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179 Cards in this Set
- Front
- Back
Is TCA cycle aerobic or anaerobic
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AEROBIC only
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TCA cycle occurs in _
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mitochondrion
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Major source of ATP
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TCA cycle
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TCA cycle requires vitamins/coenzymes. Name them
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-Coenzyme A - CoA or CoA-SH
-Niacin - NAD -RIboflavin - FAD -Thiamine - for oxidative decarboxylation -Lipoic acid - COENZYME only, not a vitamin, for oxidative decarboxylation -Biotin - for carboxylation |
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Pyruvate dehydrogenase complex
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Multienzyme complex located exclusively in mitochondrial matrix, catalyzes oxidative decarboxylation of pyruvate, forming acetyl CoA
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Energy gain of TCA cycle
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NADH and FADH2 produced by the cycle donate electons to electron transport chain.
Each NADH produces 3 ATP, and there are 3 NADH molecules so it gives 9 ATP. Each FADH2 gives 2 ATP, and there is one FADH. ALso GTP is produced when succinyl CoA is cleaved, and GTP produces ATP. TOTAL ENERGY = 12 ATP |
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What is the role of oxaloacetate
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Cycle starts with 4 carbon oxaloacetate, adds 2 carbons from acetyl CoA, loses 2 carbons as CO2 and regenerates 4 carbon compound oxaloacetate
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How is citrate formed
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-Acetyl CoA and oxaloacetate condense forming CITRATE
-Enzyme - citrate synthase -Cleavage of high energy thioester bond in acetyl CoA provides energy for this condensation -Citrate(product) is inhibitor of this reaction |
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Which reaction of TCA cycle provides large negative G to drive the cycle
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Formation of citrate
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Citrate is ismerized to _
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Isocitrate by rearrangement of the molecule
Enzyme - aconitase |
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Isocitrate is oxidized into _
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Alpha Ketoglutarate
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First oxidative decarboxylation reaction
Describe whats produced |
Oxidation of isocitrate into alpha ketoglutarate - CO2 is produced and electrons are passed to NAD+ to form NADH + H+
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Enzyme that catalyzes oxidative decarboxylation of isocitrate
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Isocitrate dehydrogenase - key regulatory enzyme of TCA cycle - allosterically activated by ADP and inhibited by NADH
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What is the second oxidative decarboxylation reaction
Describe whats produced |
Conversion of alpha ketoglutarate to succinyl CoA
CO2 is released and succinyl COA, NADH and H+ are produced |
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Two enzymes that are large multienzyme complexes and require multiple cofactors
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Alpha ketoglutarate dehydrogenase
Pyruvate dehydrogenase |
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Enzyme that catalyzes conversion of alpha ketoglutarate to succinyl CoA
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Alpha ketoglutarate dehydrogenase
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Alpha ketoglutarate dehydrogenase requires 5 cofactors - name them
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-Thiamine pyrophosphate
-Lipoic acid -CoASH -FAD -NAD+ |
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Thiamine defficiency
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-Common in alcoholics
-Decreases pyruvate dehydrogenase activity, causing pyruvate to accumulate and form lactate -Slows TCA cycle at alpha ketoglutarate dehydrogenase step -Also called beri-beri disease |
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Wet beri beri causes _
Dry beri-beri causes _ |
edema (heart failure)
Polyneuropathy |
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_ impairs thiamine absorption
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ALCOHOL
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Succinyl COA is cleaved into _
Describe reaction |
Succinyl COA is cleaved into succinate.
