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141 Cards in this Set
- Front
- Back
- Energy (oxidation of fatty acids in liver and muscle)
- Membranes (separation of cellular components) - Regulation (steroids, prostaglandins, many other bioactive molecules) - Detergents (solubilize nonpolar substances in body fluids) |
Functions of fatty acids
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Most common unsaturated fat is ______
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Oleic acid 18:1 delta 9
Double bond between 9 and 10 Nine carbons away from omega carbon |
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- Increases with chain length
- Decreases with double bonds |
Melting point
Double bonds trump chain length |
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Alpha-linoleic acid (omega-3) 18:3 d9,12,15
Linoleic Acid (omega-6). 18:2 d9,12 Arachidonic Acid (omega-6) 20:4 d5,8,11,14 |
Essential fatty acids.
Cannot make de novo |
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Fatty acid molecule in thioester linkage with CoA molecule
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Fatty Acyl CoA
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No charge on this molecule
We store them in the body Digested by lipases |
Triacylglycerols
Lipase cleavage = DAG + FFA |
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- Phosphatidylcholine
- Phosphatidylethanolamine - Phosphatidylserine - Phosphaditylinositol - Cardiolipin |
Major phospholipids
Components of cellular membranes. |
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Composes 30% of inner mitochondrial matrix.
Polar head group is in the middle of this molecule |
Cardiolipin
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When a molecule has polar and nonpolar parts.
One part soluble in water, one part solule in lipid |
Amphipathic molecule
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Phospholipases are mostly under hormonal control.
Arachadonic acid is precursor for _______________ production |
prostaglandin
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-Derived from serine and palmitic acid
- Different, nonglycerol backbone - Attach things to OH |
Ceramide
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- Sugar acid
- Negatively charged - Ceramide based |
NANA
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- Has OH at C3
- Allows for interaction with aqueous environment - If lost, becomes very hydrophobic |
Cholesterol
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- Adipose tissue
- Liver - Mammary tissue |
Major sites of lipid synthesis
Don't store fat in liver or mammary gland Fatty acid synthesis begins with glucose entering the cell. |
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- Cytosol
- Acetyl CoA - ATP and Mg2+ - HCO3- - Citrate - NADPH |
Requirements for fatty acid synthesis
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Of the following, which enzyme belongs in the committed step of Fatty Acid Synthesis:
- Malonyl CoA carboxylase - Pyruvate carboxylase - Acetyl-CoA carboxylase - Fatty acid synthetase |
- Acetyl-CoA carboxylase
Cofactors: - Citrate - Mg2+ - ATP - HCO3- - Biotin Turns Acetyl-CoA into Malonyl-CoA |
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1 palmitate + 7 CO2 + 14 NADP+ + 8 CoA + 6 H20
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Products of Fatty Acid Synthase
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Regulation:
Acetyl-CoA Carboxylase (CBX) |
Stimulated by:
- Insulin - Dephosphorylation (by insulin) - Decreased ratio of AMP/ATP - Citrate Inhibited by: - Long chain fatty acyl-CoA's - Fats from diet - Increased ratio of AMP/ATP - Phosphorylation (by AMP activated protein kinase (AMPK) - Epinephrine and glucagon - Malonyl CoA |
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What affects the citrate transporter?
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Stimulates:
- High levels of ATP (slows down the TCA cycle - citrate pumped out of mitochondria) Inhibits: - Fatty Acyl CoA |
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What neurotransmitter is a potent stimulator of appetite?
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Neuropeptide-Y
NPY |
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Inhibition of what enzyme on the Fatty Acid Synthase protein has been shown to control feeding regulation?
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Condensing enzyme
Build up of malonyl CoA is though to be the signal which inhibits NPY secretion |
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A molecule that inhibits pancreatic lipase should also be expected to inhibit what enzyme?
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Condensing enzyme on Fatty Acid Synthase
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Inhibition of the condensing enzyme of Fatty Acid Synthase did not tend to make people lose weight. What effect did it have?
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Improved lung cancer survival
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1) Generate a glycerol phosphate backbone
2) Generate phosphatidic acid by esterification of fatty acids to position 1 and 2 3) Generate a DAG by removal of the phosphate from position 3 4) Generate a TAG by esterification of a fatty acid to position 3 |
Synthesis of TAGs
Glycerol kinase phosphorylates glycerol to glycerol-3-phosphate (absent in adipose tissue) |
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The first step of TAG synthesis occurs in all tissues.
