Bioenergetics and Regulation of Metabolism

Chapter 12: Bioenergetics and Regulation of Metabolism

6 min read Updated Apr 18, 2026
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1. (12.1) A reaction is spontaneous when:
B. ΔG = ΔH - TΔS. Spontaneous = ΔG < 0 (exergonic). Non-spontaneous = ΔG > 0 (endergonic). Spontaneous reactions can still be slow - thermodynamics says nothing about rate (that's kinetics).
2. (12.1) Standard ΔG° is different from cellular ΔG because:
C. A reaction with ΔG° = +3 kcal/mol can still be spontaneous in cells if substrates are much more concentrated than products. That's why reactions like those in glycolysis run forward even when ΔG°' looks unfavorable.
3. (12.2) The standard ΔG of ATP hydrolysis to ADP + Pi is approximately:
A. ATP → ADP + Pi releases ~7.3 kcal/mol under standard conditions. In cells, where [ATP] >> [ADP], the actual ΔG is closer to -11 to -14 kcal/mol. This drives most endergonic biological reactions.
4. (12.2) Why is ATP called "high energy" even though its phosphoanhydride bonds are not unusually strong?
D. The "high-energy bond" terminology is misleading. It's really "low-energy products." ADP and Pi are more stable (more resonance structures, less electrostatic strain) than ATP. Enthalpy of the products drops, so ΔG of hydrolysis is strongly negative.
5. (12.3) Coupled reactions link:
B. Example: glucose + Pi → G6P has ΔG = +3.3 kcal/mol (uphill). Coupled to ATP → ADP + Pi (-7.3), net ΔG = -4.0, spontaneous. Hexokinase catalyzes the coupled transfer of phosphate directly, avoiding the ATP-Pi intermediate.
6. (12.3) The most common strategy cells use to drive endergonic reactions is:
A. ATP, GTP, and other high-energy phosphate transfers are the universal mechanism. Also: redox coupling (NADH/NAD+), ion-gradient coupling (Na/K-ATPase → Na-glucose transport), and high-energy thioester bonds (acetyl-CoA).
7. (12.4) In biological redox, NADH is a ______ because it ______:
C. NADH is reduced (carries electrons); it donates them to other molecules (becoming the oxidized form, NAD+). "OIL RIG" - Oxidation Is Loss, Reduction Is Gain (of electrons). Biological reducing agents: NADH, NADPH, FADH2.
8. (12.4) NAD+ is used mostly in catabolism; NADP+ (and its reduced form NADPH) is used mostly in:
D. NAD+/NADH handles catabolism; NADP+/NADPH handles biosynthesis. Cells keep NAD+ oxidized (ready to accept electrons from catabolism) but NADPH reduced (ready to donate electrons for biosynthesis). The extra phosphate on NADP+ lets enzymes distinguish the two pools.
9. (12.5) Which vitamin gives rise to the coenzyme Coenzyme A (CoA)?
B. Pantothenic acid (B5) is the pantothenate portion of CoA. CoA carries acyl groups throughout metabolism (acetyl-CoA, succinyl-CoA, palmitoyl-CoA). The "high-energy" thioester bond between CoA's sulfur and an acyl group drives acyl transfer.
10. (12.5) Pyridoxal phosphate (PLP), derived from vitamin B6, is the cofactor for:
A. PLP is the MVP of amino acid metabolism. Shuttles the amino group in transamination (ALT, AST) and forms Schiff bases essential for decarboxylation, racemization, and side-chain cleavage.
11. (12.6) The "fed state" (postprandial, 0-2 hours after eating) is characterized by:
C. Insulin dominates: glucose flows in, gets stored as glycogen, converted to triglycerides in liver and adipose, and amino acids feed protein synthesis. Catabolic pathways are suppressed.
12. (12.6) By 3 days into fasting, the body's primary fuel pattern is:
D. Glycogen is long gone (~24h). The body pivots to mobilizing fat and making glucose from protein. As ketone production ramps up, the brain gradually switches to ketones, sparing protein.
13. (12.7) Insulin is secreted in response to:
A. Beta-cells sense glucose via GLUT2 and glucokinase; ATP/ADP ratio rises, closing K-ATP channels, depolarizing the cell, and triggering Ca2+-mediated insulin exocytosis. Sulfonylurea diabetes drugs close the same channels artificially.
14. (12.7) Glucagon's main effect on the liver:
B. Glucagon is the "fasting" hormone. Via GPCR → Gαs → cAMP → PKA, it phosphorylates targets to break down glycogen and make glucose. The inverse of insulin. Epinephrine does the same in muscle and is additionally released during stress.
15. (12.8) The liver is unique because it:
D. Liver is the metabolic hub - it alone releases glucose for other tissues, makes ketones, synthesizes urea, and runs much of cholesterol/lipoprotein biology. Its central role is why liver disease has such widespread effects.
16. (12.8) Red blood cells rely exclusively on:
C. Mature RBCs have shed all organelles including mitochondria. Only glycolysis is available (yielding 2 ATP per glucose, all from substrate-level phosphorylation). They also run the pentose phosphate pathway to make NADPH for antioxidant defense.
17. (12.9) Type 1 diabetes mellitus results from:
B. Type 1 = no insulin (autoimmune beta-cell loss). Type 2 = insulin resistance + relative deficiency. Both produce hyperglycemia, but Type 1 is prone to ketoacidosis because the absence of insulin unleashes unopposed lipolysis and ketogenesis.
18. (12.9) Phenylketonuria (PKU) is caused by:
A. PAH converts Phe → Tyr. Without it, Phe builds up and Tyr becomes essential. Treatment = low-Phe diet + Tyr supplementation. Detected by newborn screening; untreated infants develop severe intellectual disability within months. Pregnant women with PKU must also strictly control Phe to protect the fetus.
19. (12.10) During the first ~10 seconds of maximal exercise, muscle primarily uses:
D. PCr + ADP → ATP + creatine, catalyzed by creatine kinase. Instant, large-capacity ATP buffer, but depletes in ~10-15 seconds. Then anaerobic glycolysis takes over. Aerobic metabolism dominates after ~2 minutes when cardiovascular response catches up.
20. (12.10) Aerobic endurance training increases which adaptations?
C. Endurance training upregulates the oxidative machinery. Trained athletes burn a higher fraction of fat at submaximal intensities, sparing glycogen. Lactate threshold rises. Mitochondrial biogenesis is driven largely by PGC-1α signaling.

Chapter 12 ties everything together. You already know the pathways. Now learn the thermodynamic principles, the master hormonal controls, the tissue-specific differences, and the clinical disorders that arise when any of them breaks. These are the big-picture concepts the MCAT tests in passages.

ATP is the Universal Currency

ATP is accepted by every cellular process. Making ATP is earning money; using it is spending. The cell’s “bank account” is its ATP/ADP ratio - it decides whether to save (anabolism) or spend (catabolism). Every pathway in this book ultimately connects back to this currency.

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