-Cleavage of high energy thioester bond of succinyl COA provides energy for substrate level phosphorylation of GDP to GTP (NOT an oxidative phosphorylation - does not involve electron transport chain) |
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Enzyme that catalyzes conversion of succinyl CoA to succinate is _
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Succinate thiokinase ( or succinyl COA synthetase)
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Succinate is oxidized to _
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Fumarate - succinate transfers two hydrogens together with their electrons to FAD forming FADH2
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Enzyme that catalyzes conversion of succinate to fumarate is _
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Succinate dehydrogenase - in inner mitochondrial membrane
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All the enzymes of TCA cycle are present in _ , except _ that is present in _
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Mitochondrial matrix
EXCEPT succinate dehydrogenase that is in inner mitochondrial membrane |
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Fumarate is converted to _
Enzyme - _ |
Malate by addition of water across double bond
Enzyme - fumarase |
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Malate is oxidized regenerating _
Enzyme ? |
Oxaloacetate, completing the cycle
Enzyme - malate dehydrogenase |
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What is produced in oxidation of malate
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Oxaloacetate and two hydrogen with electrons are passed to NAD+, producing NADH and H+
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Describe anaplerotic reactions of TCA cycle
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Anaplerotic reactions replenish intermediates of TCA cycle as they are removed for synthesis of glucose, fatty acids, amino acids or other compounds
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Key anaplerotic reaction and what enzyme catalyzes it
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Carboxylation of pyruvate to form oxaloacetate
Enzyme - pyruvate carboxylase |
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Pyruvate carboxylase requires _
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Biotin - cofactor, vitamin B
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What causes biotin defficiency
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Biotin can be complexed by Avidin - protein in egg white
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Pyruvate carboxylase is found in _ and is activated by _
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Found in liver, brain and adipose tissue (NOT in muscle) and is activated by acetyl CoA
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Pyruvate dehydrogenase catalyzes reaction that provides TCA cycle with _
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Acetyl CoA
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Pyruvate dehydrogenase is activated by _
Inhibited by _ |
Activators:
-Pyruvate -CoA -NAD+ -Ca -ADP Inhibitors: -NADH -ACetyl CoA |
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Rate of flux through TCA cycle depends on _ and _
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NADH/NAD+
ATP/ADP |
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2 major sites of regulation of TCA cycle
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-Isocitrate dehydrogenase - inhibited by NADH, activated by Ca and ADP
-Alpha oxoglutarate dehydrogenase - inhibited by NADH, activated by Ca |
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Import of proteins into mitochondria requires _
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Chaperones on both sides of the membrane
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Oxidative phosphorylation occurs in
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Mitochondria
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"Hydrogen acceptor" part of NAD + is made from _
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Niacin (vitamin B3)
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Electron transport chain is located in _
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Inner mitochondrial membrane
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How NADH and FADH2 get from matrix to membrane
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-NADH freely diffuses
-FADH2 tightly bound to enzymes that produce it within inner mitochondrial membrane |
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First stage of electron transport is _
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Transfer of electrons from NADH to coenzyme Q via NADH dehydrogenase complex to FMN to coenzyme Q
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Second stahe of electron transport is _
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Transfer of electrons from coenzyme Q to cytochrome C
(first to cytochromes b and c1) |
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Third stage of electron transport chain is _
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Transfer of electrons from cytochrome c to oxygen
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Each complex in electron transport chai uses energy from electron transfer to _
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Pump protons to cytosolic side of membrane
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Electrochemical potential consists of _
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-pH gradient
-membrane potential |
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Is inner mitochondrial membrane permeable to protons?
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No
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How do protons re enter matrix
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Through ATP synthase complex - causes generation of ATP
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How is ATP synthesized in oxidative phosphirylation
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Protons return to mitochondrial matrix through the channel made by ATP synthase --> this causes conformational change in ATP synthase --> catalyzes reaction ADP + Pi --> ATP
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_ protons are transfered out for each ATP synthesized
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4
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NADH oxidation produces _ ATP
FADH2 oxidation produces _ ATP |
2.5
1.5 |
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Describe chemiosmotic model of Peter Mitchell
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-Energy is released as electrons are passed down the chain
-This energy is used to pump protons out of mitochondrial matrix forming electrochemical gradient across membrane -Electrons move down gradient re entering matrix through pore in ATP synthase -This causes conformational change in ATP synthase leading to catalysis of ATP production |
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Describe cyanide poisoning
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Cyanide binds to Fe3+ in cytochrome aa3. As a result oxygen cannot receive electrons, respiration is inhibited, energy production is stopped and death ensues
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Describe uncoupling agents - give examples
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Uncoupling agents are poisons
Example - dinitrophenol Those agents are ionophores that allow protons from cytosol to re enter matrix without passing through ATP synthase complex - thus they uncouple electron transport and ATP production |
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When uncoupling occurs energy is lost as
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Heat
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Describe thermogenesis and brown adipose tissue
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Brown adipose tissue contains many mitochondria (gives it its color)
Inner mitochondrial membrane of brown adipose tissue contains THERMOGENIN - protein that transports proteins across membrane. This uncouples oxidative phosphorylation and produces HEAT instead of ATP |
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What happens in aspirin poisoning
