Untitled Flashcard Set

I. Lipid Classification and Properties

• Definition: Lipids are a diverse group of water-insoluble biomolecules that dissolve in nonpolar solvents like ether or chloroform.

• Major Classes: They include fatty acids, triacylglycerols, wax esters, phospholipids (phosphoglycerides and sphingomyelins), sphingolipids, isoprenoids (terpenes and steroids), and lipoproteins.

• Physical Nature: Often described as "greasy stuff," lipids like hexane are liquids due to weak hydrophobic interactions and Van der Waals forces.

• Amphipathic Molecules: Many lipids, like phospholipids and ionized fatty acids, contain both polar "heads" and nonpolar "tails". In water, they spontaneously form micelles or bilayers to sequester hydrophobic regions away from water.

II. Fatty Acid Structure and Nomenclature

• Structure: Monocarboxylic acids usually containing an even number of carbons (typically 12–20+) in an unbranched chain.

• Saturation:

  • Saturated: No carbon-carbon double bonds; they pack tightly and are solid at room temperature.

  • Unsaturated: Contain one (monounsaturated) or more (polyunsaturated) double bonds.

• Isomerism: Most natural double bonds are in the cis configuration, creating a "kink" that prevents close packing and lowers the melting point (making them liquid oils). Trans fatty acids, by-products of hydrogenation, have straight structures similar to saturated fats.

• Nomenclature:

  • $\Delta$ (Delta): Counts from the carboxylate end.

  • $\omega$ (Omega): Counts from the terminal methyl end.

• Essential Fatty Acids (EFAs): Mammals cannot synthesize linoleic acid ($\omega$-6) or $\alpha$-linolenic acid ($\omega$-3); these must be obtained from the diet.

III. Triacylglycerols (TAGs): The Storage Form

• Structure: Triesters consisting of a glycerol backbone and three fatty acids.

• Energy Efficiency: TAGs are the major energy reserve because they are anhydrous (storing 8x more energy by volume than hydrated glycogen) and more chemically reduced (releasing 38.9 kJ/g vs 17.2 kJ/g for carbs).

• Storage: Primarily stored in specialized cells called adipocytes within adipose tissue.

• Mobilization (Lipolysis): Triggered by low energy or hormones like glucagon and epinephrine, which activate protein kinase A (PKA) to phosphorylate lipases like hormone-sensitive lipase (HSL).

IV. Lipid Transport and Lipoproteins

• Exogenous Pathway (Dietary Fat):

  • Bile salts emulsify fats in the intestine.

  • Pancreatic lipase degrades TAGs into fatty acids and monoacylglycerols.

  • Enterocytes package these into chylomicrons for transport through lymph and blood.

• Endogenous Pathway (Liver-derived): The liver packages lipids into VLDL, which is converted to IDL and then LDL as TAGs are removed.

• Lipoprotein Density Classes:

  • Chylomicrons: Lowest density; transport dietary fat.

  • VLDL/LDL: VLDLs transport endogenous TAGs; LDLs are the primary cholesterol transporters to tissues.

  • HDL: Scavenges excess cholesterol from tissues for return to the liver (Reverse Cholesterol Transport).

• Clinical Note: Small dense LDLs (sdLDLs) are highly atherogenic because they easily enter arterial walls and oxidize, leading to plaque formation.

V. Fatty Acid Degradation ($\beta$-Oxidation)

• Location: Mitochondrial matrix.

• Activation: Fatty acids are converted to acyl-CoA derivatives in an ATP-dependent reaction.

• The Carnitine Shuttle: Because the inner mitochondrial membrane is impermeable to CoASH, carnitine is required to transport acyl groups into the matrix.

• The Reaction Cycle: Sequential removal of two-carbon fragments as acetyl-CoA, generating NADH and FADH$_2$.

• Special Cases:

  • Odd-chain: Yields propionyl-CoA, which can be converted to succinyl-CoA and then glucose.

  • Peroxisomes: Shorten very-long-chain fatty acids (VLCFAs) without generating ATP.

• Ketone Bodies: In starvation or diabetes, excess acetyl-CoA is converted to acetoacetate, $\beta$-hydroxybutyrate, and acetone to fuel the heart and brain.

VI. Fatty Acid Biosynthesis

• Location: Cytoplasm, primarily in the liver.

• Precursor: Excess mitochondrial acetyl-CoA is exported to the cytoplasm as citrate.