These intermediates are from what pathway? - DHAP - NADH - G3P |
Glycolysis
Phosphatidic acid and DAG are used in intermediates in other pathways too |
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In this tissue, most TAGs are from diet or synthesized by the liver
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adipose
Mammary tissue and liver produce fat de novo |
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This type of fat has the following characteristics:
- Lots of mitochondria - Expression of uncoupling protein - Uncouples ETC, generates non-shivering heat |
Brown adipose
Found in infants in the infrascapular region. Adults: cervical, supraclavicular and paravertebral depots Other sites listed: Retro-orbical, Periarticular regions, bone marrow, intramuscular, pericardial |
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Name the fat depot
- Higher basal and stimulated adenylate cyclas activity - Higher LPL activity - Lipolysis not suprressed by insulin - Greater lipid flux - Drain into the portal venous system, Non-esterified fatty acids (NEFA's) are transported to the liver = stimulates hepatic GNG |
Intra-abdominal fat
Common sites: Omental Retroperitoneal Visceral |
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Name the fat depot
- Enhanced lipid storage - Lipolysis suppressed by insulin - Insulin receptor, GLUT4, leptin and PPARy all expressed at higher levels than omental - Depots drain into the systemic venous system and NEFAs are distributed around the body. - Preadipocytes differentiate more readily |
Subcutaneous
Common sites: - Crainal - Facial - Abdominal - Gluteal |
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a protein hormone produced by adipose tissue.
Its concentration in the body provides the brain with a rough indication of adipose mass for the purposes of regulating appatite and metabolism. |
Leptin
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Secretion by adipocytes is directly proportional to adiposity.
Stimulates recruitment of additional macrophages to adipose tissue. |
Macrophage Chemo-attractant Protein1 (MCP1)
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Secreted by adipocytes as well as macrophages in the tissue in proportion to adiposity.
TNFα is a cytokine involved in the inflammatory response. |
Tumor necrosis factor α (TNFα)
Regulates immune system |
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Synthesized & secreted by adipose tissue.
Promotes/controls insulin sensitivity. |
Adiponectin
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Synthesized & secreted by adipose tissue.
Promotes/controls insulin resistance. |
Resistin
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This molecule is orexigenic (promotes increased energy intake).
Levels are decreased with increased levels of leptin |
Neuropeptide Y
Most potent appatite stimulator |
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Leptin binds to the arcuate nucleus in the hypothalmus...what affect on NPY stimulation does it have?
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Decreases NPY stimulation
Stimulates POMC neuron (leads to secretion of a-MSH), which bind to receptors that signal satiety |
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Preopiomelanocortin (POMC) is the precursor to the _____________ which bind to receptors and signal satiety
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melanocortins
Specifically, alpha-melanocyte stimulating hormone (a-MSH) |
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This deficiency does the following:
- Drives hunger - Suppresses energy expenditure - Inhibits reproductive competance |
Leptin deficiency
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A deficiency in this receptor will not allow for fat synthesis
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Proxisomal proliferator activated receptor y (PPARy)
Target of thiazolidinedione drugs/glitazones |
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What type of drugs are these?
- Actos (pioglitazone) - Avandia (rosiglitazone) They target the PPARy receptor. |
Thiazolidinedione drugs - glitazones
Move glucose out of the blood supply and into the adipocytes. Concern is for toxic levels of glucose, not obesity |
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- Fasting
- Prolonged exercise - Diabetes (Type I predominantly) - Sudden drop in environmental temperature - Trauma/Stress |
Conditions promoting lipolysis
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Hydrolysis by HSL is the rate limited step for what reaction
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Lipolysis
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Albumin binds how many free fatty acids?
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one
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Oxidation of TAG's is dependeon on serum levels of what carrier molecule?
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Albumin
1 albumin molecule carries 1 FFA |
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Malonyl CoA's role in TAG breakdown
Is malonyl CoA a product of lipolysis or FA synthesis? |
Inhibits CPT-1
Malonyl-CoA is a product of fatty-acid synthesis. Result: Do not want to make fat while breaking it down (futile cycle) |
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Fatty acids can by pass the carnithine system. It has to be less than how many carbons long?
