Medical School · Year 1 · Foundations · includes a quiz and discussion video

Lecture 8: Lipid Metabolism

Unit 1.1: Foundations of Medicine & Medical Sciences

Learning Objectives

By the end of this lecture, students will be able to:

1. Describe the pathways of fatty acid synthesis and β-oxidation, including key enzymes and regulatory steps
2. Explain the formation and utilization of ketone bodies during fasting and starvation
3. Compare lipid metabolism in the fed versus fasted state
4. Describe the transport of fatty acids into mitochondria via the carnitine shuttle
5. Identify clinical disorders of fatty acid oxidation and ketone body metabolism
6. Explain the regulation of lipid metabolism by hormones (insulin, glucagon, epinephrine)

Lecture Content

I. Overview of Lipid Metabolism

Lipids represent the body's most efficient energy storage system. While carbohydrates provide 4 kilocalories per gram, fats deliver 9 kilocalories per gram—more than double the energy density. This efficiency, combined with the hydrophobic nature of lipids (which allows storage without accompanying water), makes adipose tissue an extraordinarily compact energy reserve. A typical adult stores over 100,000 kilocalories as fat—enough to sustain life for weeks during starvation—while carbohydrate reserves (primarily glycogen) last less than a day.

Beyond energy storage, lipids serve essential structural and signaling functions. Phospholipids form the bilayer architecture of all cellular membranes. Cholesterol modulates membrane fluidity and serves as the precursor for steroid hormones and bile acids. Eicosanoids derived from fatty acids mediate inflammation, blood clotting, and vascular tone.

The major pathways of lipid metabolism operate in opposing metabolic states. Lipogenesis (fatty acid synthesis) predominates in the fed state when nutrients are abundant and insulin levels are high—excess dietary carbohydrate is converted to fat for storage. Lipolysis releases stored fatty acids from adipose tissue triglycerides during fasting. Beta-oxidation breaks down these fatty acids for energy in the fasted state. Ketogenesis produces ketone bodies during prolonged fasting or uncontrolled diabetes, providing an alternative fuel for tissues including the brain.

<image>Panel A: Fed state (warm orange) showing lipogenesis with glucose and acetyl-CoA converting to fatty acids in liver under high insulin. Panel B: Triglyceride storage depicting fatty acids incorporated into adipose tissue triglycerides in fed state. Panel C: Fasted state (cool blue) showing lipolysis releasing fatty acids from adipose and beta-oxidation converting to acetyl-CoA with ATP. Panel D: Ketogenesis showing excess acetyl-CoA forming ketone bodies in liver for brain and muscle with hormone labels (insulin, glucagon, epinephrine).</image>

II. Fatty Acid Synthesis (Lipogenesis)

When dietary intake exceeds immediate energy needs—particularly when carbohydrates are abundant—the liver converts excess acetyl-CoA to fatty acids for storage. This anabolic process occurs in the cytoplasm, requires significant energy input, and is active primarily during the fed state when insulin levels are high.

Source of Carbon: The Citrate Shuttle

Fatty acid synthesis requires cytoplasmic acetyl-CoA, but the acetyl-CoA generated from pyruvate oxidation and other catabolic reactions resides in the mitochondrial matrix. Since acetyl-CoA cannot directly cross the inner mitochondrial membrane, cells employ the citrate shuttle to transport its carbon atoms to the cytoplasm.

In the mitochondrial matrix, acetyl-CoA condenses with oxaloacetate to form citrate (the first reaction of the TCA cycle). When cellular ATP levels are high and the TCA cycle is running slowly, citrate accumulates and is transported to the cytoplasm via the citrate transporter. In the cytoplasm, ATP-citrate lyase cleaves citrate back to acetyl-CoA and oxaloacetate, regenerating the acetyl-CoA building blocks needed for fatty acid synthesis. The oxaloacetate returns to the mitochondria after conversion to pyruvate or malate.

Acetyl-CoA Carboxylase: The Committed Step

The first committed step of fatty acid synthesis is catalyzed by acetyl-CoA carboxylase (ACC), a biotin-dependent enzyme that carboxylates acetyl-CoA to form the three-carbon malonyl-CoA: Acetyl-CoA + CO₂ + ATP → Malonyl-CoA + ADP + Pᵢ.