• Rate-Limiting Step: Carboxylation of acetyl-CoA to malonyl-CoA by Acetyl-CoA Carboxylase (ACC), requiring biotin and ATP.

• Fatty Acid Synthase (FAS): A multienzyme complex that builds palmitate (16:0) using NADPH as the reducing agent.

• Regulation:

  • ACC: Activated by citrate and insulin; inhibited by palmitoyl-CoA, glucagon, and AMPK.

  • Malonyl-CoA: Potently inhibits carnitine acyltransferase I (CAT-I) to prevent $\beta$-oxidation during synthesis (avoiding a futile cycle).

VII. Membranes and Fluidity

• Fluid Mosaic Model: Describes the membrane as a noncovalent lipid bilayer (mostly phospholipids) with floating proteins.

• Fluidity Factors:

  • Unsaturation: Higher percentages of unsaturated fatty acids increase fluidity.

  • Cholesterol: Contributes stability while maintaining high fluidity.

• Lipid Rafts: Specialized microdomains enriched in cholesterol and sphingolipids that spatially organize signaling processes.

VIII. Cholesterol and Isoprenoids

• Cholesterol Synthesis: HMG-CoA is converted to mevalonate by HMG-CoA reductase (HMGR), the rate-limiting step and target of statin drugs.

• Bile Salts: Derived from cholesterol in the liver; they act as detergents to aid fat digestion.

• Eicosanoids: Hormone-like signaling molecules (prostaglandins, thromboxanes, leukotrienes) derived from 20-carbon fatty acids like arachidonic acid.

To prepare for Part A of your Exam 3, which focuses on Chapter 10 (Electron Transport and Oxidative Phosphorylation) and TCA cycle regulation from Chapter 9, you should focus on the following key concepts and clinical applications.

I. Regulation of the Citric Acid Cycle (Chapter 9)

The Citric Acid Cycle (TCA) is precisely regulated to match the cell's energy and biosynthetic needs.

• Three Irreversible Steps: The cycle is primarily controlled at three key enzymes: citrate synthase, isocitrate dehydrogenase, and $\alpha$-ketoglutarate dehydrogenase.

• Allosteric Inhibitors: High energy signals like ATP and NADH inhibit these enzymes. Reaction products such as succinyl-CoA and citrate also act as inhibitors.

• Allosteric Activators: Low energy signals like ADP and AMP activate the cycle. Calcium ions ($Ca^{2+}$) are critical activators in the mitochondrial matrix, stimulating the PDHC, isocitrate dehydrogenase, and $\alpha$-ketoglutarate dehydrogenase to match energy production with demand.

• The PDH Complex: Pyruvate dehydrogenase (PDHC) links glycolysis to the TCA cycle. It is inhibited by Acetyl-CoA, NADH, and ATP. It is also regulated by phosphorylation; pyruvate dehydrogenase kinase inactivates it, while pyruvate dehydrogenase phosphatase (activated by $Ca^{2+}$ and insulin) reactivates it.

II. Electron Transport and Oxidative Phosphorylation (Chapter 10)

This chapter explains how cells extract energy from reduced coenzymes to synthesize ATP.

• The Components: Electrons flow through four complexes in the inner mitochondrial membrane (IMM): Complex I (NADH dehydrogenase), Complex II (Succinate dehydrogenase), Complex III (Cytochrome $bc_1$), and Complex IV (Cytochrome oxidase).

• Mobile Carriers: Coenzyme Q (Ubiquinone) carries electrons from Complexes I and II to Complex III. Cytochrome c carries electrons from Complex III to Complex IV.

• Final Electron Acceptor: Oxygen ($O_2$) is the terminal electron acceptor, combining with protons and electrons to form water ($H_2O$).

• Chemiosmotic Theory: Proposed by Peter Mitchell, this explains how the ETC pumps protons from the matrix to the intermembrane space, creating a proton gradient (protonmotive force) that drives ATP synthase.

• ATP Synthase (Complex V): Consists of the $F_0$ unit (a proton channel) and the $F_1$ unit (the catalytic motor). Its "binding change mechanism" involves three conformations for the catalytic sites: Open (O), Loose (L), and Tight (T).

• ETC Inhibitors:

  • Rotenone and Amytal: Block Complex I.

  • Antimycin A: Blocks Complex III.

  • Cyanide ($CN^-$), Carbon Monoxide ($CO$), and Azide: Block Complex IV.

  • Oligomycin: Inhibits ATP synthase by blocking the proton channel.

