Outline for Prelim II

Outline for Prelim II - Outline for Prelim II Lipogenesis...

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Outline for Prelim II: Lipogenesis: making f.a from acetyl CoA (acetyl CoA comes from carbs and a.a.- not from diet directly) **ACC- acetyl-coA carboxylase > converts acetyl CoA to malonyl coA > palmitate CPT1- transports acyl coA into mitochondria for B-oxidation NADP is required for the synthesis of F.a FASN- enzyme that can do all the activites on a signle polypeptide chain Malonyl CoA is building block for lipid synthesis Esterification: f.a from diet converted to TG (fat). From diet Lipolysis: TG broken down to f.a. B-oxidation: f.a. converted to acetyl CoA (which can make cholesterol through cholesterogenesis) Lose two carbons from carboxyl end (not methyl end) ATGL, HSL, MGL: all hormones that break TG down into ffa **All f.a. must be activated. Activated by Acyl CoA synthetase. This turns FFA into acyl-CoA (acyl CoA can then enter into the mitochondria through CPT1) Ketones: generated in liver Liver cannot use ketone bodies for energy. Acetyl CoA is precursor for B-hydroxybutyrate <-> acetoacetate & Acetone All ketones B-hydroxybutyrate- measure this to know if ketoacidosis is present **Malonyl CoA inhibits CPT1 and B-oxidation Short chain FA bind to albumin when entering the bloodstream Long chain FA are converted to TG and then packaged into chylomicrons and enter the lymph system. Brain and muscle can convert ketone bodies back into acetyl CoA for metabolism. Eiconsonoids: Arachinodonic acid is precursor Can make prostaglandins, thromboxanes, and leukotrienes Aspirin inhibits cyclo-oxygenase. That’s why you take aspirin to reduce fever, because prostaglandins cause fever Fatty acids need to be esterified to become TG
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Cholesterol biosynthesis: HMG CoA reductase: high amount of cholesterol in the blood inhibits that enzyme. Carnitine required for oxidation of long chain fatty acid Statins inhibit HMG CoA, which reduces cholesterol, which increases LDL receptors AMPK activates catabolism Inhibits ATP consumption AMPK- energy sensor. AMPK can phosphorylate ACC which inhibits ACC. This decreases levels of malonyl CoA. SREBP: regulates gene transcription of enzymes involved in lipid metabolism Sterols inhibit movement of SREBP from ER into golgi When sterols are present, insig remains attached to SCAP, and therefor SREBP cannot move into the golgi. If it cannot go into the golgi, then it cannot act as a transcription factor for genes involving lipid
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This note was uploaded on 09/09/2011 for the course NS 331 taught by Professor Mccormick during the Spring '10 term at SUNY Buffalo.

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Outline for Prelim II - Outline for Prelim II Lipogenesis...

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