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High concentrations of salicylate partially uncouple mitochondria
-Increased AMP and decreased ATP stimulate glycolysis -Glycolysis leads to increased blood concentration of lactate which leads to metabolic acidosis |
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Role of mitochondria in cell death
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Ischemia can result in inadequate oxygen supply to maintain proton gradient and ATP synthesis
-Mitochondrion permeability transition pore opens and protons and ions flood mitochondria leading to its swelling and bursting |
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Oxidative phosphorylation disease are usually due to _
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mutations in mitochondrial DNA
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LHON
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Lebers Hereditary Optic Neuropathy - sudden blindness in young males, less common symptoms mild dementia, ataxia, peripheral neuropathy
-Inherited maternally -caused by various mutations in complexes I, II and IV polypeptides encoded by mitochondrial DNA -90 % caused by mutations of NADH dehydrogenase |
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MERRF
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Myotonic epilepsy and Red Ragged Fiber disease - myoclonus, ataxia, muscle weakness, deafness and progressive dementia
-Caused by mutations in mitochondrial RNA |
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MELAS
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Mitochondrial myopathy, encephalomyopathy, lactic acidosis and stroke-like episodes
-Progressive neurodegenerative disease, onset 5-15 years -Caused by mutations in tRNA |
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Mitochondrial disease
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Age related decline in oxidative capacity may be due to continuous oxidative damage to mitochondrial DNA
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Definition of glycolysis
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Catabolism of glucose to pyruvate or lactate
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Aerobic glycolysis
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Glucose to pyruvate
ATP is produced by both oxidative and substrate level phosphorylation |
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Anaerobic glycolysis
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Glucose to lactate
ATP is produced by substrate level phosphorylation only |
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Principal function of glycolysis
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Production of ATP from glucose
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Where does glycolysis occur
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In cytosol of every cell of the body
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HK and PFK1 reactions involve what
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Phosphorylation with ATP - glucose in converted to glucose 6 phosphate and then to fructose - 6 - phosphate
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Which steps of glycolysis produce ATP
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1. 1,3- BPG reacts with ADP to produce 3 - phosphoglycerate and ATP, catalyzed by phosphoglycerate kinase
2. Phosphoenolpyruvate reacts with ADP to produce ATP and pyruvate --> last reaction of glycolysis, enzyme - pyruvate kinase 2. |
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Anaerobic glycolysis is important in some tissues. They are _
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renal medulla and skeletal muscle
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Some tissue types entirely depend on anaerobic glycolysis They are -
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RBC and some areas of the eye - do NOT have mitochondria
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Yield of aerobic glycolysis
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2 molecules of ATP are used and 4 molecules of ATP are made - net gain of 2 ATP molecules and 2 molecules of NADH
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Yield of anaerobic glycolysis
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2 molecules of ATP only
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Two ways by which electrons are passed to electron transport chain
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Glycerol phosphate shuttle and malate aspartate shuttle
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List biosynthetic functions of glycolysis
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Glycolysis provides precursors for
-Fatty acid biosynthesis from pyruvate -Triacylglycerol formation from glycerol - 3- P -Amino acid formation from alanine, serine, glycine, cysteine -Ribose 5-P for nucleotide synthesis from glyceraldehydes 3 p ans fruktose 6 P -2,3 BPG for Hb - |
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Describe Cori cycle
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In muscle glucose is turned into lactate via glycolysis --> lactate goes to liver where its taken up -->In the liver lactate is turned back to glucose via gluconeogenesis
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Explain how and under what conditions lactic acidemia occurs
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An increase in lactate blood levels causes lactic acidemia. This condition can result from hypoxia or alcohol ingestion. Lack of oxygen slows electron transport chain, resulting in increased NADH. High NADH causes more then normal amount of pyruvate to be transferred into lactate
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Main regulatory enzyme of glycolysis is _
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PFK1 - catalyzes reaction that transfers fructose - 6- phosphate into fructose - 1,6 bisphosphate using ATP and producing ADP
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In muscle PFK 1 is activated by _
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AMP - during exercise AMP levels are high and ATP levels are low. Glycolysis is promoted by PFK1 and ATP is generated. ATP and citrate inhibit PFK1. When ATP is high, cell doesnt need ATP and glycolysis is inhibited. High citrate means that enough substrate is entering TCA cycle so glycolysis slows down
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In adipose and liver PFK1 is activated by _
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fructose - 2,6 bisphosphate
PFK2 makes 2,6 bisphosphate from fructose - 6- P after meal. Fructose 2,6 bisphosphate activates PFK1 and glycolysis is stimulated. Liver uses glycolysis for production of fatty acids and triacylglycerol |
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Which hormone promotes glycolysis
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High insulin - fed state
Insulin causes phosphatases to be stimulated. Phosphatase dephosphorylates PFK2 causing it to become more active in producing 2,6 bisphosphate which activates PFK1 and promotes glycolysis |
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Which hormone inhibits glycolysis
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High glucagon - fasting state
PFK 2 is phosphorylated which makes it less active and converts fructose 2,6 bisphosphate back to fructose 1,6 phosphate, making PFK1 less active and decreasing glycolysis |
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Enzyme inhibitor
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Molecule that binds to enzyme and decreases rate of reaction
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Irreversible inhibitor
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Binds covalently, inhibition progresses with time, effect cannot be overcome by dilution or dialysis but can be overcome by adding more enzyme
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Reversible inhibitor
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-Bind by weak interactions
-At equilibrium with enzyme -Can be overcome by dialysis or dilution |
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Covalent inhibitor
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Irreversible inhibitor that covalently modifies specific amino acid side chains at the active site in progressive chemical reaction