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Less than 12 carbons long
Useful therapy for various disease states where CPT-1 or CPT-2 are deficient |
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- Oxidation (FADH2 produced)
- Hydration - Oxidation (NADH produced) - Thiolase |
Steps of even chain Fatty Acid Oxidation in the matrix of mitochondria
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- Fatty Acyl CoA (FADH2 produced)
- Trans d2 enoyl-CoA - B-Hydroxy acyl CoA (NADH produced) - B-Keto acyl CoA = Products (FA CoA + acetyl CoA) |
Products of even chain Fatty acid oxidation in matrix of mitochondria
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- Rate of fatty acid delivery to the tissue (albumin levels)
- rate of fatty acyl translocation across the inner mitochondria matrix (carnithine levels) |
Rate of B-oxidation is determined
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- Isomerase
- Hydration - Oxidation (NADH produced) - Thiolase |
Steps of odd-chain fatty acid oxidation in matrix of mitochondria.
Note: FADH2 not produced, thus, yields less energy |
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- cis d2 enoyl CoA
- trans d2 enoyl CoA - B-hydroxy acyl-CoA - B-keto acyl-CoA Products (FA CoA + acetyl-CoA) |
Products of odd-chain fatty acid oxidation
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Final process of odd-chain fatty acid oxidation.
Priopionyl CoA -> Methyl Malonyl CoA Methyl Malonyl CoA -> Succinyl CoA Succinyl CoA -> TCA |
First reaction is a carboxylation reaction (needs biotin, ATP, HCO3-)
Second reaction is a mutase that requires vitamin B12 |
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8 Acetyl CoA + AMP + PPi + 7 NADH + 7 H+ + 7 FADH2
Total: 106 ATP produced How many are lost due to activation? |
1 is lost for ATP activation
1 is lost for PPi activation Net = 108 ATP |
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Acetyl-CoA levels when carbohydrate and fat breakdown is balanced:
1 mL/dL in circulation |
When fat breakdown preddominates, AcCoA is in excess and carbohydrates are unavailable or not properly utilized.
Decreased concentration of OAA Ketogenesis predominates |
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- Elevated gluconeogenesis
- Increased delivery of fatty acids to liver - Increased ketogenesis - Ketone spillage to urine |
Metabolic consequences of ketogenesis
Hormones: decreased insulin, increased glucagon |
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50 um after a meal
200-400 um after an overnight fast 1-2 mM after a three day fast 6-8 plateau upon prolonged starvation |
Serum concentrations of beta-Hydroxy Butryate
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Ketone body synthesis occurs in what organnelle in what organ?
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Liver only: mitochondrial matrix
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This molecule is the only water soluble lipid derived energy carrying product
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B-hydroxybutyrate
Cannot be utilized by the liver, must enter circulation |
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B-hydroxybutryate is converted back into acetoacetate.
It is then catalyzed by a reaction using succinyl-CoA as a cofactor |
Products:
2 AcCoA's, which combine with OAA to form 2 citrates |
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These pathways occur in what organelle?
1. Activate the polar head group (choline or ethanolamine) and condense with a DAG 2. Activate the glycerol backbone and condense with a polar head group |
Occur in the endoplasmic reticulum
Difference is what is activated to build phospholipid |
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Lung surfactant.
Coats alveolar sacs Reduces surface tension 10x less pressure for inflation Absense = respiratory distress syndrome |
Lecithin
Occurs in infants who do not have enzyme to make phosphatidylcholine |
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Pick one:
Between phosphatidylethanolamine or phosphatidylcholine, which one can be catalyzed to form phosphatidylserine? |
Phosphatidylethanolamine
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- Major player in signaling
- Binds to ER or SR - Signals calcium to be dumped into cytoplasm |
Phosphatidylinositol
(remember, IP3 from physiology) |
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Two phosphatidic acids linked by glycerol moiety
- Critical membrane lipid: 30-35% of inner mitochondrial membrane |
Cardiolipin
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An ester linkage rather than an ester at C1
Synthesized in peroxisomes (where some FA metabolism and plant FA digestion occurs) |
Plasmalogens (ether lipids)
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A plasmologen with choline in the R group will be found where?
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In the heart
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A plasmologen with ethanolamine in the R group will be found where?