III. Clinical Application: Carbohydrate Metabolism During a Heart Attack

For the four True/False questions regarding a heart attack, the sources provide the following metabolic consequences of ischemia (inadequate blood flow) and hypoxia (low oxygen).

Introductory Sentence: “During a heart attack, the flow of oxygen-rich blood to the heart muscle is interrupted by blockage of a coronary artery. How would you expect carbohydrate metabolism in the heart to change?”

• Consequence 1: Shift to Anaerobic Glycolysis. Because the heart is highly sensitive to hypoxia, it shifts from aerobic fatty acid oxidation (which normally provides >50% of its energy) to anaerobic glycolysis to produce ATP. (TRUE)

• Consequence 2: Increased Glycolytic Flux. Flux through glycolysis increases dramatically because levels of allosteric inhibitors like citrate fall when the TCA cycle slows down. (TRUE)

• Consequence 3: Lactate Accumulation and Acidosis. The reliance on anaerobic glycolysis leads to a rapid increase in lactate production, causing intracellular acidosis. (TRUE)

• Consequence 4: Falling ATP and Ion Imbalance. Energy production by glycolysis is inefficient, so ATP levels fall. This causes ion pumps (like the $Ca^{2+}$ ATPase) to fail, leading to high cytoplasmic calcium levels and the activation of damaging proteases like calpains. (TRUE)

• Consequence 5: Mitochondrial Damage. Low ATP and high $Ca^{2+}$ cause the mitochondrial permeability transition pore (mPTP) to open, which leads to membrane potential collapse and the release of cytochrome c, triggering apoptosis (programmed cell death). (TRUE)

• Consequence 6: Reperfusion Injury. When oxygen is reintroduced (reperfusion), the reenergized ETC leaks electrons, creating a burst of Reactive Oxygen Species (ROS) that inflict further oxidative damage on heart tissue. (TRUE)

G3p shuttle

Lose proton gradient = no ATP

Dinitrophenol (DNP) has a pKa of around 7. Important for ino gradient. Outside the membrane, it is neutral. It crosses the OMM without effort. There are a lot more protons in IMM space. DNP stays protonated in the IM space. It crosses the IMM, too, and can lose some of the proton and release h+ into the matrix. It decreases the gradient as dnp moves into the matrix. 

pH = pKa - half ROH and half RO.

Brown fat - contains mitochondria with Fe proteins, giving it the color. It can do electron transport or TCA. It has an H+ channel in the imm. Regulated by epinephrine (activated). Used to increase heat. Dissipate the gradient and don't make ATP = heat. Non-shivering thermogenesis. 

Reactive oxygen species - “leaks” from the electron transport chain. Oxygen in ETC is not always reduced to water. Normal reaction: reoxidize NADH to NAD+, which releases electrons. Electrons can escape. Oxygen is supposed to be reduced to water at the same time. Oxygen will not make it all the way to water. Oxygen gas can diffuse across membranes! Oxygen becomes superoxide, which can be converted into hydrogen peroxide. Can also get hydroxyl radicals. 

SOD1 and SOD2 - antioxidant enzymes. Get rid of superoxide, which makes H2O2.  Peroxiporin - channel allowing h2o2 through

O2 + e- -> O2- + e- -> O2(2-) - > (w/ 2h+) h2o2 

ROS react with our cells to make carbon-centered radicals, too. 

Antioxidants can detoxify, such as vit e, vit c, glutathione, ubiquinone, NADPH, fruits, veggies, tea, coffee, and chocolate. 

Glutathione - tripeptide w reactive cysteine - disulfides

As we age, more ROS!

Fatty acids with double bonds get damaged by ROS

The alpha carbon is adjacent to the carboxylate, and the omega end is the terminal carbon. 

Saturated - no double bonds, unsaturated - double bond (s)

Omega 3 -  alkene 3 carbons from omega end (ANTI INFLAMMATORY)

Omega-6 - alkene 6 carbons from omega end

Triacylglycerol - fat that we store. glycerol with three ester bonds to three fatty acids.

18 carbons and no double bonds - 18:0 (sat)

18 carbons and one double bond - 18:1 (unsat)

16:0

Lots of even numbers

Insoluble in water - gallbladder secretes detergents

Palmitic acid is very common, oleac acid is common, etc

Linolenic acid - omega three

Fats can be apart of membranes

Unsaturated fatty acids have bends

Phospholipases hydrolyze fatty acids from phospholipids.