ACC is the rate-limiting enzyme of fatty acid synthesis and a critical regulatory point. The enzyme is allosterically activated by citrate (signaling abundant acetyl-CoA and energy) and inhibited by palmitoyl-CoA (the end product of fatty acid synthesis, providing feedback inhibition). Hormonal regulation occurs through phosphorylation: insulin promotes dephosphorylation, activating ACC and stimulating lipogenesis; glucagon and epinephrine stimulate phosphorylation via protein kinase A, inactivating ACC. AMP-activated protein kinase (AMPK), the cellular energy sensor, phosphorylates and inhibits ACC when cellular energy is low.

Malonyl-CoA, beyond serving as the building block for fatty acid synthesis, plays a crucial regulatory role by inhibiting carnitine palmitoyltransferase I (CPT-I), thereby preventing fatty acid entry into mitochondria for oxidation. This reciprocal regulation ensures that fatty acid synthesis and oxidation do not occur simultaneously.

Fatty Acid Synthase: Building the Chain

Fatty acid synthase (FAS) is a large, multifunctional enzyme complex that catalyzes all subsequent reactions of fatty acid synthesis. In mammals, FAS is a homodimer, with each monomer containing seven distinct enzymatic activities and an acyl carrier protein (ACP) domain that holds the growing fatty acid chain via a phosphopantetheine prosthetic group (the same group found in coenzyme A).

Each elongation cycle adds two carbons from malonyl-CoA to the growing chain through a sequence of four reactions: condensation releases CO₂ while joining the two-carbon unit to the chain; reduction uses NADPH to reduce a ketone group; dehydration removes water to form a double bond; and a second reduction uses NADPH to saturate the double bond. The cycle repeats seven times, with the final product being palmitate—a saturated 16-carbon fatty acid.

The overall reaction summarizes the resource requirements: Acetyl-CoA + 7 Malonyl-CoA + 14 NADPH + 14 H⁺ → Palmitate + 7 CO₂ + 14 NADP⁺ + 8 CoA-SH + 6 H₂O. Note the substantial NADPH requirement; the pentose phosphate pathway is the primary source, with the malic enzyme contributing additional NADPH.

<image>Panel A: Fatty acid synthase homodimeric structure with two monomers head-to-tail showing seven functional domains and ACP with phosphopantetheine tether. Panel B: Loading and condensation steps with acetyl on KS domain, malonyl on ACP, forming 4-carbon product with CO2 release. Panel C: Reduction and dehydration cycle with NADPH reducing ketone, water removal forming double bond, second NADPH saturation. Panel D: Product translocation to KS domain for cycle repeat with carbon count progression (4C to 16C) and palmitate release by thioesterase.</image>

III. Transport of Fatty Acids into Mitochondria

While fatty acid synthesis occurs in the cytoplasm, β-oxidation takes place in the mitochondrial matrix. Long-chain fatty acids cannot simply diffuse across the inner mitochondrial membrane; they require a specialized transport system known as the carnitine shuttle.

The Carnitine Shuttle Mechanism

The process begins with fatty acid activation in the cytoplasm. Fatty acyl-CoA synthetase (also called acyl-CoA synthetase or thiokinase) catalyzes the ATP-dependent attachment of coenzyme A to the fatty acid, forming fatty acyl-CoA. This reaction consumes the equivalent of two ATP (ATP → AMP + PPᵢ, with pyrophosphate subsequently hydrolyzed to drive the reaction forward).

The activated fatty acyl-CoA then encounters the outer surface of the inner mitochondrial membrane, where carnitine palmitoyltransferase I (CPT-I) transfers the fatty acyl group from CoA to carnitine, producing fatty acyl-carnitine and releasing free CoA. CPT-I is the rate-limiting enzyme for fatty acid oxidation and represents the critical regulatory point.

Fatty acyl-carnitine crosses the inner membrane via carnitine-acylcarnitine translocase, an antiporter that exchanges acyl-carnitine for free carnitine. On the matrix side, carnitine palmitoyltransferase II (CPT-II) reverses the first transfer, moving the fatty acyl group from carnitine back to intramitochondrial CoA. The regenerated carnitine returns to the cytoplasm, and the fatty acyl-CoA is now positioned for β-oxidation.

