Fatty Acid Synthesis and Regulation Quiz

Lipid Metabolism

• Lipids, primarily triacylglycerols (TAGs), constitute ~95% of dietary lipids.
• The remaining 5% consists of sterols (mainly cholesterol), and phospholipids.
• Cholesterol exists mostly as free cholesterol, while ~10-15% is in the form of cholesterol esters.

Digestion and Absorption of Lipids

• Lingual lipase in the mouth primarily targets short- or medium-chain fatty acids (in milk fat). Its activity decreases with age but is high in neonates.
• Gastric lipase in the stomach acts on lipids, which need emulsification, requiring emulsifiers like polysaccharides, phospholipids, and proteins. Its optimal pH is 4-6.
• The presence of fat in the stomach triggers the release of hormones like CCK, secretin, GIP, and GLP-1. These hormones regulate pancreatic and gallbladder function.
• Mechanical mixing by peristalsis and detergent properties of bile salts emulsify hydrophobic fat droplets, increasing the surface area for enzyme action in the small intestine. Phospholipids also contribute to emulsification.
• Bile acids/bile salts are synthesized in the liver from cholesterol, stored in the gallbladder, and released into the small intestine to aid lipid digestion and absorption.

Digestion of Lipids

• Pancreatic lipase is released into the duodenum and activated by calcium and colipase.
• Pancreatic lipase removes fatty acids from TAGs containing long-chain fatty acids, yielding fatty acids and 2-monoacylglycerol.
• Cholesteryl esterase produces cholesterol and free fatty acids. Activity is enhanced by bile salts.
• Phospholipases (A₁, A₂) act on phospholipids, removing fatty acids and forming lysophospholipids.
• Lysophospholipids are further degraded by lysophospholipase A₁.

Absorption of Lipids by Intestinal Mucosal Cells

• Free fatty acids, free cholesterol, 2-monoacylglycerol, and lysophospholipids form micelles in the aqueous environment of the small intestine.
• Micelles are absorbed at the brush border of enterocytes.
• Fatty acids with short/medium chain length do not require micelles for absorption.
• Products are absorbed and resynthesized into TAGs, cholesteryl esters, and phospholipids within enterocytes.

Resynthesis of Triacylglycerols/Phospholipids/Cholesteryl Ester

• In enterocytes, free fatty acids are converted to fatty acyl-CoA.
• Triacylglycerols are synthesized from 2-monoacylglycerol and fatty acyl-CoA, utilizing monoacylglycerol acyltransferase and diacylglycerol acyltransferase.
• Phospholipids are formed by reacylation of lysophospholipids.
• Cholesteryl esters are formed by acyl-CoA:cholesterol acyltransferase.

Absorption of Bile Salts

• Bile salts remain in the intestinal lumen, and are absorbed in the distal ileum by an active transport mechanism utilizing Na-bile salt co-transport.

Lipid Malabsorption (Steatorrhea)

• Steatorrhea is characterized by the increased excretion of lipids and fat-soluble vitamins in feces (over 5g/day).
• This can be caused by defects in the digestion and/or absorption of lipids.

Secretion of Lipids from Enterocytes

• Chylomicrons are synthesized in enterocytes from TAGs, cholesterol esters, and phospholipids, surrounded by apolipoproteins.
• Chylomicrons are released into lacteals (lymph).
• Lymph containing chylomicrons drains into the bloodstream.

Chylomicrons

• Chylomicrons are assembled in intestinal mucosal cells.
• Chylomicrons have the lowest density and are the largest.
• TG is the highest percentage of lipids and have the lowest percentage of proteins in chylomicrons.
• they carry dietary lipids to peripheral tissues and are responsible for the milky appearance of plasma shortly after a meal.

Metabolism of Chylomicrons

• Nascent chylomicrons acquire apo C-II and apo E from HDL in the plasma.
• Lipoprotein lipase, activated by apo C-II and located on capillary walls, degrades TAG into free fatty acids and glycerol.
• The chylomicron remnant, with apo E, is taken up by the liver. In the liver, lysosomal enzymes degrade all components returning the amino acids, free cholesterol, and fatty acids.
• The receptor is recycled.

Fate of Fatty Acids

• Fatty acids are oxidized in various tissues to produce energy.
• Glycerol is processed by the liver to form glycerol 3-phosphate which enters pathways for energy production (glycolysis or gluconeogenesis).