Detergents in gallbladder released into small intestine to digest fats. Pancreatic lipase helps hydrolyze esters. Ths is needed for transfer into cells and fat remodeling.

CoA carrier of fatty acids

What is ester hydorylsus? 

Adipocyte: fat cell - long term storafe. No glycogen.

Fat is anhydrous

Hormone - sensitive lipase responds to insulin and glucagon.

Lipolysis - release of fatty acids from fat cells. Phopshorylated perilipin - on. Start breaking down triacylglyercol. Glycerol can go to gluconeogenesis. Free fatty acids clup in bloodstream. Become cholesterol particles, need fatty acid binding protein to transport, serum albumin.

Moving fat to muscles -  mitochondria ! fat cell - blood - muscle cell - mitochondria

Fatty acaid reacts with coA -> thioester. Take ROH of carnitine plus acyl coa anad get carnitine ester. Use atp to make thioester

Outside cells - trig or fats bound to protein

Carnitine derivative is the one that crosses the matrix to get burned (oxidized completely).

Transferase: carnitase stuff

Fatty acid + coA needs ATP (uphill) - > AMP + PPi -> 2Pi - atp is invested (2)

Fatty acids metabolized from alpha end, cleaved between alpha and beta carbon, cut everything in two carbon pieces. BETA OXIDATION OF FATTY ACIDS - beta carbon gets oxidized (loses h, gain O)

Alkane to alkene make FADH2

Add water across double bond

Remove water, make nadh and h+

Thiolase breaks ketone bond (into acetyl coa piece)

Each cycle yields FADH2 and NADH.

Fatty acid beta oxidation makes: acetyl coa, fadh2, nadh.

TCA makes: CO2, NADH, FADH2

ETC makers: O2 to h2o - > h+ gradient, use it to make ATP

16:0 fatty acid - how many ATP?

Palmitic acid+7FAD+7NAD+ + 7CoAsh - > 8 acetyl coa + 7 FADH2 + 7 NADH + 7H+

= 28 atp from beta oxidation

8 acetyl coa = 80 atp

= 108 - 2 ATP = 106 ATP from 16:0

Metabolism of unsaturated fatty acid

• Decrease FADH2 yield

Even-Numbered Chains

1. Activation: Subtract 2 ATP (one-time cost to start).

2. beta-Oxidation Cycles: Calculate $n / 2) - 1.

3. Each cycle yields: 1 NADH (2.5 ATP) + FADH_2 (1.5 ATP) = 4 ATP.

4. Acetyl-CoA: Calculate n / 2

   • Each enters the TCA cycle for 10 ATP each.

5. Sum: (Cycles x 4) + (AcetylCoA x 10) - 2.

Odd-Numbered Chains

1. Activation: Subtract 2 ATP.

2. beta-Oxidation Cycles: Calculate (n - 3) / 2

   • Each cycle yields 4 ATP.

3. Acetyl-CoA: Calculate (n - 3) / 2.

   • Each yields 10 ATP.

4. Propionyl-CoA (The final 3 carbons):

   • The last fragment is Propionyl-CoA, which converts to Succinyl-CoA.

   • This process consumes 1 ATP but eventually yields 5 ATP (Net: 18.5 ATP total for that final 3-carbon unit, including the final NADH, FADH_2 produced in the last round).

5. Sum: Add the cycles, the acetyl-CoA, the propionyl-CoA net, and subtract activation.

Acetyl coa from fatty acid enters into the citric acid cycle/tca cycle. It reacts with oxaloacettate to make citrate. Without carbs, fire dies out - oaa can leave to make glucose in liver which limits fatty acid burning. Fatty acids can not become glucose because acetyl coa cannot be converted to pyruvate.

Conversion of acetyl coa to ketone bodies is made by the liver

When making ketone bodies, you need 3 acetyl-CoA

• FAMINE pathway

Acetoacetate can be reduced in the liver. It can lose CO2 and generate acetone.