Regulation: The Malonyl-CoA Switch

The carnitine shuttle provides an elegant mechanism for reciprocal regulation of fatty acid synthesis and oxidation. In the fed state, high insulin activity stimulates acetyl-CoA carboxylase, producing malonyl-CoA. This malonyl-CoA allosterically inhibits CPT-I, blocking fatty acid entry into mitochondria even if fatty acids are available. Simultaneously, the malonyl-CoA provides building blocks for fatty acid synthesis—the cell commits to storage rather than oxidation.

In the fasted state, glucagon and epinephrine inhibit ACC through phosphorylation, malonyl-CoA levels fall, and CPT-I inhibition is relieved. Fatty acids can now enter mitochondria for oxidation. This reciprocal regulation prevents the wasteful futile cycle of simultaneously synthesizing and degrading fatty acids.

<image>Panel A: Fatty acyl-CoA synthetase in cytoplasm activating fatty acid with ATP to AMP + PPi producing fatty acyl-CoA. Panel B: CPT-I (green) on inner membrane outer surface transferring acyl group to carnitine (blue) producing acyl-carnitine, releasing CoA. Panel C: Carnitine-acylcarnitine translocase (purple channel) antiport exchange with acyl-carnitine entering matrix and free carnitine exiting. Panel D: CPT-II (red) transferring acyl to matrix CoA for beta-oxidation with malonyl-CoA inhibition of CPT-I (red X) regulatory callout.</image>

IV. β-Oxidation of Fatty Acids

Once inside the mitochondrial matrix, fatty acyl-CoA undergoes β-oxidation—so named because oxidation occurs at the β-carbon (carbon 3) of the fatty acid chain. This cyclic pathway progressively shortens the fatty acid chain by two carbons per cycle, releasing acetyl-CoA and generating reduced coenzymes (NADH and FADH₂) for ATP synthesis.

The Four Reactions of Each Cycle

Each cycle of β-oxidation consists of four enzymatic reactions that modify the β-carbon.

The first oxidation step, catalyzed by acyl-CoA dehydrogenase, introduces a trans double bond between the α and β carbons. FAD serves as the electron acceptor, being reduced to FADH₂. Multiple acyl-CoA dehydrogenase isoenzymes exist with different chain-length specificities: VLCAD for very long chains (C12-C22), LCAD for long chains (C12-C18), MCAD for medium chains (C4-C12), and SCAD for short chains (C4-C6).

Hydration, catalyzed by enoyl-CoA hydratase, adds water across the double bond to form L-3-hydroxyacyl-CoA.

The second oxidation, catalyzed by L-3-hydroxyacyl-CoA dehydrogenase, oxidizes the hydroxyl group to a ketone, generating NADH.

Finally, thiolysis (catalyzed by thiolase, also called β-ketothiolase) cleaves the bond between the α and β carbons in the presence of CoA-SH, releasing acetyl-CoA and leaving a fatty acyl-CoA shortened by two carbons. This shortened acyl-CoA reenters the cycle.

Energy Yield from β-Oxidation

Each cycle produces one FADH₂ (approximately 1.5 ATP via the electron transport chain), one NADH (approximately 2.5 ATP), and one acetyl-CoA (approximately 10 ATP when oxidized through the TCA cycle and oxidative phosphorylation). A 16-carbon palmitate molecule requires seven cycles of β-oxidation, ultimately producing eight acetyl-CoA, seven FADH₂, and seven NADH.

Calculating the total ATP yield from complete palmitate oxidation: 8 acetyl-CoA × 10 ATP = 80 ATP; 7 FADH₂ × 1.5 ATP = 10.5 ATP; 7 NADH × 2.5 ATP = 17.5 ATP. The gross total is 108 ATP. Subtracting the 2 ATP equivalents consumed during initial activation (ATP → AMP + PPᵢ) yields a net of 106 ATP per palmitate molecule—compared to 30-32 ATP from glucose, highlighting the energy density of fatty acids.

<image>Panel A: Step 1 oxidation with acyl-CoA dehydrogenase (FAD to FADH2) producing trans-enoyl-CoA with double bond (red) at beta-carbon. Panel B: Step 2 hydration adding H2O producing L-3-hydroxyacyl-CoA with hydroxyl (blue) and step 3 oxidation (NAD+ to NADH) producing 3-ketoacyl-CoA with ketone (yellow). Panel C: Step 4 thiolysis with CoA-SH cleaving to produce acetyl-CoA (exiting to TCA cycle) and shortened acyl-CoA recycling. Panel D: Summary box showing per cycle yield (1 FADH2, 1 NADH, 1 acetyl-CoA = 14 ATP) with palmitate C16 to 7 cycles to 8 acetyl-CoA.</image>

V. Variations in β-Oxidation

Odd-Chain Fatty Acids

Most naturally occurring fatty acids have even numbers of carbons, but odd-chain fatty acids (found in some plant oils, fish, and ruminant fat) require special handling. β-Oxidation proceeds normally until the final three-carbon unit, which cannot be cleaved into two acetyl-CoA molecules. Instead, the product is propionyl-CoA.