Oxidation of Fatty Acids

• Fatty acid oxidation typically proceeds in three stages.

Functions of Fatty Acid Oxidation

• Fatty acid oxidation provides energy for cellular and metabolic work.
• Fatty acid oxidation in various tissues provides energy.

Oxidation of Fatty Acids in Tissues

• All tissues except red blood cells and brain use fatty acids for energy.
• Skeletal and heart muscle significantly rely on fatty acids for energy production.

Physiological Conditions for Fatty Acid Oxidation

• In the fasted state, fatty acid oxidation increases due to the depletion of glycogen in the liver and the need for glucose production.
• During prolonged exercise or physical activities, fatty acid oxidation plays a significant role in providing energy.

Transport of Fatty Acids

• Fatty acyl-CoA synthetase is required for the activation into fatty acyl CoA to be transported into the mitochondria.
• FAT/CD36 is a key transporter in the heart, skeletal muscles, adipocytes, and the intestine.

Activation of Free Fatty Acids

• Fatty acids are activated to fatty acyl-CoA before metabolism.
• Acyl-CoA synthetases are located in the cytosol, endoplasmic reticulum, mitochondria, and peroxisomal membranes.

Types of Fatty Acid Oxidation

• Fatty acid oxidation occurs in three ways: α-oxidation, β-oxidation and ω-oxidation.

Transport of Long-chain Fatty Acids into Mitochondria

• Beta-oxidation takes place within the mitochondrial matrix.
• The inner mitochondrial membrane is impermeable to CoA.
• Specialized carriers (carnitine) are necessary for long-chain acyl groups to be carried from cytosol to mitochondria.
• The process is called the carnitine shuttle.

Steps in LCFA Transport

• Fatty acyl CoA reacts with carnitine, catalyzed by carnitine acyltransferase 1 (CAT-I), to produce fatty acyl carnitine and CoA.
• The resulting acyl carnitine crosses the inner mitochondrial membrane.

Regulation of CAT-I

• CAT-I is a rate-limiting enzyme in fatty acid oxidation.
• Malonyl CoA, an intermediate in fatty acid synthesis, allosterically inhibits CAT-I to regulate both processes simultaneously.

Steps in LCFA Transport

• Fatty acyl carnitine, inside the mitochondrial matrix, reacts with CoA, catalyzed by carnitine acyltransferase II (CAT-II), forming fatty acyl CoA and carnitine.
• The fatty acyl CoA is then available for beta-oxidation.

Carnitine Shuttle

• Long-chain fatty acyl CoA is transported from the outside of the mitochondria to the inside.
• Carnitine-acylcarnitine translocase is used to facilitate this exchange.

Sources of Carnitine

• Carnitine can be obtained from the diet or synthesized in the liver and kidneys from lysine and methionine.

Carnitine Deficiencies

• Primary deficiencies, like CAT-I/II deficiency, can cause severe metabolic problems and even death, especially during fasting.
• Secondary deficiencies may arise from various medical conditions or nutritional imbalances.

Entry of Short/Medium Chain FA into Mitochondria

• Carnitine and CAT systems are not needed for short (under 12 carbon) chain FAs.
• FAs are activated into their CoA forms within the mitochondrial matrix

Reactions of Beta-Oxidation

• Beta-oxidation is the process to successively remove two-carbon units in the form Acetyl-CoA from the carboxyl end of the fatty acyl chain.
• The products of beta-oxidation are Acetyl-CoA, FADH₂, and NADH+.

Four Steps of Beta-Oxidation

• The process is repeated four times four steps until the fatty acyl chain is entirely broken down to acetyl-CoA.

1. Dehydrogenation
2. Hydration
3. Oxidation
4. Thiolysis

Types of Fatty Acyl-CoA Dehydrogenases

• Different enzymes for various chain lengths are responsible for dehydrogenation reactions in fatty acid oxidation (LCAD>12 carbon; MCAD 6-12 carbons; SCAD 4-6 carbons).

Reaction Products

• Acetyl-CoA is oxidized through the citric acid cycle to produce CO₂ and H₂O.
• FADH₂ and NADH+ are oxidized by mitochondrial electron transport system (ETS) yielding ATP.

Fate of the FADH₂ and NADH+ H⁺

• The reduced coenzymes (FADH₂ and NADH+) transfer their electrons to the mitochondrial electron transport system.
• Electrons moved down the chain to generate ATP.