Beta-hydroxybutyrate is also a ketone body

Liver does not use ketone bodies; they can go to the heart, brain

They can be converted back to acetyl coa

• Beta-hydroxybutyrate re oxidized with NAD+

• Uses TCA cycle intermediates

• Thiolase is not expressed in the liver

• Acetyl coa can go into TCA

• OAA is not limited in brain

acetoacetate

Beta-hydroxybutyrate 

Odd-chain fatty acids

How to use the leftover 3 carbon piece:

Propionyl-CoA

Carboxylase enzyme - same as pyruvate to OAA

Needs biotin

Net increase of succinyl-CoA

Fatty acid biosynthesis 

Insulin is fat fertilizer

8 acetyl coA +14NADPH + 14H+ + 7ATP -> palmitic acid + 14 NADP+ + 7ADP + 7Pi + 8CoAsh + 6H2O

Needs NADPH from PPP

Happens in the cytosol of the liver

When you have eaten insulin + glucagon -

Fatty acid synthase complex and ACC

High citrate, acetyl-CoA, ATP, NADH (slows TCA)

Move citrate and make ATP

Acetyl-CoA doesn't cross the membrane

Malate to pyruvate releases CO2 and makes NADPH

Fatty acid synthesis

 uses reductass

Acetyl-CoA can be used to make fatty acids

Malate can become pyruvate with malic enzyme, and NADPH is made and used for fatty acid synthesis

One nadph for FA synth for each citrate laevaing matric

1. Acetyl-CoA + ATP + CO2 -> malonyl coA +ADP +pi w/ carbxylase enzyme, also requires biotin.

2. Acetyl coa attaches to ACP

3. Acetyl synthase + malonyl ACP: lose CO2 (driving force), make a transient carbanion (very reactive)

4. Carbanion reacts with two carbon piece 

• Ketone to alcohol to alkene to alkane -- reverse of fatty acid oxidation

Three thiols:

CoA

ACP

Fatty acid synthase

Fatty acid oxidation vs synthesis comparison table

Regulation of acc:

• Acc can be phosphorylated

• PKA = protein kinase A (also glycogen breakdown signal)

• Feast: make fatty acids (insulin on)

• Famine: oxidize fatty acids (glucagon on)

• Insulin is fat fertilizer

• Movement of fat is a slow step

• Citrate stabilizes the polymer form

• Activated by: citrate

• Inhibited by: palmitoyl-CoA (product of FA synthesis, feedback inhibition) (reduced ability to make malonyl-CoA)

Below is your material converted into a clean, structured, exam-optimized study guide using the prompt framework (tight formatting, hierarchy, and high-yield emphasis).

Lipid Metabolism + TCA/ETC Study Guide

I. 🔵 Lipid Classification & Properties

Overview

• Lipids = hydrophobic biomolecules soluble in nonpolar solvents (e.g., ether, chloroform)

• Function: energy storage, membranes, signaling

Major Classes

• Fatty acids

• Triacylglycerols (TAGs) → storage

• Phospholipids / Sphingolipids → membranes

• Steroids (cholesterol)

• Isoprenoids

• Lipoproteins

Amphipathic Behavior

• Polar head + nonpolar tail

• Self-assemble into:

  • Micelles

  • Bilayers

II. 🔵 Fatty Acids

Structure

• Long hydrocarbon chain + carboxyl group

• Usually even-numbered carbons

Saturation

Key Concepts

• Cis double bonds → kinks → ↑ fluidity

• Trans fats → behave like saturated fats

Nomenclature

• Δ (delta): from carboxyl end

• ω (omega): from methyl end

Essential Fatty Acids

• ω-3 (α-linolenic acid) → anti-inflammatory

• ω-6 (linoleic acid)

III. 🔵 Triacylglycerols (TAGs)

Structure

• Glycerol + 3 fatty acids (ester bonds)

Why Efficient Storage

• Anhydrous

• Highly reduced → ~9 kcal/g

Storage

• Stored in adipocytes

• No glycogen storage in fat cells

Lipolysis (Mobilization)

🟢 Trigger:

• Glucagon / Epinephrine → PKA activation

🟢 Mechanism:

1. Perilipin phosphorylated

2. Hormone-sensitive lipase (HSL) activated

3. TAG → fatty acids + glycerol

IV. 🔵 Lipid Transport

Exogenous Pathway (Dietary)

1. Bile salts emulsify fat

2. Pancreatic lipase digests TAGs

3. Packaged → chylomicrons

Endogenous Pathway (Liver)

• VLDL → IDL → LDL

Lipoproteins

🔴 Clinical

• Small dense LDL → highly atherogenic

V. 🔵 Fatty Acid Oxidation (β-Oxidation)

Location

• Mitochondrial matrix

Step 1: Activation

• FA + CoA + ATP → Acyl-CoA

• Costs 2 ATP equivalents

Carnitine Shuttle

• Required to enter mitochondria

• Malonyl-CoA inhibits this step

β-Oxidation Cycle (repeat)

Each cycle:

