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38 Cards in this Set
- Front
- Back
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Describe the digestion of TG's, including the formation of micelles.
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TG's are neutral lipids that come from the diet or are stored. Bile salts emulsify and pncreatic lipase breaks down TG's. Micelles form and take the products of enzyme digestion to be absorbed. Products are FFA, 2-monoacylglycerol, Cholesterol
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Define Amphipathic
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Polar on one side, non-polar on other side.
Hydrophobic on one side, hydrophilic other side |
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Define Emulsion
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Large Lipid Droplets
Visible Cloudiness No Organized Structure Unstable Stabilized by emulsifying agents |
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Define Micelles
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Highly organized structures with polar groups oriented outwards and non-polar groups oriented inward
Happens when polar lipids are added to water at very low concentrations |
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Name the principle digestive enzymes that are necessary for digestion
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Pancreatic Lipase - for TG degradation
Cholesteryl Ester Hydrolase - for cholesteryl ester degradation Phospholipase A2 - for phospholipid degradation |
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Explain how bile participates in the digestive process
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Bile salts are derivatives of cholesterol and act as emulsyfying agents. Effective detergents because of their amphipathic nature.
Main purpose is to form micelles. Necessary for absorption of cholesterol and vitamins AEK |
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Steps in which TGs are absorbed by intestinal epithelium
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TG->(pancreatic lipase)-> 2-monoacylglycerol + FFA (Packed in a micelle)-> (Intestinal cell absorption)-> resynthesis to TG -> packed into chylomicrons
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Route in which chylomicrons reach the cells of the body
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Chylomicrons move through the lymphatic system and bloodstream to tissues ->Lipoprotein lipase in the capillary is activated by the apo C-II attached to the chylomicron and hydrolyse TG & Cholesterol to fatty acids and cholesterol
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Describe the role of HDL in the formation of Chylomicrons and VLDL
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Nascent Chylomicrons have Apo-A1 and B-48. Once released from intestinal cell, HDL attaches Apo-CII and Apo-E to the Chylomicron (via A1 receptor).
Nascent VLDL has Apo B-100. Gets Apo C-II and Apo-E from HDL |
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Describe the role in which Chylomicron remnants are removed from from circulation and the role of APO-E
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As Chylomicrons circulates through the blood stream, Lipoprotein Lipase degrades TGs and Cholesterol. The Chylomicrons decrease in size and increase in density.
Apo-CII is returned to HDL and the remaining particle is called a chylomicron remnant. The Apo-B48 and Apo-E are recognized by hepatocyte plasma membrane and take up the remnant. The remnant is degraded to AAs, free cholesterol, glycerol, FAs by lysosomes |
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Describe the role of Lipoprotein lipase
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Enzyme found at the capillaries of tissues that degrades TGs and Cholesterol inside chylomicrons. Forms 2-monoacylglycerol & FFAs.
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Role of Apo-CII
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An Apoprotein attached to the outside of a chylomicron and VLDL that activates lipoprotein.
Given by HDL |
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Describe the various classes of lipoproteins and relative amounts of TG, cholesterol in each class
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Chylomicrons - released from small intestine/ lowest in density/ largest in size/ has most lipid and smallest %of protein/ Carries dietary TGs/ Nascent form has Apo A1, Apo B48/ Gets Apo-CII & APo E
VLDL - Gets TGs from liver/ has APO B100 as nascent/ Gives up TG following lipoprotein lipase LDL - Formed from VLDL after TG, phospholipid exchange from HDL/ Highest % of cholesterol/ provides cholesterol to tissues HDL - Smallest lipoprotein/ 60% apolipoprotein/ Two Types (HDL2 & HDL3) |
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Role of Serum Albumin in fat transport
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Serum Albumin is used to transport FFA
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Describe the production and utilization of glycerol
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Hormone sensitive lipase catalyzes the hydrolytic release of FAs and glycerol from storage.
Adipocytes cannot metabolize released glycerol because they lack Glycerol Kinase enzyme. Glycerol is transported to the liver where it is converted to DHAP |
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How is Glycerol-P formed in muscle, adipose tissue and liver
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Glycerol-3-Phosphate is formed from Glycerol by Glycerol Kinase. Glycerol-3-Phosphate can then be shuttled to glycolysis.
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Describe the role of LCAT (and APO-A1) and HDL in Cholesterol mobilization and transport.
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HDL removes non-esterified cholesterol from extrahepatic tissue and esterifies it using Phosphotidylcholine Cholesterol Acyltransferase (PCAT/LCAT).
LCAT is produced in the liver and activated by Apo-A1 on HDL The resulting cholesterol ester is very hydrophobic and is trapped inside the HDL and cannot be passively transferred through membranes. The enzyme that transfers esterified cholesterol to VLDL is cholesteryl ester transfer protein (CETP) in exchange for TG and PLs. the Cholesteryl esters remain in LDL until taken up by a cell. |
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Describe the production and utilization of glycerol
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Hormone sensitive lipase catalyzes the hydrolytic release of FAs and glycerol from storage.
Adipocytes cannot metabolize released glycerol because they lack Glycerol Kinase enzyme. Glycerol is transported to the liver where it is converted to DHAP |
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How is Glycerol-P formed in muscle, adipose tissue and liver
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Glycerol-3-Phosphate is formed from Glycerol by Glycerol Kinase. Glycerol-3-Phosphate can then be shuttled to glycolysis.
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Describe the role of LCAT (and APO-A1) and HDL in Cholesterol mobilization and transport.