Energy Yield from Beta-Oxidation of Palmitic Acid

• Complete oxidation of a 16-carbon palmitic acid molecule yields 129 ATP.

Oxidation of Unsaturated Fatty Acids

• Unsaturated fatty acids undergo β-oxidation but with additional steps to handle the presence of double bonds.

1. Some unsaturated fatty acids (specifically those with a double bond at an odd numbered carbon) need a specific isomerase enzyme to correct the bonding before proper oxidation can proceed.
2. Other unsaturated fatty acids require an additional enzyme (2,4-dienoyl CoA reductase) given additional unsaturation/double bonds at the odd numbered carbons.

Alpha Oxidation

• Alpha oxidation is a process of removing one carbon atom from the carboxyl end of branched-chain fatty acids.
• The process occurs in the endoplasmic reticulum using a monoxygenase enzyme, consuming oxygen and releasing CO₂ and H₂O.

Phytanic Acid

• Phytanic acid is a 20-carbon branched-chain fatty acid.
• It is an oxidation product phytol (from chlorophyll) present in animal fat and milk products.
• The oxidation of phytanic acid is crucial to metabolize it to a less-toxic form in mammals.

Refsum's Disease

• Refsum's disease is caused by a deficiency in phytanate alpha-hydroxylase and leads to phytanic acid buildup within the body's tissues.

Omega Oxidation

• Omega oxidation is a pathway for fatty acid degradation where the initial oxygenation occurs at the terminal methyl group or omega carbon of the fatty acid chain.
• In this process, the terminal methyl group gets converted to an alcohol molecule and finally to a carboxalic acid molecule.
• The dicarboxylic acids thus produced can then undergo B-oxidation to yield other metabolites.

Regulation of Beta-Oxidation

• The rate of beta-oxidation is primarily governed by the availability of fatty acids. The presence of malonyl-CoA, an intermediate in fatty acid biosynthesis, allosterically inhibits carnitine acyltransferase I (CAT I).
• Other factors that can regulate the rate are insulin and glucagon, which alter the rate of lipolysis, the release of fatty acids from storage sites.

Fatty Acid Oxidation During Fasting

• During fasting, stored triacylglycerols in adipocytes are hydrolyzed to release fatty acids.
• Fatty acids released from adipocytes are transported to the liver, where they are subsequently oxidized.
• These released fatty acids can also be used by tissues such as the heart muscle, brain, and renal cortex for fuel.

Fatty Acid Oxidation in the Fed State

• In a well-fed state (high carbohydrate/energy intake), fatty acid synthesis is upregulated, while fatty acid oxidation is downregulated.
• The high energy/carbohydrate intake provides substrates readily available for synthesis, and the lower level of fatty acids reduces the demand for oxidation.

Role of Insulin in Fatty Acid Synthesis

• Insulin plays a critical role in regulating both lipogenesis and lipolysis.
• It stimulates glucose uptake into adipose tissues, and, in turn, promotes the generation of substrates like glycerol 3-phosphate and acetyl-CoA for fatty acid synthesis.
• Conversely, high insulin levels have an inhibitory effect on lipolytic processes by attenuating the signaling pathways activated by glucagon or other counter-regulatory hormones, leading to a decreased release of fatty acids to the blood stream.

Fatty Acid Elongation

• Palmitate is the primary precursor for the synthesis of longer chain fatty acids.
• The process of fatty acid elongation primarily occurs in the endoplasmic reticulum.

Biosynthesis of Unsaturated Fatty Acids

• Palmitate and stearate are the precursors for the synthesis of unsaturated fatty acids like palmitoleate and oleate in animal cells.
• The introduction of double bonds is catalyzed by fatty acyl-CoA desaturases.

Essential Fatty Acids

• Some unsaturated fatty acids (e.g., linoleic acid, α-linolenic acid) are essential, meaning the body cannot synthesize them and they must be obtained from the diet.
• Essential fatty acids serve as precursors for other unsaturated fatty acids and eicosanoids.

Eicosanoids

• Eicosanoids are 20-carbon lipid-derived molecules that play crucial roles as cell-to-cell signals.
• They are synthesized from the fatty acid precursor arachidonic acid and their production is tightly regulated to prevent unwanted effects.

Main Sites of Eicosanoid Biosynthesis

• Eicosanoids are produced in various cell types, including endothelial cells, leukocytes, platelets, and kidneys.