Propionyl-CoA is converted to succinyl-CoA through a three-step pathway. Propionyl-CoA carboxylase (biotin-dependent) carboxylates propionyl-CoA to D-methylmalonyl-CoA. Methylmalonyl-CoA racemase converts the D-isomer to L-methylmalonyl-CoA. Finally, methylmalonyl-CoA mutase (vitamin B₁₂-dependent) rearranges L-methylmalonyl-CoA to succinyl-CoA, which enters the TCA cycle. This pathway represents an anaplerotic input—unlike acetyl-CoA, the carbons from propionyl-CoA can contribute to net glucose synthesis.

Unsaturated Fatty Acids

Unsaturated fatty acids contain one or more double bonds that may not be in the correct position or configuration for the standard β-oxidation enzymes. Additional enzymes are required: enoyl-CoA isomerase repositions double bonds from the cis-Δ³ position to the trans-Δ² position required by enoyl-CoA hydratase; 2,4-dienoyl-CoA reductase handles polyunsaturated fatty acids by reducing one double bond. These extra steps bypass one FADH₂ production, slightly reducing ATP yield from unsaturated fatty acids.

Very Long-Chain Fatty Acids and Peroxisomes

Fatty acids longer than about 22 carbons cannot be handled by the mitochondrial β-oxidation system. These very long-chain fatty acids (VLCFAs) undergo initial chain-shortening in peroxisomes. Peroxisomal β-oxidation uses different enzymes, and notably, the first oxidation step transfers electrons directly to oxygen, producing hydrogen peroxide (H₂O₂) rather than FADH₂—making peroxisomal oxidation less energy-efficient. Once shortened to medium-chain length, the fatty acids exit peroxisomes as acyl-carnitines and complete oxidation in mitochondria.

VI. Ketone Body Metabolism

During prolonged fasting, starvation, or uncontrolled diabetes, the liver produces ketone bodies—water-soluble molecules that provide an alternative fuel for tissues including the brain.

The Three Ketone Bodies

The ketone bodies are acetoacetate, β-hydroxybutyrate, and acetone. Strictly speaking, β-hydroxybutyrate is not a ketone (it has a hydroxyl group instead), but it is grouped with the ketones metabolically. β-Hydroxybutyrate is the most abundant circulating ketone body. Acetone, produced by spontaneous decarboxylation of acetoacetate, is volatile and exhaled—it produces the fruity breath odor characteristic of diabetic ketoacidosis.

Ketogenesis: When and Why

Ketogenesis occurs exclusively in the liver, specifically in hepatic mitochondria. It becomes active when two conditions coincide: first, fatty acid oxidation is high, generating abundant acetyl-CoA; second, the TCA cycle cannot accommodate all this acetyl-CoA because oxaloacetate has been diverted to gluconeogenesis.

During fasting, glucagon stimulates lipolysis in adipose tissue, flooding the liver with fatty acids. Hepatic β-oxidation proceeds vigorously. Simultaneously, glucagon activates gluconeogenesis, consuming oxaloacetate to make glucose for tissues that cannot use fatty acids (brain, red blood cells). With oxaloacetate depleted, acetyl-CoA cannot enter the TCA cycle efficiently. The excess acetyl-CoA is shunted to ketone body synthesis.

The pathway begins when two acetyl-CoA molecules condense to form acetoacetyl-CoA (thiolase). HMG-CoA synthase then adds a third acetyl-CoA to form 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA). HMG-CoA lyase cleaves HMG-CoA to release acetoacetate and regenerate acetyl-CoA. Acetoacetate can be reduced by β-hydroxybutyrate dehydrogenase to β-hydroxybutyrate (using NADH), establishing an equilibrium that favors β-hydroxybutyrate when the mitochondrial NADH/NAD⁺ ratio is high. HMG-CoA synthase is the rate-limiting enzyme for ketogenesis.

