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Introductory Biochemistry

by: Kiera Waelchi III

Introductory Biochemistry BCH 3023

Kiera Waelchi III
GPA 3.66


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This 6 page Study Guide was uploaded by Kiera Waelchi III on Wednesday September 23, 2015. The Study Guide belongs to BCH 3023 at University of South Florida taught by Staff in Fall. Since its upload, it has received 58 views. For similar materials see /class/212626/bch-3023-university-of-south-florida in Biochemistry and Molecular Biology at University of South Florida.

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Date Created: 09/23/15
1 Cholesterol Metabolism Describe the functions of cholesterol meUm Absent in plant tissues Constituent of cell membranes Precursor of steroid hormones Elevated levels correlate with increased coronary artery disease and atheroschlerosis Cannot be degraded to C02 i Liver converts cholesterol in bile 2 Outline Cholesterol Synthesis 3 a Takes place in cytosol AcetylCoA AcetoacetylCoA combine to form C HMGCoA reductase key regulatory step i HMGCoA is reduced by NADPH to form mevalonate 6Carbon sugar Decarboxylase i Decarboxylation of mevalonate to form 5carbon llactive isoprenes Condensation i Several isoprenes join together in groups of 5 to form squalene C3O Cyclization i Squalene cyclized into lanasterol C30 Decarboxylation 3X i Three carboxyl groups released to give the 27C cholesterol Ubiquinone coenzyme Q is an intermediate in this pathway Explain how the pathway is regulated and also pretty much all the other objectives a 57 Hormonal control LAANG LAAAAAANG TERM i Glucagon suppresses hepatic cholesterol synthesis by phosphorylation of HMS CoA reductase inactivation ii Insulin enhances the dephosphorylation and thus promotes the synthesis of cholesterol 9 JUST AS PDH AND MUDAFUCKIN ACCCASE Feedback regulation SHORT TERM MU DAFUCKA i High cholesterol levels inhibit cholesterol synthesis 1 Accomplished by increasing rate of HMGCoA reductase degradation 2 Decreases rate of enzyme synthesis The Statins DRUGSSSS i Competitive inhibitors of HMGCoA reductase ii Used to treat hypercholesterolaemia Resins i Bind bile salts in the intestine and prevent their entrance into the enterohepatic circulation ii Forces body to use cholesterol stores in order to decrease total body cholesterol iii Causes steatorrhea 4 Discuss bile stone formation a Cholelithiasis b Bile is primarily composed of cholesterol which is solublized by phospholipids and bile acids c When there is more cholesterol than phospholipid cholesterol crystallizes around an insoluble nucleus gall stone Lipoprotein Metabolism 1 Categorize the different types of lipoproteins and their functions a Lipid transporters i Exogenous 1 Absorbed from the intestines ii Endogenous 1 Synthesized by the liver iii HDL pathway 1 Reverse cholesterol transport b Types i HDL 1 Chief composition of protein and phospholipid ii LDL 1 Chief cholesterol composition 2 Transport cholesterol and cholesterol esters iii IDL INTERMEDIATE iv VLDL 1 One chief constituent of TAG v Chylomicrons INTESTINES WHICH GIVE DIET TAGS T0 ADIPOSE AND LIVER 1 Chief constituent of TAG 2 In the intestines 3 Supply cholesterol and fatsoluble vitamins to the liver 2 Describe the general structure of lipoproteins particles i Hydrophobic core of TAG cholesteryl esters amp fatsoluble vitamins ii Amphipathic coat consisting of phospholipid and free cholesterol iii Apoproteins associated with particle surface 3 Describe how TAG rich particles interact with lipoprotein lipases a Capillaries rich in lipoprotein lipases on the endothelial cell membrane b making them smaller and increasing their density thus MUDAFUCKA GIVING VLDLlDL LDL c Lipoprotein remnant receptors REGULATION i After all TAGS are hydrolyzed lipoproteins are internalized via receptor mediated endocytosis and broken down 4 Discuss chylomicron metabolism a Chylomicrons produced in the intestines b TAGs hydrolyzed via lipoprotein lipase AND Produces chylomicron remnant c Liver recognizes chylomicron remnant apoE protein via LDL receptors d Individuals deficient in LDL receptors do not accumulate chylomicron remnants 5 Outline the conversion of VLDLs into lDls and then to LDLs a LPLase in capillaries recognize apoCll apoenzyme AND SUCK UP DA Hydrolyze TAG b Newly synthesized VLDLs aquire apoCll and apoE apoenzymes from circulating HDL c VLDLs have relatively short halflife due to LPLase d Hepatic TAG lipase i After hydrolysis of TAGs and conversion to lDL the molecule