Main Steps of Eicosanoid Biosynthesis

• PLA₂ activation releases arachidonate.
• The COX or LO pathway, with subsequent modifications, produces various eicosanoids.

Phospholipase A2 Activation

• Several factors, like cytokines, hormones, and other local mediators activate the release of arachidonate through their effects on PLA-2 activity.
• Release of arachidonate from the membrane phospholipids is catalyzed by PLA-2 activity.

Arachidonate Release

• Arachidonate can be released from membrane phospholipids by PLA-2 activation.

Eicosanoid Biosynthesis Pathways

• Eicosanoids are synthesized through different pathways:
• COX (cyclooxygenase) pathway: produces prostaglandins and thromboxanes.
• LO (lipoxygenase) pathway: produces leukotrienes, lipoxins, and HETEs.
• CYP450 pathway: produces epoxyeicosatrienoic acids (EETs) and HETEs.

Cyclooxygenase (COX) Pathway

• The COX pathway uses the fatty acid precursor arachidonic acid to produce prostaglandins and thromboxanes.
• Cyclooxygenase catalyzes the addition of two molecules of oxygen to arachidonic acid to form PGG2, which is converted to PGH2 by hydroperoxidase.

Prostaglandin H Synthase

• Prostaglandin H synthase (PGHS) is an enzyme in the COX pathway consisting of two isoforms that produce prostaglandins and thromboxanes.
• Aspirin inhibits the enzyme activity in a vital step that produces PGH2.

Products of the COX Pathway

• Platelets use thromboxane synthase from PGH2 to produce thromboxanes (TXA2, TXB2).
• Vascular endothelial cells produce prostacyclin synthase, converting PGH2 into prostacyclin (PGI₂).

Inhibition of the COX Pathway

• Aspirin inhibits COX enzymes by acetylating a specific serine residue.

Lipoxygenase (LOX) Pathway

• The LOX pathway uses arachidonic acid and produces various metabolites like leukotrienes, lipoxins, and HETEs.
• The main enzymes involved are lipoxygenases, with different types acting on different portions of the arachidonate molecules.

Peptidoleukotrienes Biosynthesis

• Peptidoleukotrienes are short-lived lipid signaling molecules produced mainly through 5-lipoxygenase activity. They display various important roles and have potent biological effects.

Eicosanoid Synthesis by CYP450s

• Cytochrome P450s (CYP450s) are monooxygenases that produce several hydroxyeicosatetraenoic acids (HETEs) and epoxyeicosatrienoic acids (EETs) during eicosanoid synthesis.
• Two classes of products result including epoxyeicosatrienoic acids (EETs) which are further metabolized by epoxide hydrolases to dihydroxyeicosatrienoic acids (DiHETEs), and HETEs.

Structural Features of the Various Metabolic Products

• Prostaglandins have a cyclopentane ring structure.
• Thromboxanes have a six-membered oxygen-containing ring structure.
• Leukotrienes have three conjugated double bonds plus an additional unconjugated double bond.
• Lipoxins consist of conjugated trihydroxytetraenes.

Prostaglandin Nomenclature

• The three classes of prostaglandins (A, E, and F) are distinguished by the functional groups around the cyclopentane ring.
• Subscripts provide information concerning the number of double bonds and the configuration of the 9-OH group.

Biological Effects of Eicosanoids

• Eicosanoids regulate diverse physiological functions, mainly by interacting with specific receptors, and, in turn, controlling numerous metabolic pathways.
• Biological effects vary depending on several factors including the type of eicosanoid(s), local concentration (because they have short half-lives), type of receptors, and availability of receptors themselves.

Mechanisms of Action of Eicosanoids

• Eicosanoids exert their effects through interactions with specific receptors.
• They bind to either the same cell that synthesized them (autocrine effect) or to neighboring cells (paracrine effect).
• The signaling pathway involved depends on the type of receptor and the consequent activation/inhibition of specific intracellular signals.

Effects of Prostaglandins

• Prostaglandins mediate inflammation, regulate pain and fever, regulate blood pressure, and are involved in blood clotting and other reproductive processes.

Biological Role of Thromboxanes

• Thromboxanes primarily mediate vasoconstriction and platelet aggregation.

Biological Role of Leukotrienes

• Leukotrienes are potent constrictors of the bronchial airways, increasing vascular permeability and leukocyte attraction and activating various other cell defense and damage processes during inflammation.