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Explain organophosphorous compounds and give examples
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Sarin + malathione - inhibit acetylcholinesterase which blocks transmission at NMJ. They covalently modify serine at the active site of acetyl cholinesterase
Sarin - chemical weapon Malathione - insecticidde |
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Aspirin as covalent inhibitor
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Aspirin covalently modifies cyclooxygenase
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How are covalent inhibitors used in treatment of myasthenia gravis
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In myasthenia gravis you dont have enough of Ach so by blocking covalently an enzyme that degrades Ach you increase concentration of Ach at NMJ which helps to reduce symptoms of myasthenia gravis
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Mechanism based inhibitor
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Substrate or transition state analogs which initially are processed by normal catalytic mechanism, after which they are converted into intermediate resembling transition state that binds covalently to enzyme. Also called suicide inhibitors
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Allopurinol
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Purine analog
-Mechanism based inhibitor of xanthine oxidase -Reduces uric acid production and is used in treatment of gouty arthritis |
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Penicillin
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Mechanism based inhibitor
-Inhibits transpeptidase essential for synthesis of bacterial cell walls, it contains strained peptide bond that resembles transition state |
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Heavy metals as inhibitors
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Heavy metals like lead or mercury can bind non specifically and irreversibly to many groups on enzymes and can replace essential metal ions in enzymes - Ca, Mg, Zn
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Lead inhibits
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ALA - dehydratase and ferrochelatase which will lead to symptoms similar to porphyrias
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Competitive inhibitors
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Compete with substrate for active site of enzyme and form enzyme substrate complex
You can reverse it by adding more substrate |
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In competitive inhibition, Km _ and Vmax _
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Km increases
Vmax stays same |
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Non competitive inhibitors
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Inhibitors that bind to enzyme or enzyme substrate complex at site other then active site thus decreasing activity of enzyme
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In non competitive inhibition Km _ and Vmax _
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Km same
Vmax decreases |
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Explain action of sulfonamides
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-Competitive inhibitor
-Folic acid is essential for nucleotide synthesis, folic acid is made of PABA and sulfonamides mimic PABA and competitively inhibit dihydropteroate synthetase in bacteria -First anti-bacterial agents |
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Explain action of methotrexate
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-Chemotherapy drug
Methotrexate mimicks folic acid and competitively inhibits dihydrofolate reductase |
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Warfarin
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-Competitively inhibits vitamin K epoxide reductase which regenerates active form of vitamin K, which is essential for some clotting factors
-ANTI- COAGULANT |
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Statin
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-Anti hyperlipidemic drug
-Competitively inhibits HMG CoA reductase - rate limiting step of cholesterol synthesis |
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ACE inhibitors
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-Captopril and enalopril
-Competitively inhibits ACE - angiotensin converting enzyme -ACE is used to convert angiotensin I to angiotensin II in lungs which elevates blood pressure Inhibiting ACE leads to lower blood pressure, captopril competes with angiotensin I for binding to ACE active site |
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Allosteric enzyme
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Enzyme that binds activators or inhibitors at site other then active site
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Allosteric activator
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Forces enzyme to bind substrate more readily
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Allosteric inhibitor
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causes enzyme to bind less readily
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T state is _
R state is _ |
T state - low affinity
R state - high affinity |
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In cooperative binding when there is no substrate enzyme is in _ state, when it binds enzyme is in _ state
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T state
R state |
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Inhibitors bind and stabilize _ state
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T
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Activators bind and stabilize _ state
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R
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Enzyme that is activated by phosphorylation
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Glycogen phosphorylase
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Ca calmodulin
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-important in muscle contraction, Ca binds to calmodulin and calmodulin activates glycogen phosphorylase kinase
|
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G proteins
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Activated by binding GTP, they hydrolyze GTP and are no longer active after that
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Zymogens
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Inactive precursors - prevent enzymes from cleaving proteins prematurely at sites of synthesis or secretion
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Pepsinogen
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Catalyzes its own cleavage as pH of stomach drops
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Protein kinase A
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PKA is activated by cAMP --> activates phosphorylase kinase -> activates glycogen phosphorylase
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After heart attack there is an increase in in blood levels of
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MB isozyme of creatine kinase
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Equation for G
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G = H- TS OR
G = G' + RT ln [products]/[reactants] |
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If G<0, then reaction is
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EXERGONIC - reaction will proceed spontaneously and energy will be released
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If G >0, then reaction is
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ENDERGONIC - reaction will not go spontaneously and there is gain of energy
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If G= 0, reaction is
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in equilibrium
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At equilibrium, G' =
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-RT ln Keq
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What information does G provide and what information it does not provide
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Provides information about free energy changes and provides definition of where equilibrium lies but it DOES NOT give information about rate of reaction
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ATP is consumed by what kind of processes?