enters the liver ii HTGL removes any remaining TAGs leaving only LDLs containing cholesterol esters iii LDls contain apoB1OO apoprotein 1 Longer halflife 6 Outline the receptormediated process involving LDL receptors a LDL i Primary plasma carrier of free cholesterol and cholesterol esters to extrahepatic tissues b LDL receptors i Engqu LDLs via receptor mediated endocytosis ii LDL broken down into cholesterol NEFA and aminoacids iii ACAT 1 Esterifies excess cholesterol and stores it in the cell c Regulation i Excess intracellular cholesterol 1 lnhibits HMGCoA reductase cholesterol synthesis 2 Decreases LDLreceptor gene expression cholesterol absorption d Foam cells i LDLs that remain in circulation can become oxidized and form atheroschlerotic plaques ii Macrophages remove these foam cells via scavenger receptors 7 Describe the reverse cholesterol transport mechanism a HDLs i Primary function is to transfer cholesterol and cholesterol esters back to the liver via Reverse Cholesterol Transport 1 Reduces level of free cholesterol Help prevent the oxidation of LDLs iii Phospholipid iv Act as apoprotein reservoirs and recyclers by salvaging them from other proteins v Steps 1 Liver produces nascent HDLs that impact peripheral tissues absorbing cholesterol 2 Lecithin 39 39 39 39 39 LCAT a Synthesized in the liver to esteri HDL cholesterols using phosphatidylcholine in the blood Responsible for the ability to reduce level of free cholesterol 397 O Esterification makes the cholesterol hydrophobic and transfers them inside the HDL Entrapment d Enzyme requires activation by enterocyte and hepatocytes 3 Can then swap esters with VLDLs and chylomicrons for TAG molecules a Uses an enzyme known as Cholestryl Ester Transfer Protein CEPT 8 Differentiate between ACAT and LCAT a ACAT AcylCoA acyl transferase i Synthesizes cholesteryl esters from free cholesterol on the cytoplasmic face of the ER b Peroxinase lnhibits LDL oxidation 9 Describe Tangier disease a Rare autosomal disorder b Low plasma HDL c Accumulation of cholesterol d Engorged macrophages accumulate in lymphoid tissue e Cause by defect in ABCl transporter which is involved in HDL removal of membrane cholesterol f Plasma LDLs one third of normal 10 List the functions of the major apolipoproteins a A1 i ActivatesCATin HDL b All i Activator of hepatic lipase ii lnhibitsCATin HDL c BlOO i Receptor binding d C11 activator for LPLase e E i Receptor Binding 11 Explain how oxidized LDL particles are involved in foam cell development and atherosclerosis a Macrophages remove oxidized LDLs and become engorged on them fixing themselves in the intima of the artery 12 Differentiate between primary and secondary hyperlipidaemias a Primary i Not due to identifiable underlying disease b Secondary i Disorder is a manifestation of some other disease 1 Diabetes 2 Hypothyroidism 3 Alcohol abuse 13 Describe type I II III and IV hyperlipoproteinaemias a Familial LPLase deficiency i LPLase deficiency Abnormal production of LPLase iii ApoCll deficiency b H Familial Familial hypercholesterolaemia i LDL receptor defects ii Increase in blood cholesterol C III hyperlipidaemia i ApoE abnormalities ii lnterferes with chylomicron and VDLD remnants removal iii Serum TAG is elevated d N Familial Familial hypertriglyceridaemia i Overproduction of VLDL 1 2 3 Control of Glycolysis and Gluconeogenesis Discuss the regulation of glycolysis in skeletal muscle a Activated by phosphofructokinase i Activated by 1 F26 bP 2 AMP ii Inhibited by 1 ATP 2 Citrate 3 H b Inactivated by F16 bPase i Inhibited by 1 F26 bP 2 AMP c Gluconeogenesis and glycolysis are reciprocally regulated to prevent quotfutile cycle d Desribe how during starvation precursors are channelled into gluconeogenesis a Cortisol causes proteins from muscles and connective tissue to be broken down into amino acids to make glucose b Body is able to shift to utilizing fats to make glucose when carbohydrate supply is low Discuss the links between lipolysis gluconeogenesis and glycolysis especially the role of acetylCoA glucose sparing a Correlate with the postabsorptive phase b Blood moved back into the blood supply c Glycogenolysis is first source of glucose d Lipolysis breaks TAGs into glycerol and fatty acids i Triggered by epinephrine and glucagon 39 Glycerol can make glucose or function in glycolysis entering through DHAP Fatty acids can also be used in many aerobic cells 1 Deemed to be quotglucose sparing because it leaves glucose for anaerobic cells such as neurons


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