Biological Roles of Lipoxins

• Lipoxins are unlike other eicosanoids in that they limit inflammatory reactions.

Biological Effects of HETEs

• HETEs participate in host defenses (bacterial infection) and influence blood pressure regulation (vasoconstriction), and participate in controlling renal function.

Biological Roles of Hepoxilins

• Hepoxilins have effects on glucose-induced insulin secretion.
• They are thought to have a compensatory effect during oxidative stress by potentially elevating glutathione peroxidase levels to better protect cells.

Biosynthesis of Triacylglycerols

• The synthesis of triacylglycerols (TAGs) is a process that occurs in most tissues, including the liver and adipocytes.
• The pathway primarily utilizes glycerol 3-phosphate and fatty acyl-CoAs
• Activated fatty acids are derived from several sources:
• Dietary fats
• Endogenous synthesis
• Different substrates and enzymes are used by the small intestine vs the primary tissues.

Synthesis of Glycerol Phosphate

• Glycerol kinase catalyzes the process in the Liver when excess glucose or glycerol are present. This produces glycerol phosphate as substrate for TAG synthesis
• In adipose tissue, elevated glucose levels and consequent insulin secretion are necessary to obtain the substrate glycerol phosphate for TAG synthesis

Formation of Activated Free Fatty Acids

• Long-chain fatty acids are converted to fatty acyl-CoA for participation in triacylglycerols (TAG) synthesis.
• Fatty acyl-CoA synthetase catalyzes this conversion.

Synthesis of a Molecule of TAG

• This intricate process includes several steps:

1. Combining glycerol phosphate with a fatty acyl-CoA to form lysophosphatidic acid.
2. The removal of CoA from lysophosphatidic acid, forming phosphatidic acid.
3. The formation of diacylglycerol (DAG).
4. The combination of DAG with the third fatty acyl-CoA yielding triacylglycerol (TAG).

Fate of TAGs in Liver and Adipose Tissues

• Adipose tissue: TAGs are stored within the cytosol of adipocytes.
• Liver: TAGs are mostly packaged into VLDLs, which transport these lipids to peripheral tissues.

Synthesis of Phospholipids

• Glycerophospholipids are synthesized in most cells (excluding mature red blood cells) within the endoplasmic reticulum and the Golgi complex. Liver is a major site of phospholipid synthesis.
• Several types of phospholipids can be synthesized depending on the head groups from a phosphatidic acid backbone

Synthesis of Phosphatidylcholine (PC)

• PC is a key phospholipid in the body and its synthesis can take various pathways.
• In most cells, choline is a substrate for PC; in the liver another pathway is possible starting with phosphatidylserine.

Synthesis of Phosphatidylethanolamine (PE)

• Ethanolamine, obtained from the diet or from other precursor molecules, is phosphorylated and subsequently attached to diacylglycerol.

Synthesis of Phosphatidylserine (PS)

• PE reacts with serine to form PS via PE-serine transferase, which is a base exchange reaction.

Synthesis of Phosphatidylinositol (PI)

• CDP-diacylglycerol reacts with inositol to form phosphatidylinositol, by an enzyme called PI synthase.

Synthesis of Cardiolipin

• Cardiolipin is synthesized from two phosphatidic acid molecules and one glycerol molecule. It can be found in various tissues.

Synthesis of Plasmalogens

• Plasmalogens are one type of phospholipids in which the fatty acid at position 1 of glycerol is linked through an ether linkage, not an ester linkage

Degradation of Phospholipids

• Phospholipases (A₁, A₂, C, and D) are the key enzymes involved in the degradation of phospholipids.

Degradation of Sphingomyelin/Glycosphingolipids

• Sphingomyelin and glycosphingolipids are broken down by lysosomal enzymes, such as sphingomyelinase and ceramidase for sphingomyelin.

Sphingolipidoses

• Sphingolipidoses are a group of inherited metabolic disorders associated with the accumulation of specific sphingolipids in lysosomes.
• Gaucher disease, Niemann-Pick disease, and Fabry disease are examples of sphingolipidoses.