Ketone Body Utilization

Ketone bodies produced by the liver are released into the bloodstream and taken up by peripheral tissues, particularly brain, heart, skeletal muscle, and kidney. Critically, the liver itself cannot use ketone bodies—it lacks succinyl-CoA:3-oxoacid-CoA transferase (SCOT), the enzyme required for activation.

In peripheral tissues, β-hydroxybutyrate is oxidized back to acetoacetate. SCOT transfers CoA from succinyl-CoA to acetoacetate, forming acetoacetyl-CoA. Thiolase then cleaves acetoacetyl-CoA to two acetyl-CoA molecules that enter the TCA cycle. The brain normally relies on glucose but can adapt to derive 50-75% of its energy from ketone bodies during prolonged fasting—a critical survival adaptation.

<image>Panel A: Liver ketogenesis with two acetyl-CoA forming acetoacetyl-CoA via thiolase, then HMG-CoA synthase (rate-limiting) adding third acetyl-CoA. Panel B: HMG-CoA lyase releasing acetoacetate and beta-hydroxybutyrate dehydrogenase reducing to beta-hydroxybutyrate with "liver lacks SCOT" note. Panel C: Peripheral tissues (brain, heart, muscle icons) ketolysis reversing pathway via SCOT producing acetyl-CoA for TCA cycle. Panel D: Physiological context box explaining fasting gluconeogenesis depletes oxaloacetate shunting acetyl-CoA to ketogenesis.</image>

VII. Regulation of Lipid Metabolism

The opposing pathways of lipid metabolism—synthesis versus oxidation—are coordinated by hormonal signals that reflect the body's nutritional state.

Fed State: Insulin Dominance

After a meal, elevated blood glucose stimulates insulin secretion from pancreatic β-cells. Insulin promotes energy storage and macromolecule synthesis while inhibiting catabolic pathways.

Insulin activates acetyl-CoA carboxylase (ACC) through dephosphorylation, increasing malonyl-CoA production. This has two consequences: malonyl-CoA provides substrate for fatty acid synthesis, and it inhibits CPT-I, blocking fatty acid oxidation. Insulin also promotes expression of lipogenic enzymes (ACC, FAS) through activation of transcription factor SREBP-1c.

In adipose tissue, insulin inhibits hormone-sensitive lipase (HSL), preventing triglyceride breakdown and fatty acid release. It also activates lipoprotein lipase on capillary endothelium, promoting uptake of dietary triglycerides from chylomicrons and VLDL.

The net effect: dietary carbohydrates are converted to fatty acids, transported as VLDL to adipose tissue, and stored as triglycerides.

Fasted State: Glucagon and Catecholamine Dominance

During fasting, falling glucose levels decrease insulin and increase glucagon. Sympathetic activation releases epinephrine during stress or exercise.

Glucagon and epinephrine, acting through cAMP and protein kinase A (PKA), phosphorylate and inactivate ACC. Malonyl-CoA levels fall, relieving CPT-I inhibition and allowing fatty acid entry into mitochondria for β-oxidation. Simultaneously, PKA phosphorylates and activates hormone-sensitive lipase in adipose tissue, stimulating triglyceride hydrolysis and releasing fatty acids into the circulation.

In the liver, low malonyl-CoA permits hepatic β-oxidation, generating acetyl-CoA. With oxaloacetate diverted to gluconeogenesis, excess acetyl-CoA drives ketogenesis. Ketone bodies are exported to provide fuel for extrahepatic tissues, sparing glucose for tissues that absolutely require it.

<image>Panel A: Fed state with citrate shuttle exporting acetyl-CoA, ACC active (dephosphorylated) producing malonyl-CoA, FAS synthesizing palmitate for VLDL export. Panel B: Fed state malonyl-CoA inhibiting CPT-I (red X), adipose lipoprotein lipase active, HSL inactive, triglycerides accumulating. Panel C: Fasted state with adipose HSL phosphorylated/active releasing fatty acids, liver CPT-I active (low malonyl-CoA), beta-oxidation generating acetyl-CoA. Panel D: Ketogenesis from acetyl-CoA (limited TCA due to gluconeogenesis) with insulin/glucagon seesaw graphic and enzyme phosphorylation status.</image>

VIII. Clinical Correlations

Diabetic Ketoacidosis (DKA)

Diabetic ketoacidosis represents the extreme consequence of uncontrolled lipid mobilization. In type 1 diabetes, absolute insulin deficiency combined with elevated glucagon creates a metabolic state mimicking severe starvation despite hyperglycemia. Lipolysis is maximally activated, flooding the liver with fatty acids. Hepatic β-oxidation and ketogenesis proceed at overwhelming rates.