Regenerated? |
Consumed by muscular contraction, active transport and biosynthetic reactions, regenerated by oxidation of food stuff
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When ATP is hydrolyzed, _ is released
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Free energy - used to drive reactions that require energy
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Define biochemical work
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Biochemical work occurs in anabolic pathways which are pathways that synthesize large molecules - DNA, glycoge, triacylglycerols from smaller compounds. Biochemical work also occurs when toxic compounds are converted to non toxic compounds that can be excreted (liver converts ammonium to urea that can be excreted).
In general formation of new bond requires energy and therefore requires biochemical work |
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Estimated daily use of ATP
|
Heart - 16
Brain - 6 Kidneys - 24 Liver- 6 Skeletal muscle (rest) - 0.3 Skeletal muscle (running) - 23.6 |
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3 METHODS OF ATP PRODUCTION
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OXIDATIVE PHOSPHORYLATION - production of ATP is coupled to electron transport chain to O2, in inner mitochondrial membrane
SUBSTRATE LEVEL PHOSPHORYLATION - transfer from substrate to product, requires ADP + Pi -> ATP HIGH ENERGY PHOSPHATE GROUP TRANSFER- creatine phosphate is high energy phosphate reservoir and shuttle in brain, muscle and sperm |
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High energy phosphorylated molecules other then ATP
|
Acetyl CoA
1,3 - BPG phosphoenolpyruvate creatine phosphate |
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Reduction potential
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Measure in volts of energy change when compound accepts an electron - becomes reduced - measure of willingness of compounds to accept electrons
|
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Negative reduction potential means
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Greater energy is available for ATP generation when compound passes electrons to O2
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As food is oxidized electrons are passed to _
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FAD and NAD
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NAD derived from _ and accepts _ electrons
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Niacin - one electron
|
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FAD derived from _ and accepts _ electrons
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Riboflavin - 2 electrons
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NAD and FAD are _ and substrate is _
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Reduced
Oxidized |
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Anabolic processes
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-Reductive processes
- Occur when molecules are being built (stored as fuels) -Primarily during fed state |
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Catabolic processes
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Oxidative processes
-Occur when molecules are being burnt for energy -During fasting and fed states |
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What do cells first do when they are in fed state
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MEET THEIR ENERGY NEEDS (then they store energy if they can)
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Fate of carbs in fed state
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-Digested to monosaccharides and absorbed in blood
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Major monosaccharide
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Glucose
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Glucose in fed state has 2 fates -
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-Oxidized for energy
-Enters biosynthetic pathway - making TAG or glycogen |
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Fate of proteins in fed state
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-Digested to individual amino acids and abdorbed in blood
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Proteins in fed state can be _
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-Turned into other proteins
-Turned into N containing compounds -Converted to glucose (liver) -Oxidized for energy |
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Fate of fats in fed state
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-Digested to fatty acids
-Built into TAG particles -Delivered to adipose tissue |
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How do carbs, fats and proteins get to organs
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Absorbed by intestinal epithelial cells
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What happens when blood glucose is elevated
|
Insulin is secreted by beta cells of pancreas
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What happens to glucose in liver
|
-First, glucose is oxidized to CO2 and H2O through insulin induced glycolysis and oxidative phosphorylation) to meet energy needs of liver
-Excess glucose is stored as glycogen -Excess acetyl CoA is used to make fatty acids, fatty acids are combined with glycerol to make TAG and are packaged into VLDL particles for export from liver |
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What happens to glucose in brain
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Glucose is internalized by brain and is completely oxidized to CO2 and H2O through glycolysis and oxidative phosphorylation to meet energy needs of brain
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What happens to glucose in RBC
