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Notes on Chapter 20 through regulation of fatty acid metabolism.

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by: ChasePrater

Notes on Chapter 20 through regulation of fatty acid metabolism. 4510

Marketplace > Middle Tennessee State University > 4510 > Notes on Chapter 20 through regulation of fatty acid metabolism
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These notes cover a big portion of chapter 20. They are a compilation of the powerpoint, notes I take in class, and material from the book. Some of it may be too much detail, if you feel like it is...
Biochemistry II
Dr. Ooi
Class Notes
biochemistry, Lipid Metabolism, metabolism, fatty acid metabolism




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This 6 page Class Notes was uploaded by ChasePrater on Saturday March 19, 2016. The Class Notes belongs to 4510 at Middle Tennessee State University taught by Dr. Ooi in Spring 2016. Since its upload, it has received 103 views.


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Date Created: 03/19/16
Biochem 2 Review 3 Chapter 20: lipid metabolism Triacylglycerols (triglycerides/fats) - Storage and transport form of fats - highly concentrated energy storage molecule, so therefor the major form of energy storage in people - when fully oxideized to CO2 and water, it gives over twice the energy per carbon than glucose. - Stored in adipose tissue, and undergo beta-oxidation to give acetyl CoA, FADH2 and NADH. Lipid Digestion - Takes place at lipid-water interfaces because fats are hydrophobic but enzymes are hydrophilic. - The rate of the reaction is determined by surface area of interface, so bile salts are released to increase the surface area. Bile Salts: - amphipathic cholesterol derivatives made in the liver that act like detergents to break apart big globs of fat in the small intestine into smaller micelles. Pancreatic lipase: - Chops off the fatty acid side chains of triglycerides at the 1 and 3 position to give 2 fatty acids and a monoacylglycerol. - This enzyme works better when it reaches the lipid-water interface, this is called Interfacial activation. - Requires a colipase to bind to C-terminal to make a hydrophobic shelf, which helps it bing lipids. - Colipase also hydrogen bonds to stabilize the open conformation. - Active site in near N-terminal. Absorption of Lipids - Intestinal cells absorb fatty acids via intestinal mucosa, which then form complexes with I-FABP ( intestinal fatty acid binding protein) to protect the cell from the detergent like properties of the fatty acid. - I-FABP also helps to increase fatty acid solubility. Lipid Transport - After fatty acids are absorbed, they are turned back into triglycerides and are then packaged in a type of lipoprotein called a chylomicrons. - Next these are released into the lymph and eventually enter the large veins, which then deliver chylomicrons to other tissues. - They bind to skeletal muscle and adipose tissue where the triglycerides are hydrolyzed by lipoprotein lipase, and the products are taken up by the cell. - The chylomicron remnants (contain cholesterol) are shipped back to liver - Other lipoproteins are VLDL,HDL,IDL, and LDL. - VLDL: carry cholesterol and fat to muscle and adipose tissue where lipoprotein lipase degrades it. Glycerol is oxidized to DHAP, and other remnants are converted to IDL and the LDL(contains mostly just cholesterol). If cells need cholesterol, they either make it or put out LDL receptors. - HDL: removes cholesterol from tissues (does the opposite of LDL). Begin in liver and small intestine, then float around and pick up cholesterol that is on the surface of cells. The picked up cholesterol is dumped in the liver. Fatty Acid Oxidation Activation of fatty acids: Requires one ATP - They have to be activated before they can enter matrix and be oxidized. - Happens on outer mitochondrial membrane, and is catalyzed by acyl-CoA synthetase (thiokinases). - Forms a high energy thioester bond in the acyl-CoA product. Transport across Mito. Membrane - Rate limiting step for fatty acid oxidation. - For long chain fatty acids the acyl group of the acyl-CoA is given to a carnitine in the cytosol. - Then the acyl-carnitine unit is carried into the mito. Matrix by carnitine carrier protein as free carnitine is pumped into cytosol. - Short (2-4) and medium length (4-12) chains do not need carnitine to cross into matrix. - Palmitoyl transferase II transfers the acyl group back to a CoA and frees the canitine. Beta-oxidation - One cycle of four reactions to chop 2 carbons at a time. - 1. Acyl-CoA dehydrogenase (AD) forms trans double bond between alpha and beta carbons. (oxidation that makes FADH2) - 2. Enoyl-CoA hydratase (EH) catalyzes hydration of the double bond forming beta-hydroxyacyl-CoA. (hydration) - 3. beta-hydroxyacyl-CoA undergoes dehydrogenation by 3-L- hydroxyacyl-CoA dehydrogenase (HAD). (oxidation that makes NADH) - 4. Beta-ketoacyl-CoA thiolase (KT or thiolase) cleaves Alpha- beta carbons to form acetyl-CoA and a new chain that is 2 carbons shorter. (cleavage) - Acyl-CoA DH: has three isozymes for short. Medium, amd long chains. It is linked to the electron transport chain. - Completele oxidation of one palmitate has a net yield of 106 ATP. Oxidation of Unsaturated fatty acids 3 Problems - 1. Cis double bond isn’t a substrate for EH. One enzyme (isomerase) is needed to fix the problem. - 2. A double bond at an even carbon isn’t a substrate for EH. Two enzymes are needed to solve this problem. - 3. Sometimes odd number double bonds create a stable conjugated diene. This odd numbered diene must be converted to an even numbered diene by a dienoyl-CoA isomerase. Odd