1. Oxidation → FADH₂

2. Hydration

3. Oxidation → NADH

4. Cleavage → Acetyl-CoA

ATP Yield (Even Chain)

Example: 16:0 (Palmitate)

• 7 cycles → 7 NADH + 7 FADH₂

• 8 acetyl-CoA

Total:

• β-oxidation: 28 ATP

• TCA: 80 ATP

• −2 ATP activation

Net = 106 ATP

General Formula

• Cycles = (n/2) − 1

• Acetyl-CoA = n/2

Special Cases

Odd-chain FA

• → Propionyl-CoA → Succinyl-CoA

• Requires biotin

Unsaturated FA

• ↓ FADH₂ → less ATP

Peroxisomes

• Shorten very-long-chain FA

Ketone Bodies (Fasting)

• Produced in liver

• From acetyl-CoA

Types:

• Acetoacetate

• β-hydroxybutyrate

• Acetone

🟡 Liver cannot use ketones

VI. 🔵 Fatty Acid Synthesis

Location

• Cytosol (liver)

Key Idea

• Opposite of β-oxidation

Rate-Limiting Step

🟢 Acetyl-CoA → Malonyl-CoA

• Enzyme: Acetyl-CoA Carboxylase (ACC)

• Requires:

  • ATP

  • Biotin

Fatty Acid Synthase (FAS)

• Builds palmitate (16:0)

• Uses NADPH

Overall Reaction

• 8 acetyl-CoA → palmitate

Regulation

🟡 Malonyl-CoA inhibits β-oxidation

NADPH Sources

• Pentose phosphate pathway

• Malic enzyme

VII. 🔵 Membranes

Fluid Mosaic Model

• Lipid bilayer + proteins

Fluidity Factors

Lipid Rafts

• Cholesterol-rich signaling domains

VIII. 🔵 Cholesterol & Derivatives

Synthesis

🟢 Rate-limiting:

• HMG-CoA reductase

Products

• Bile salts

• Steroid hormones

• Eicosanoids

IX. 🔵 TCA Cycle Regulation

Key Enzymes

• Citrate synthase

• Isocitrate dehydrogenase (rate-limiting)

• α-Ketoglutarate dehydrogenase

Regulation

PDH Complex

• Links glycolysis → TCA

X. 🔵 Electron Transport Chain (ETC)

Complexes

Key Concept

• Proton gradient → ATP synthesis

ATP Synthase

• Uses H⁺ gradient

• States: O, L, T

Inhibitors

Uncoupling

• DNP dissipates proton gradient

• Brown fat uses uncoupling → heat

XI. 🔵 Reactive Oxygen Species (ROS)

Formation

• Electron leakage → superoxide

Detox

• SOD → H₂O₂

• Antioxidants:

  • Vitamin C/E

  • Glutathione

  • NADPH

🔴 ROS damage:

• Lipids (especially unsaturated FA)

• Proteins

• DNA

XII. 🔵 Heart Attack Metabolism

Key Shifts

• ↓ O₂ → ↓ ETC

• ↑ Anaerobic glycolysis

Consequences

• ↑ Lactate → acidosis

• ↓ ATP → ion pump failure

• ↑ Ca²⁺ → protease activation

• ROS burst (reperfusion injury)

🔴 Common Mistakes

• Forgetting −2 ATP activation cost

• Confusing ACC vs FAS

• Assuming fat → glucose (not possible)

• Forgetting malonyl-CoA inhibits carnitine shuttle

• Thinking liver uses ketones (it does not)

🟡 Quick Reference (Cheat Sheet)

• TAG = storage

• β-oxidation = mitochondria

• FA synthesis = cytosol

• ACC = rate-limiting synthesis

• Carnitine shuttle = entry step

• Malonyl-CoA blocks oxidation

• 106 ATP from palmitate

• TCA inhibited by ATP/NADH

• ETC needs O₂

🧠 Active Recall Questions

1. Why are TAGs more energy-dense than glycogen?

2. What inhibits the carnitine shuttle?

3. Where does β-oxidation occur?

4. What is the rate-limiting enzyme of FA synthesis?

5. Why can’t fatty acids form glucose?

6. What activates ACC?

7. What is the role of HDL?

8. How many ATP from 16:0?

9. What happens to odd-chain fatty acids?

10. What causes ROS formation?

11. What happens metabolically during hypoxia?

12. Why does DNP produce heat?

If you want, I can compress this further into a 1-page ultra-high-yield cram sheet or convert it into Anki-style active recall cards aligned with how you study.