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Glucose is taken up by RBC and is metabolized to lactate through anaerobic glycolysis
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What happens to excess blood glucose
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It is taken up by insulin dependent transporters that are present in muscle and adipose
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What happens to glucose in muscle
|
It is oxidized to CO2 and H2O to meet energy needs or is stored in form of glycogen
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How are fatty acids delivered to adipose
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Through chylomicrons (dietary fat) or VLDL particles (newly synthesized fat)
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Glycerol and fatty acids make
|
TAG
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Describe digestion of carbohydrates
|
Starch - main carbohydrate we get from plants and other carbohydrates are digested with help of salivary and pancreatic amylase to disaccharides. Disaccharides are cleaved to monosaccharides by enzymes found on brush border of intestinal epithelial cells. ONLY monosaccharides are absorbed by intestinal epithelial cells. Then glucose enters portal circulation
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Describe digestion of proteins
|
Proteins are digested first by PEPSIN in stomach and then by different enzymes in intestine. Individual amino acids are absorbed by intestinal epithelial cells and enter portal circulation
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Describe digestion of fats
|
Triacylglycerol is primary diet fat. Triacylglycerol is emulsified in the intestine by bile salts and digested by pancreatic lipase to 2-monoacylglycerols and fatty acids which are packaged into micelles and absorbed into intestinal epithelial cells where they are reconverted into triacylglycerols
After digestion and resynthesis, triacylglycerols are packaged in chylomicrons that first enter lymph and then blood. |
|
What happens 1 hour after meal
|
-Blood glucose levels fall
-Insulin secretion decreases -Glucagon levels increase |
|
When does fasting state begin
|
2-4 hours after meal
|
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During fasting blood glucose levels are maintained at
|
80-100 mg/dL
|
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Blood glucose during fasting is maintained by 2 mechanisms
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-Glycogen breakdown
-Gluconeogenesis |
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Which hormone is increased during fasting
|
Glucagon - alpha cells of pancreas
|
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What happens in liver during fasting
|
-Liver glycogen begins to break down into glucose
-Glucose is exported from liver to brain |
|
What happens in brain during fasting
|
Glucose is exported from liver to brain where its oxidized to CO2 and H2O through aerobic glycolysis to meet energy needs
|
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What happens to fats in fasting state
|
In response to low insulin levels triacylglycerol is broken down into glycerol and fatty acids.
Fatty acids released from adipose tissue are taken up by muscle to oxidize it to CO2 and H2O to meet its energy needs They are also taken up by liver to meet its energy needs after what they are converted to ketone bodies |
|
In fasting state ketone bodies made by liver can be used by _
|
Muscle to meet its energy needs
|
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What happens to amino acids in fasting state
|
Amino acids are released after protein degradation in muscle and are carried to liver (mostly in form of alanine) where they are converted to glucose through gluconeogenesis
Amino groups are removed from amino acids and are converted to urea which is excreted in urine |
|
Lactate in fasting state is sent from RBC to _
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Liver where its converted to glucose through gluconeogenesis
|
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What happens to glycerol in fasting state
|
Glycerol released from adipose tissue via hormone sensitive lipase - taken up by liver and converted to glucose through gluconeogenesis
|
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Main organ to maintain blood glucose during fasting is _
|
liver
|
|
Carbon sources for gluconeogenesis
|
-Lactate
-Glycerol -Alanine |
|
What happens to ketone bodies during starvation
|
During starvaton levels of ketone bodies in blood are very high and beyond the level that can be utilized by muscle - BRAIN will utilize ketone bodies for energy during starvation
|
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What happens in muscle during starvation
|
Muscle protein is degraded and alanine is released and taken up by liver
|
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What happens in liver during starvation
|
Liver will continue to use alanine, glycerol and lactate to make glucose
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What happens to glucose in starvation
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Glucose will be exported from the liver and will be utilized by RBC for energy and to make NT in the brain
|
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What happens to fatty acids in starvation
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They are converted to ketone bodies in liver and utilized by brain
|
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Does liver use ketone bodies to meet its energy needs during starvation
|
NO
|
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Name two ketone bodies used for energy
|
Acetoacetate
Hydroxybutarate Acetone is also a ketone body but its not used for energy |