Chain Fatty Acids Last round of beta oxidation gives an acetyl-CoA and a propionyl-CoA, which can be converted to succinyl-CoA. Metabolism of propionyl-CoA: 3 enzymes. - 1. Propionyl-CoA carboxylase requires ATP and a biotin to form S-methymalonyl-CoA. - 2. Methylmalonyl-CoA racemase converts it to R form. - 3. Methylmalonyl-CoA mutase rearranges the carbon skeleton to form succinyl-CoA. - Uses coenzyme B12, which contains a corrin ring with a cobalt center. This cobalt’s 6 ligand is to C5 of deoxyribose, which forms an extremely rare carbon- metal bond. Lack of this coenzyme casues pernicious anemia. - Uses a free radical mechanism. - Succinyl-CoA is converted to pyruvate before it enters TCA cycle. Peroxisomal beta-oxidation Peroxisome - starts oxidation of very long chain fatty acids ( more than 22) - Acyl-CoA synthetase activates chain. - 1. Acyl-CoA oxidase: gives electrons directly to O2 instead of forming FADH2. Since a FADH2 is not entering the ETC, this makes 2 fewer ATP than mitochondrial oxidation. - The rest of the steps are the same as in mitochondrial oxidation. - Peroxisomal thiolase (enzyme of last step) doesn’t work with chains that are 8 or less, so the rest of the chain is converted to canitine esters. They are shipped to mito for further oxidation. Zellweger Syndrome - Casued by a deficit in the import enzymes into peroxisomes - Liver, kidney and muscle problems, and can be fatal. Ketone Bodies - Produced when a surplus of acetyl-CoA is generated from beta oxidation, and what doesn’t enter the TCA cycle gets oxidized to acetoacetate, acetone, or D-beta-hydroxybutyrate. - Are an important fuel source for heart and skeletal muscle - Main fuel source for brain when glucose levels are low (starvation). Formation of Ketone Bodies - 1. Two acetyl-CoA are condensed by thiolase to form acetoacetyl-CoA - 2. A third Acetyl-CoA is condensed by HMG-CoA synthase to form HMG-CoA. Rate limiting step! - 3. HMG-CoA is degraded by HMG-CoA lyase to make acetyl- CoA and acetoacetate. - Acetoacetate can become D-beta-hydroxybutyrate, or acetone and CO2. - This step only uses one NADH. Ketosis - Acetoacetate is made faster than its broken down. - Blood pH drops - Found in people with diabetes because their bodies do not know there is glucose in the blood and thinks you need energy, therefore it makes ketone bodies. Metabolism - Easily broken down - Liver puts acetoacetate and beta-hydroxybutyrate into blood where it is carried to tissues. - Once it reaches the tissues it is condenced with succinyl-CoA to form two acetyl-CoA, which now enter the TCA. Fatty acid biosynthesis Adding 2 carbon units at a time; doing the opposite of beta-oxidation. Takes place in the cytosol of the liver when there is an excess of energy. 3 Stages - Acetyl-CoA leaves mito via tricarboxylate transport system - Acetyl-CoA carboxylase turns it into malonyl-Coa Rate limiting step! - Fatty acid synthase builds the chain. Tricarboxylate transport system - Acetyl-Coa must turn into citrate to be able to leave mito. - Pyruvate and bicarbonate come together to form oxaloacetate (uses ATP), which is then condensed with actetyl-Coa to form citrate using Citrate Synthase. - In cytosol, citrate is turned back into oxaloacetate (OAA) and acetyl-Coa by ATP-citrate lyase (uses ATP). - OAA is then reduced to malate by the enzyme malate dehydrogenase (malate DH) using a NADH. - Malate is decarboxylated to pyruvate with the formation of a NADPH and CO2 by malic enzyme. - Pyruvate is transported back into the mito to complete the cycle. Carboxylation of acetyl-Coa - First committed step and regulatory step of FA synthesis. - Acetyl-CoA carboxylase: requires biotin - Allosterically stimulated by citrate, and inhibited by long chain fatty acyl-Coa’s - inactivated when phosphorylated AMPK, which is activated by ADP and inactivated by ATP. - Hormonal control: Insulin removes phosphate (activiating synthesis); glucagon and epinephrine promote phosphorylation. Assembling FA chain - Acetyl group attaches to a cysteine ACP, and a malonyl group is added to another ACP. - Acetyl group is condensed to the middle carbon of the malonyl group forming acetoacetyl-ACP and CO2. - Beta-ketoacyl-ACP reductase reduces it using NADPH and forms D-isomer - Beta-ketoacyl-ACP dehydrase dehydrates it forming a trans alpha-beta bond. - Double bond is oxidized by enoyl-ACP reductase using another NADPH. - The chain is now 2 C’s longer and is transferred to the cysteine ACP where the first acetyl group was, and another malonyl group comes in and attaches to the open ACP. - These steps are repeated, adding 2C units to the thioester end six more times forming palmitoyl-ACP. - Palmitoyl thioesterase breaks the thioester bond, releasing palmate and regenerating the enzyme. Long chain FAs - Made using elongases; found in mito and endoplasmic reticulum (ER). - In mito: acetyl units are added, and uses NADPH - In ER: adds malonyl-Coa with acetyl-Coa; uses CoA instead of ACP. Regulation of FA metabolism Short term - Glucagon and epinephrine stimulate oxidation and inhibit FA synthesis; Insulin does opposite. - Concentration of FAs in the blood, which is controlled by breakdown of triglycerides. HORMONE SENSITIVE TRIACYLGLYCEROL LIPASE is activated when glucagon or epinephrine raise cAMP levels. - Allosteric activators: Palmitoyl-CoA. - Allosteric inhibitors: NADPH, acetyl-Coa, citrate. - Membrane transport modulators: palmitoyl-Coa stimulates; Malonyl-Coa inhibits. - NADH inhibits 3-hydroxyacyl CoA DH and acetyl-Coa inhibits thiolase. Long Term: synthesis of enzymes. Synthesis of Triglycerides Glycerol comes from glycolytic pathway or OAA via glycerneogenesis.


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