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HDL removes non-esterified cholesterol from extrahepatic tissue and esterifies it using Phosphotidylcholine Cholesterol Acyltransferase (PCAT/LCAT).
LCAT is produced in the liver and activated by Apo-A1 on HDL The resulting cholesterol ester is very hydrophobic and is trapped inside the HDL and cannot be passively transferred through membranes. The enzyme that transfers esterified cholesterol to VLDL is cholesteryl ester transfer protein (CETP) in exchange for TG and PLs. the Cholesteryl esters remain in LDL until taken up by a cell. |
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Describe the production and utilization of glycerol
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Hormone sensitive lipase catalyzes the hydrolytic release of FAs and glycerol from storage.
Adipocytes cannot metabolize released glycerol because they lack Glycerol Kinase enzyme. Glycerol is transported to the liver where it is converted to DHAP |
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How is Glycerol-P formed in muscle, adipose tissue and liver
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Glycerol-3-Phosphate is formed from Glycerol by Glycerol Kinase. Glycerol-3-Phosphate can then be shuttled to glycolysis.
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Describe the role of LCAT (and APO-A1) and HDL in Cholesterol mobilization and transport.
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HDL removes non-esterified cholesterol from extrahepatic tissue and esterifies it using Phosphotidylcholine Cholesterol Acyltransferase (PCAT/LCAT).
LCAT is produced in the liver and activated by Apo-A1 on HDL The resulting cholesterol ester is very hydrophobic and is trapped inside the HDL and cannot be passively transferred through membranes. The enzyme that transfers esterified cholesterol to VLDL is cholesteryl ester transfer protein (CETP) in exchange for TG and PLs. the Cholesteryl esters remain in LDL until taken up by a cell. |
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What is the role of hormone sensitive lipase?
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Hormone sensitive lipase hydrolizes triacylglycerol from fat storage and makes FFA + Glycerol for metabolism to CO2.
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and what makes hormone sensitive lipase hormone sensitive?
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HSL is hormone sensitive lipase because it is activated by EPI, NE, Glucagon
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Explain how FFA are processed before being oxidized in the matrix of the mito.
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FFA must be activated before resynthesis. FA activation is catalyzed by ACYL CoA SYNTHETASE. This occurs on the outer mitochondrial membrane. The resulting FA-CoA is transfereed into the inner mitochondrial membrane by CARNITINE PALMITOYL TRANSFERASE I (CPTI) and makes fatty acyl carnitine. a second Carnitine Palmitoyl Transferase (CPTII) brings the FA-Carnitine into the matrix and back to FA-CoA.
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What are the steps of B-Oxidation of FAs?
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Degredation of FAs proceeds 2 c's at a time.
Step 1 Oxidation FAD is used up and FADH2 is made Step 2 Hydration Enoyl-CoA hydratase is used Step 3 Oxidation NAD+ is used and NADH is made Step 4 Thiolysis Acyltransferase (thiolase) is used. Adds CoA to the B Carbon. Releaseing a shorter FA and Acetyl CoA |
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Energy yeild of B-Oxidation
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NADH 2.5 ATP
FADH2 1.5 ATP Acetyl-CoA 10 ATP 14 ATP Per Cycle |
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Describe the metabolic steps in Ketone Body synthesis
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3 Ketone Compounds
1. 3-Hydroxybutyrate 2. Acetoacetate 3. Acetone Steps FA-CoA or Acetyl CoA ->Acetoacetyl Coa -(HMG-CoA Synthase)-> HMG-CoA -(HMG-CoA Lyase) -> Acetoacetate Acetoacetate forms: 1. 3-hydroxy butyrate from (3hydroxybutyrate dehydrogenase) 2. Acetone (decarboxylation) |
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When do ketone bodies accumulate?
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Ketones are increased during 1. fasting
2. high fat diets 3. diabetes |
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How and where are Ketone Bodies oxidized in the body?
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Ketone Bodies:
made in liver utilized outside of liver -HMG-CoA is an enzyme only found in significant quantities in liver. -the liver lacks CoA transferase, cannot utilize ketone bodies itself |
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Steps of unsaturated FAs Oxidation
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For Mono Unsatuarated FAs:
Only one enzyme (Enoyl CoA Isomerase). Converts Cis to Trans. Proceeds to 2nd step of B-Oxidation For Poly Unsaturated FAs: 2 Enzymes needed 1. 2,4 Dienoyl CoA reductase (energy needed: NADPH) 2. cis-enoyl isomerase |
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Steps of odd chain FA oxidation
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Odd chain FA produces
1. Acetyl CoA 2. Proprionyl CoA -Only Proprionyl Coa goes to citric acid cycle = converted to glucose after succinyl coa conversion |
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Most important regulatory enzyme for FA degradation
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Malonyl-CoA inhibits Carnitine Palmitoyl Transferase I (CPTI)
Malonyl-CoA is formed as an early intermediate in FA synthesis. when FA synthesis occurs, FA oxidation is inhibited. |
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The rate limiting enzyme for FA synthesis
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Acetyl CoA Carboxylase
-Contains Biotin! |
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Regulation for Acetyl CoA Carboxylase
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Citrate = activator
Long chain FA = inhibitor Hormonal regulators 1.insulin-activator (phosphatase) 2. glucagon/epinephrine-inhibitor (kinase) |
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Role of ATP + Citrate Lyase in FA synthesis
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ATP + Citrate Lyase convertas transported citrate from the Mito to Acetyl-CoA
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Why is glucose needed to make fat?
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to make Acetyl-CoA
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