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Myelin
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- Aggregates platlets at 10^-11 M
- Potent anti-hypertensive - Involved in allergic response |
Platelet Activating Factor
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This fat is derived from serine and two fatty acids, one of which is bound to a nitrogen
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Ceramide
Serine with a fatty acid linked to Nitrogen - only place you'll see it |
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This sphingolipid is critical in neural tissue
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sphingomyelin
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Could be converted into a glucocerebroside
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Galactocerebroside
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- Addition of NANA to a glucocerebroside forms a _________
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Ganglioside
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- Sugar acid
- Negatively charged - CMP sugar |
NANA (N-acetylneuraminic acid)
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1. UDP-Glc
2. UDP-Gal 3. UDP-GalNac 4. CMP-NANA 5. UDP-Gal |
Ordered sequential steps in formation of ganglioside GM1
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The lysomsome uses specific glycosyl hydrolases for sqequential removal of each sugar residue
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Degradation of gangliosides
Lack of hydrolase to cleave the bond between Gal-GalNAC = GM2 accumulates. This is called Tay-Sach's disease |
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Carbohydrate moieties of glycolipids on the surface of cells.
When present on the surface of cells, the ABO carbs are linked to ____________ and are therefore the glycosphingolipid class |
sphingolipid
ABO markers confer antigenic determinants on the cell, especially RBCs |
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H-antigen
A-antigen B-antigen |
H antigen gives O blood type
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Molecule when carbon six is a methyl group instead of a carboxyl group
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Fucose
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The only sphingolipid that has a phosphate group
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Sphingomyelin
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Acety-CoA -> Mevalonate
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First step of cholesterol synthesis
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Mevalonate -> Isopentynyl-PP
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Second step of cholesterol synthesis
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Isopentynyl PP -> Geranyl-PP -> Farnesyl-PP -> Squalene
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Third step of cholesterol synthesis
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Cyclization of squalene and formation of cholesterol
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Fourth step of cholesterol synthesis
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- Incorporation into lipoproteins
- Bile salts - Steroid hormones |
Liver
Steroid hormones produced in adrenal and gonads |
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- Liver
- Intestine - Adrenal cortex - Gonads |
Major sites of cholesterogenesis
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All cell types can synthesize cholesterol, but they derive it from plasma lipproteins secreted by the _______ and ______.
If they do not provide an adequate supply, de novo synthesis of cholesterol is activated |
Liver and intestine
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Cholesterol feedback mechanism targets what enzyme?
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HMG-CoA reductase
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1. Cholesterol will block transcription of the HMG-CoA reductase gene (means there will be no HMG CoA reductase mRNA. No mRNA = no protein)
2. An AMP activated protein kinase phosphoyrlates and inactivates HMG CoA Reductase 3. HMG-CoA Reductase is the target of the statin family of drugs. These drugs function as competitive inhibitors of the enzyme |
Regulation of cholesterol synthesis.
Protein kinase A phosphorylates and inactivates HMG CoA reductase. Rationale: Low ATP = do not want to make cholesterol |
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These drugs reduce:
- Total cholesterol levels - LDL - apo B - TAGs Increase HDL |
Statins
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Getting rid of bile salts is important in lowering ones cholesterol. What substance helps?
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Fiber
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- Coronary artery disease
- Multiple sclerosis - Bone Fractures - Alzehimers disease - Aortic valve disease - Cancer |
Statins are used to treat these diseases
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___% of total cholesterol produces goes to bile salt production
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80%
Bile salts act as a detergent, has both hydrophobic and hydrophilic molecules |
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1) Hdryxylate the steroid nucleus
2) Cleave the side chain to generate a bile acid 3) Conjugate the acid to a glycine or taurine |
Set of reactions that take place in the liver for bile salt production
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Primary bile salts
Gives cholesterol an acid function. Removes three carbons from cholesterol (C27) to C24 Cholic acid or Chenocholic acid. Pka of acid = 6.0. Pka of intestine = 6.0 What's the problem? |
Problem: Only 50% of the compund is ionized.
Want all of the groups ionized. Note: Cholic acid has three hydroxyls while Chenocholic acid only has two. |
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Rate limiting step of primary bile salt production:
Cholesterol reduction to 7-a-hydroxycholesterol |
7-a-hydroxylase requires:
- O2 - P450 cytochrome containing iron - NADPH |
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3a, 7a-hydroxycholesterol gives rise to what two products?
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1) Chenocholic acid or
2) 3,7,12 hydroxycholesterol ---> Cholic acid |
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Secondary bile salt
Conjugation lowers the pKa. Activate the carboxyl group of the side chain by making the CoA derivative. |
Once Acetyl-CoA has been added, can add glycine or taurine to complete conjugation.
Glycocholate = pka 4 Taurocholate = pka 2 |
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Built from dietary lipid in the epithelial cells of small intestine.
