Lecture 15 Summary
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- FrontMaster model of lipid metabolismBackFed state and fasting state are the central framework for the entire lecture
- FrontFed stateBackMetabolic state after eating
- FrontMain hormone in fed stateBackInsulin
- FrontMain metabolic goals in fed stateBackStore fat and build fat
- FrontFed state dietary lipid pathwayBackDietary fat is packaged into chylomicrons, LPL releases fatty acids into tissues, adipose stores them as triacylglycerol, and the liver converts glucose to fatty acids and triacylglycerol for export as VLDL
- FrontRole of adipose tissue in fed stateBackStores fatty acids as triacylglycerol
- FrontRole of liver in fed stateBackConverts glucose to acetyl-CoA, synthesizes fatty acids, forms triacylglycerol, and exports it as VLDL
- FrontFasting stateBackMetabolic state with low insulin and high glucagon
- FrontMain hormones in fasting stateBackGlucagon high and insulin low
- FrontMain metabolic goals in fasting stateBackBreak fat and use fat
- FrontFasting state lipid pathwayBackTriacylglycerol is broken down by HSL, fatty acids travel in blood bound to albumin, undergo beta-oxidation to form acetyl-CoA, and excess acetyl-CoA is converted into ketone bodies
- FrontGold rule of lipid metabolismBackInsulin promotes storage and glucagon promotes mobilization
- FrontMajor dietary lipidBackTriacylglycerol makes up about 90 percent of dietary lipid
- FrontFunction of bile saltsBackEmulsify dietary fat
- FrontPancreatic lipase reactionBackTriacylglycerol is digested to free fatty acids and 2-monoacylglycerol
- FrontFirst route of chylomicron transportBackChylomicrons enter lymph first rather than blood directly
- FrontApo B-48BackStructural apoprotein of chylomicrons
- FrontApo C-IIBackActivates lipoprotein lipase
- FrontApo EBackHelps liver uptake of chylomicron remnants
- FrontLocation of lipoprotein lipaseBackCapillary endothelium
- FrontFunction of lipoprotein lipaseBackHydrolyzes triacylglycerol to fatty acids and glycerol
- FrontMain activator of lipoprotein lipaseBackApo C-II
- FrontHormonal effect of insulin on LPLBackInsulin stimulates lipoprotein lipase
- FrontMain enzyme of lipolysisBackHormone-sensitive lipase
- FrontSignal that activates HSLBackPKA activated by cAMP
- FrontHow free fatty acids are transported in bloodBackBound to albumin
- FrontEnzyme for fatty acid activationBackAcyl-CoA synthetase
- FrontEnergy cost of fatty acid activationBackTwo ATP equivalents
- FrontRegulated step of carnitine shuttleBackCPT I
- FrontEffect of malonyl-CoA on CPT IBackMalonyl-CoA inhibits CPT I
- FrontLocation of beta-oxidationBackMitochondria
- FrontProducts of beta-oxidationBackAcetyl-CoA, NADH, and FADH2
- FrontSite of ketone body synthesisBackLiver mitochondria
- FrontTrigger for ketone body formationBackHigh acetyl-CoA and low oxaloacetate
- FrontThree ketone bodiesBackAcetoacetate, beta-hydroxybutyrate, and acetone
- FrontLiver and ketone bodiesBackThe liver makes ketone bodies but cannot use them
- FrontReason liver cannot use ketone bodiesBackThe liver lacks SCOT
- FrontRBC and ketone bodiesBackRed blood cells cannot use ketone bodies
- FrontLocation of fatty acid synthesisBackCytosol
- FrontRate-limiting enzyme of fatty acid synthesisBackACC1
- FrontFinal product of fatty acid synthaseBackPalmitate
- FrontCarbon length of palmitateBackSixteen carbons
- FrontEffect of citrate on ACCBackActivates ACC
- FrontEffect of palmitoyl-CoA on ACCBackInhibits ACC
- FrontEffect of insulin on fatty acid synthesisBackActivates synthesis
- FrontEffect of glucagon on fatty acid synthesisBackInhibits synthesis
- FrontKey link between synthesis and oxidationBackMalonyl-CoA blocks CPT I and prevents oxidation during synthesis
- FrontMetabolic role of malonyl-CoABackActs as a switch that promotes fatty acid synthesis and inhibits beta-oxidation
- FrontRole of oxaloacetate in acetyl-CoA fateBackIf oxaloacetate is present acetyl-CoA enters the TCA cycle, and if oxaloacetate is low acetyl-CoA is diverted to ketone bodies
- FrontTransport problem of lipidsBackLipids are hydrophobic and require specialized transport systems
- FrontMicelles in lipid handlingBackTransport lipids in the intestine through the aqueous environment
- FrontChylomicrons in lipid handlingBackTransport dietary lipids
- FrontAlbumin in lipid handlingBackTransports free fatty acids in blood
- FrontEnergy logic of lipid metabolismBackWhen glucose is available the body stores fat, and when glucose is low the body burns fat
- FrontExam trap about chylomicronsBackChylomicrons do not go to the liver first
- FrontCorrect route of chylomicron travelBackLymph to blood to tissues
- FrontExam trap about liver and ketonesBackThe liver does not use ketone bodies
- FrontEnzyme missing in liver ketone utilizationBackSCOT
- FrontExam trap about fatty acid synthesis locationBackFatty acid synthesis does not occur in mitochondria
- FrontCorrect location of fatty acid synthesisBackFatty acid synthesis occurs in the cytosol
- FrontExam trap about malonyl-CoA and CPT IBackMalonyl-CoA does not activate CPT I
- FrontCorrect effect of malonyl-CoA on CPT IBackMalonyl-CoA inhibits CPT I
- FrontExam trap about free fatty acid transportBackFree fatty acids do not travel freely in blood
- FrontCorrect transport form of free fatty acidsBackFree fatty acids require albumin in blood
- FrontPrediction if ACC is activeBackFatty acid synthesis increases and beta-oxidation decreases
- FrontPrediction if insulin is highBackHSL activity decreases and LPL activity increases
- FrontPrediction if oxaloacetate is lowBackTCA cycle entry of acetyl-CoA decreases and ketone body formation increases
- FrontFed state ultra-condensed summaryBackChylomicrons deliver dietary fat, LPL releases fatty acids for storage, glucose supports fatty acid synthesis, ACC is active, and malonyl-CoA is increased
- FrontFasting state ultra-condensed summaryBackHSL releases fatty acids, albumin transports them, beta-oxidation produces acetyl-CoA, and ketone bodies increase
- FrontMaster switch for fatty acid synthesisBackACC
- FrontMaster switch for fatty acid oxidationBackCPT I
- FrontMaster inhibitor of fatty acid oxidation during synthesisBackMalonyl-CoA
- FrontTransport form of dietary fatBackChylomicrons
- FrontTransport form of free fatty acidsBackAlbumin
- FrontTransport form of ketone bodiesBackThey travel freely because they are water-soluble
- FrontFive highest-yield facts to memorizeBackInsulin versus glucagon effects, malonyl-CoA inhibits CPT I, Apo C-II activates LPL, HSL mediates lipolysis, and the liver makes but cannot use ketone bodies
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