS XXX/YYY PHOSPHOLIPID METABOLISM PPARA LIPIDS FFAs XXX/YYY REGULATION OF LIPID METABOLISM BY PPARalpha SPHINGOSINE CERAMIDES SUGARS GSLs XXX/YYY SPHINGOLIPID METABOLISM 1,25(OH)D CHOL CHOLESTEROL ESTER BILE SALTS STEROID HORMONES Ac-CoA Ac-CoA LIPE XXX/YYY METABOLISM OF STEROIDS MAGs TAG XXX/YYY TRIGLYCERIDE METABOLISM AA EICOSANOIDS CYTOKINES CAR ACYLCARNITINE Fatty acyl-CoA Ac-CoA Ac-CoA Ac-CoA VLCFA-CoA VLCFA-CoA CITRATE XXX/YYY FATTY ACID METABOLISM KETONE BODIES ACA-CoA KETONE BODY METABOLISM XXX/YYY PLASMALOGEN DHAP Fatty acyl-CoA Fatty alcohols WAXES WAX AND PLASMALOGEN BIOSYNTHESIS XXX/YYY LIPIDS LIPIDS LIPIDS LIPIDS LIPID PARTICLE ORGANIZATION XXX/YYY

Click the highlighted Ketone body metabolism 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

Anchor ketogenesis inside lipid metabolism on the live Reactome overview map.

2

Whole-Pathway Overview

Pan and zoom the curated WikiPathways β-oxidation / ketogenesis figure before you start answering.

3

Fill in the Blank

Recall β-OH-butyrate (BHB) as the most abundant fasting plasma ketone.

4

Disruptor

Predict why insulin deficiency in T1DM cascades into severe DKA via lipolysis + low OAA.

5

Sequence Ordering

Trace 2 acetyl-CoA -> acetoacetyl-CoA -> HMG-CoA -> acetoacetate -> BHB.

6

Match the Pairs

Pair each enzyme (HMG-CoA synthase, lyase, BHB DH, thiophorase) with its precise role.

7

Numeric Input

Calculate ATP yield from full BHB oxidation (~21 ATP) using canonical TCA + ETC stoichiometry.

8

Select All That Apply

Identify TRUE facts: liver lacks thiophorase, RBCs cannot use ketones, DKA dipstick BHB blind spot.

9

Odd One Out

Distinguish acetyl-CoA (precursor) from the three actual ketone bodies.

10

MCAD Hypoketotic Hypoglycemia Fill-in

Recognize why FAO defects produce LOW ketones with hypoglycemia (no acetyl-CoA to drive ketogenesis).

Public leaderboard

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

Ketones in 60 seconds

Ketones are the liver's response to prolonged fasting / DKA: high fatty-acid oxidation -> flood of acetyl-CoA -> oxaloacetate is drained for gluconeogenesis -> acetyl-CoA cannot enter the TCA -> HMG-CoA synthase shunts it into ketones.

Three molecules circulate: acetoacetate, β-hydroxybutyrate (most abundant), and acetone (volatile, fruity-breath byproduct). The BHB / acetoacetate ratio reports the mitochondrial NADH / NAD+ ratio.

The liver MAKES ketones but cannot USE them, because hepatocytes lack thiophorase (succinyl-CoA:acetoacetate CoA-transferase). Brain, heart, and muscle have thiophorase and consume ketones eagerly during fasting.

DKA pathology = no insulin -> uninhibited lipolysis -> massive ketone production + osmotic diuresis. Standard urine dipsticks miss BHB - so when the patient improves and BHB shifts back to acetoacetate, the dipstick can paradoxically look 'worse' even as plasma ketones fall.

FAQ

Why don't RBCs use ketones?

Red blood cells have NO mitochondria. They are obligate glucose-on-glycolysis cells with lactate as their endpoint. Even in deep starvation when ketones supply most other tissues, the brain reserves glucose for the RBCs and the renal medulla.

Why does the BHB-to-acetoacetate ratio matter clinically?

It reflects the mitochondrial NADH / NAD+ ratio. Severe shock or alcoholic ketoacidosis push BHB up disproportionately - which standard dipsticks miss. Always measure plasma BHB directly when the picture is severe.

Why is the brain's switch to ketones so important?

After ~3 days of fasting, ketones supply >50% of brain energy. This dramatically reduces the brain's glucose demand - protecting muscle from being broken down for gluconeogenic precursors. It is the metabolic basis of why we can fast for weeks without losing all lean mass.

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.