Acetoacetate and β-hydroxybutyrate are moderately strong acids that consume buffer capacity, producing metabolic acidosis with a high anion gap. Patients present with Kussmaul respirations (deep, rapid breathing to blow off CO₂ and compensate for acidosis), fruity breath odor (acetone), altered mental status, and severe dehydration from osmotic diuresis. Treatment requires insulin (to suppress lipolysis and ketogenesis), fluid replacement, and careful electrolyte management.

Medium-Chain Acyl-CoA Dehydrogenase (MCAD) Deficiency

MCAD deficiency is the most common inherited disorder of fatty acid oxidation, affecting approximately 1 in 15,000 births. MCAD catalyzes the first oxidation step for medium-chain fatty acids (C6-C12). Patients can oxidize long-chain fatty acids until they are shortened to medium-chain length, at which point β-oxidation halts and medium-chain acyl-carnitines accumulate.

Clinical presentation typically occurs in infancy during a fasting episode (often precipitated by an intercurrent illness). Unable to complete fatty acid oxidation, the child cannot generate ketone bodies normally (hypoketotic hypoglycemia—low glucose without the expected elevation of ketones). Hypoglycemia can cause seizures, coma, or sudden death. Diagnosis is by newborn screening (elevated octanoylcarnitine on blood spot) or acylcarnitine profile. Treatment involves avoiding fasting through frequent feeding and carbohydrate supplementation during illness.

Carnitine Deficiency and CPT Deficiencies

Primary carnitine deficiency results from mutations in the OCTN2 transporter that reabsorbs carnitine in the kidney. Without sufficient carnitine, long-chain fatty acids cannot enter mitochondria, causing progressive cardiomyopathy and muscle weakness. Treatment with carnitine supplementation is effective if started before irreversible damage.

CPT-I deficiency affects primarily the liver isoform, impairing hepatic fatty acid oxidation. Patients present with hypoketotic hypoglycemia during fasting, similar to MCAD deficiency.

CPT-II deficiency has several forms. The adult myopathic form presents with episodes of muscle pain, rhabdomyolysis, and myoglobinuria triggered by prolonged exercise, fasting, or cold exposure. The severe infantile form causes liver failure, cardiomyopathy, and early death.

Zellweger Syndrome

Zellweger syndrome represents the severe end of the peroxisome biogenesis disorder spectrum. Without functional peroxisomes, patients cannot oxidize very long-chain fatty acids, synthesize plasmalogens, or metabolize certain bile acid intermediates. VLCFAs accumulate in tissues and plasma.

Affected infants have severe hypotonia, seizures, distinctive facial features, liver dysfunction, and fail to thrive. Death typically occurs in the first year of life. Diagnosis is confirmed by elevated plasma VLCFA levels and absent peroxisomes on liver biopsy.

Summary

Lipid metabolism encompasses opposing pathways that operate reciprocally depending on the body's nutritional state. Fatty acid synthesis (lipogenesis) occurs in the cytoplasm, primarily in liver, using acetyl-CoA transported from mitochondria via the citrate shuttle. Acetyl-CoA carboxylase is the rate-limiting enzyme, producing malonyl-CoA for chain elongation by fatty acid synthase. The carnitine shuttle transports long-chain fatty acyl-CoA into mitochondria for β-oxidation, with CPT-I as the rate-limiting step inhibited by malonyl-CoA. Each cycle of β-oxidation removes two carbons as acetyl-CoA while generating NADH and FADH₂. Complete oxidation of palmitate yields 106 net ATP—far more than glucose. During prolonged fasting, when acetyl-CoA exceeds TCA cycle capacity, the liver produces ketone bodies for export to brain and other tissues. Insulin promotes lipogenesis and inhibits oxidation; glucagon and epinephrine have opposite effects. Clinical disorders include diabetic ketoacidosis, MCAD deficiency, carnitine/CPT deficiencies, and peroxisomal disorders.

Key Terms

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