Dietary TAG delivery system |
Chylomicrons
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Remains after TAG removed from chylomicron
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Chylomicron remnant
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Synthesized and secreted by the liver. TAG rich
End product of fatty acid synthesis in liver |
VLDL
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Higher density particle after TAG removal in the periphery by lipoprotein lipase.
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IDL
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Further degradation of TAG of IDL geenrates a particle rich in cholesterol and cholester esters, and of a higher density.
Cholesterol delivery particle |
LDL
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Synthesized and secreted in an immature form by liver and gut.
Matures by interacting with chylomicrons and VLDL in circulation where it exchanges lipids and proteins |
HDL
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1. Transfers apolipoproteins to other lipoproteins (directs metabolism of chylomicrons and VLDL)
2. Picks up lipids from other lipproteins 3. Picks up cholesterol from cell membranes 4. Converts cholesterol to cholesterol esters (LCAT) 5. Transfers cholesterol esters to other LP's, which transport them to liver |
Mechanisms in which HDL works
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Receptor:
B48, C, E |
Chylomicron
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Receptor:
B48, E |
Chylomicron remnant
B48 + E are recognized by liver |
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Receptor:
B100, C, E |
VLDL
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Receptor:
B100, E, (some C) |
IDL
E recognized by liver |
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Receptor:
B100 |
LDL
B100 recognized by liver and peripheral cells and tissues |
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Receptor:
A, C, E |
HDL
Recognized by liver and steroidogenic tissues |
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Same gene in both intestine and liver, but RNA editing stops transcription early.
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B-apoliprotein gene
Stops the transcription of Apo B in intestine |
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Recognizes B100 and E
Binds with preferance for LDL, but will bind VLDL, IDL, and chylomicron remnants. Expression is high in liver and adrenal. Expressed in most other tissues |
LDL receptor
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Recognizes apo E
Binds chylomicron remnants and VLDL Expression is high in liver, brain and lung. Modest elsewhere |
LDL receptor related protein (LRP)
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Binds various types of molecules including LDL that has been subjected to oxidative damage.
Involved in foam cell formation and atherosclerosis |
Macrophage Scavenger Receptor
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Synthesized by adipose and muscle tissue.
Transported to the surface of the vascular endothelium where it binds to heparan sulfate proteoglycans. |
Lipoprotein lipase (LPL)
Responsible for the hydrolysis of TAGs present in chylomicrons, VLDL and IDL to free fatty acids and glycerol. FFA's are taken into adipose tissue for resynthesis of TAG or to muscle for oxidation |
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- Can be displaced by giving a bolus of heparin
- Useful in detecting deficiency in lipase |
Heparine Secretatogue
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Synthesized in the liver and associated with the liver plasma membranes.
Digests TAG associated with partially degraded lipoproteins |
Hepatic Triglyceride lipase (HTGL)
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Mediates the exchange of lipid components between lipoproteins.
Transfers cholesterol esters from HDL to VLDL, IDL or LDL in exchange for TAGs |
Cholesterol Ester Transfer Protein (CETP)
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Associated with HDL particle
Esterifies cholesterol remaining on the surface of HDL. This changes the polarity of the compound and the cholesterol ester moves to the inside of the particle. Changes the shape of HDL from a disc to a sphere |
Lecithin cholesterol acyl transferase (LCAT)
Phosphatidylcholine + cholesterol -> cholesterol ester + lyso-phosphatidylcholine |
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Located in the lysosome
Responsible for hydrolysis of LDL derived cholesterol esters to free cholesterol and a fatty acid |
Lysosomal acid lipase
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Intracellular enzyme mediates the esterification of cholesterol for storage
Acey CoA + cholesterol -> cholesterol oleate (18:1) |
Acyl CoA Cholesterol Acyl Transferase (ACAT)
Another enzyme that makes cholesterol esters. |
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Pancreatic lipase needs colipase.
TAGs are broken down into 2 FFA's and a B-monoacylglycerol in the intestine. |
Colipase protects lipase from bile salt inhibition
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Unique to epithelial cell: Beta-acylmonoglycerol pathway.
1. TAG is pcaked with Apo A/B48/phospholipid/cholesterol 2. Forms a chylomicron 3. Goes to lymph |
Chylomicrons are too big for blood supply.
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This apoprotein is critical.