Metabolism of Cholesterol

• Cholesterol biosynthesis occurs in most vertebrate cells, predominantly in the liver.
• Sterols are precursors that can be converted into other molecules.
• Cholesterol is derived from the diet (200-300mg/day) and synthesis in the body (700mg/day).
• Liver and Intestine plays major roles in cholesterol regulation and production

Cholesterol Biosynthesis (Steps)

• Mevalonate synthesis from Acetyl-CoA
• Isoprenoid unit production from mevalonate
• Squalene Formation from isoprenoids
• Lanosterol Formation from Squalene
• Cholesterol formation from Lanosterol

Regulation of Cholesterol Synthesis

• The rate of cholesterol synthesis is primarily controlled by HMG-CoA reductase.
• Regulation includes decreased synthesis in starving animals, inhibition by dietary cholesterol, and regulation by hormones like insulin.

Increase and Decrease in Cholesterol

• Increased cholesterol levels can result from uptake of cholesterol-containing lipoproteins via receptors, from synthesis (de novo or from other sources), and from cholesterol ester hydrolysis by enzymes.
• Decreased cholesterol levels might occur from efflux from the membrane, esterification by enzymes (ACAT), utilization for the synthesis of other steroid hormones, or the formation of other molecules (e.g. cholic acid).

Cholesterol Balance in Tissues

• Factors influencing cholesterol levels: dietary fats, cholesterol, carbohydrates, hereditary elements, blood groups, calorie intake, minerals, dietary fibers, physical exercise, individual's lifestyle.

Metabolism of Lipoproteins

• Lipoproteins are complex particles encapsulating lipids within a protein shell, enabling transport throughout the body.
• Several classes are based on density (chylomicrons, VLDL, LDL, HDL) or electrophoretic mobility.

Apolipoproteins

• Different apolipoproteins serve crucial functions in lipoprotein metabolism (e.g., recognition sites, enzyme activators).

Metabolism of VLDL

• VLDL is synthesized by hepatocytes and secreted into the bloodstream after its formation.
• VLDL travels in the bloodstream and is metabolized while being transported by lipoprotein lipase activity.
• This leads to the release of fatty acids and glycerol into peripheral cells. The remaining particle (VLDL-remnants) is eventually taken up by the liver to be further metabolized.

Catabolism of VLDL

• Catabolism of VLDL is similar to chylomicron metabolism, involving lipoprotein lipase, free fatty acid release, and the formation of VLDL remnants (IDL).
• Further metabolism leads to LDL production in the bloodstream.

Metabolism of LDL

• LDL is produced during VLDL degradation and taken up by the arterial tissues and liver.
• LDL is a primary carrier of cholesterol to the cells; their levels in the blood are crucial.
• Cells take up LDL through LDL or other receptors.

Metabolism of HDL

• HDL is synthesized in both the liver and intestines, but apo C and E are synthesized in the liver and are added to HDL in the bloodstream.
• HDL is central in reverse cholesterol transport, removing excess cholesterol from peripheral cells and tissues and returning it to the liver for metabolism or excretion.
• This process involves LCAT (Lecithin-Cholesterol Acyltransferase), which esterifies cholesterol, and other important proteins.

Summary of Lipoprotein Formation and Fate

• Chylomicrons transport dietary lipids to peripheral tissues.
• VLDLs transport endogenous lipids.
• LDL transports cholesterol to peripheral cells.
• HDL mediates reverse cholesterol transport (taking cholesterol back to the liver for use or storage).

Role of HDL in Receptor-Mediated Endocytosis

• HDL contributes apo C and apo E to nascent VLDL and chylomicrons for receptor-mediated uptake by the cells they are transported to.

Clinical Significance of Lipoprotein Metabolism

• Fatty liver results from impaired VLDL secretion, leading to fat accumulation in the liver.

Fatty Liver (Types)

• More synthesis of triglycerides: High carbohydrate/fat diets and Diabetes Mellitus.
• Defective VLDL synthesis: Impaired apo-protein(B) synthesis may not form VLDL effectively leading to fatty liver
• Defects in phospholipids provision: Insufficient choline, methionine, inositol, or essential fatty acids can impede synthesis of phospholipids required for appropriate lipoprotein functioning/formation.
• Impaired glycosylation or improper processing of lipoproteins: Orotic acid.

Test your knowledge of fatty acid synthesis. Questions cover the mechanisms of insulin's effect on fatty acid synthesis, the enzymes involved in fatty acid elongation and desaturation, and the hormonal regulation of lipogenic enzymes. Also covers regulation of acetyl-CoA carboxylase.