Interacts with LDL to activate lipase on adipose and muscle cells |
Apo C2
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Name the molecule:
Liver recognizes apo E Apo E gives receptor recognition Binds to LRP (LDL Receptor Like Protein) |
Chylomicron remnant
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From epithelial cell
-> Thoracic duct -> Systemic circulation -> HDL donates apo C2 and E to chylomicron -> LPL on capillary endothelium of adipose and muscle tissues activated by apo C2 -> Digest TAG's to 3 FFA and a glycerol. Fatty acids taken up by adipose (storage) or muscle (oxidation). Glycerol to tissue where it can be reutilized. -> Remnant (particle without TAGs) gives up apo C2 back to HDL, then off to liver -> Receptor on liver recognizes apo E on remnant -> LIVER! Remnant internalized, components digested |
The steps of chylomicron degradation
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Short and medium chain (C4-C12) fatty acids generated by the action of pancreatic lipase are able to by-pass the re-synthesis of TAG in the epithelial cells of the small intestine.
These FA's can move directly into systemic circulation where they are picked up by albumin and delivered to tissues where they can be converted to fatty acyl CoA's and used to re-synthesize TAGs or be oxidized. |
Useful if an individual has a problem with chylomicron formation.
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Sucrose with fatty acids esterified where there is an OH
Cannot be hydrolized and is excreted unchanged |
Olestra
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- Made in the liver de novo
- Stuffed with TAG and delivers fatty acids to adipose and muscle - Then turns into LDL |
VLDL molecule
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HDL picks up cholesterol from LDL
HDL donates C2 and E to LDL This makes HDL more/less hydrophobic? |
Less
LCAT esterifies the cholesterol to a cholesterol ester to keep it hydrophobic |
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These two apo's aid in receptor recognition
This one apo activates LPL |
Apo B100 and E
Apo C2 |
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Esterification is unimportant/critical for transport of cholesterol in the body?
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critical
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- Cell overloaded with cholesterol
- Only cell that doesn't downregulate is the liver - Regulation occurs at the level of the gene |
Regulation of cholesterol - turn off synthesis of LDL receptor and HMG-CoA reductase
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- Excess cholesterol is stored as cholesterol oleat (ACAT)
This makes another cholesterol ester inside of the cell and stores it |
ACAT
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Lysosomal acid lipase hydrolyzes the cholesterol ester.
This regenerates the B100 receptor and allows cholesterol to exit the lysosome for the cytoplasm |
Action of Lysosomal acid lipase
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1. Secreted into circulation by liver and gut. Contains (apo A, C and E)
2. Small and discoid in nature. Nearly devoid of cholesterol esters and TAGs 3. Donates apos C2 and E to VLDL and chylomicrons 4. Picks up cholesterol from other lipoproteins and the membranes of extrahepatic cells. 5. Cholesterol converted to cholester esters by LCAT, which is stilated by apo A1 6. As particl fills with cholester esters, it becomes spherical. Known as HDL3 |
The Role of HDL.
Notes: A1 stimulates LCAT HDL3 = spherical shape (aka, not the usual shape which is discoid) |
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CETP can mediate the transfer of cholesterol esters from HDL3 to VLDL
OR HDL3 can bind to the surface of cells and transfer its cholesterol esters to the cell, the dissociate and re-enter circulation AND Mediate the transfer of TAGs from VLDL to HDL3. |
Reverse Cholesterol Transport
Results in the movement of cholesterol from areas of excess to areas of need. CETP is a free enzyme. HDL2 = smaller particle |
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Apos C2 and E donated back to HDL
HTGL removes TAG at the liver HDL particles become smaller and are designated HDL2 |
Mechanism of CETP action
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Plaques form in walls of major arteries - impedes blood flow.
Composed of smooth muscle cells, connective tissues, lipids and debris |
Atherosclerosis
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1. Damage to endothelial cells of the arterial wall.
2. Macrophages arrive at site to deal with the damage. 3. Macrophages have "scavenger receptor" that will bind and internalize "oxidized LDL" 4. Macrophages become engorged with LDL derived lipid material. Turn into Foam Cells, the earliest physical sign of atherosclerosis. 6. Macrophages in the lesion release growth factors and stimulate growth of endothelial cells. 7. Cells in the lesion secrete collagen and other molecules that leads to the build up of a fibrous cap. Cells trapped and die (this is a plaque) 8. Rupture and hemorrhage of encapsulated plaque may cause the acute formation of a clot, which further occludes the vessel -> myocardial infarction |
Mechanism of Atherosclerosis
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Synthetic HDL - based on gold nanoparticle.
Binds cholesterol and can potential eat away at cholesterol containing plaques |
The future of treatment for atherosclerosis
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