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80 Cards in this Set
- Front
- Back
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Can amino acids be stored?
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NO
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What are the sources of free amino acids?
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Digestion and Protein Turnover
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Places where proteins are digested
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Stomach, intestinal lumen, intestinal epithelium, intestinal cell interior
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Name of enzyme embedded in intestinal cell epithelium.
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Aminopeptidase
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What is the mark of destruction for a protein?
How does it attach to a protein? |
Ubiquitin
Through an isopeptide bond |
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Protein degradation
1. What complex degrades peptides? 2. What does it degrade marked peptides into? 3. And then? 4. The 3 fates of the substrate 5. The 3 fates of the carbon skeleton |
1. Proteasome
2. Peptide fragments + recycled ubiquitin 3. Amino acids 4. Biosynthesis Amino group plucked for urea cycle Carbon skeleton 5. Glucose/Glycogen synthesis Cellular respiration Fatty acid synthesis |
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What can seriously determine the half life of proteins?
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The N terminal residues
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What are some processes regulated by protein degradation?
(8) |
Gene transcription
Cell cycle progression Organ formation Circadian rhythms Inflammatory response Tumor suppression Cholesterol metabolism Antigen processing |
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What is the major site of amino acid degradation?
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The liver
but it also occurs in the muscle |
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What is the first step in Amino Acid degradation?
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The removal of nitrogen
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How do amino acids get rid of their amino groups?
What is the enzyme involved? |
All amino acids transfer their amino groups to alpha ketoglutarate (an alpha keto-acid), forming glutamate.
Aminotransferase |
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How does glutamate get rid of the ammonia ion?
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By oxidative deamination
Catalyzed by glutamate dehydrogenase, which turns NAD+ into NADH (hence, oxidative!) Schiff base is hydrolyzed into alpha ketoglutarate, releasing free ammonia Free ammonia forms urea |
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How many atp equivalents are used in the formation of urea?
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4 atp's
3 atp --> 2 ADP + 2Pi + AMP+ PPi 2 atps --> in formation of carbamoyl phosphate 1 atp (two equivalents) citruline + L-aspartate ---> argininosuccinate |
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In urea:
1. The urea cycle begins with formation of 2. What is combined to make this molecule 3. what enzyme catalyzes the reaction 4.. What compound provides the other amino group to form urea? 5. Where do these reactions occur? |
1. Carbomoyl phosphate
2. CO2 and free NH3 3. Carbamoyl phosphate synthetase 4. Aspartate 5. Mitochondrial matrix |
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What are the stages of molecules in the urea production cycle, starting with carbamoyl phosphate?
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Carbamoyl phosphate
Citruline Argininosuccinate Arginine Ornithine |
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How is the urea cycle linked to gluconeogenesis?
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In the urea cycle, one of the byproducts is fumarate.
argininosuccinate --> arginine byproduct: fumarate fumarate --> malate --> Oxaloacetate --> glucose |
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How is the urea cycle linked to gluconeogenesis?
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In the urea cycle, one of the byproducts (argininosuccinate converted to arginine) is fumarate
fumarate --> malate --> Oxaloacetate --> glucose |
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If urea cycle is broken, what happens?
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Excess NH4+ accumulates in the blood.
Ammonia + glutamate --> glutamine. The osmotic effects lead to brain swelling. |
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What are the entry points for amino acids when they are degraded to their carbon skeletons?
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Alot of krebs cycle intermediates
(glucogenic) Pyruvate alpha-keto-glutarate Succinyl Coa Fumarate Oxaloacetate Ketogenic Acetyl CoA Acetoacetyl CoA |
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Inborn errors of amino acid metabolism:
an example |
phenylketonuria:
person lacks the enzyme for turning phenylalanine into tyrosine. causes severe mental retardation |
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Renal glutamine metabolism produces bicarbonate
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glutamine --> alpha keto glutarate + 2NH4+
alpha-ketoglutarate --> glucose + CO2 |
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What process helps with buffering in the blood? Takes away acidity?
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alpha-ketoglutarate produces CO2 in krebs cycle on its way to succinyl coA
CO2 takes on H+ (neutralizing ketone bodies) Part of H+ is excreted attached to NH4+, increasing pH |
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Can the carbon skeleton from alpha keto glutarate be used in gluconeogenesis in the kidney?
Bicarbonate as a buffer is lost over time. How? |
Yes
It is protonated, decarboxylated to form CO2 which is breathed out of the lungs. |
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Synthesis of catecholamines:
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Tyrosine -> dopamine -> norepinephrine -> epinephrine
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Synthesis of Serotonin:
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Tryptophan --> oxidized, decarboxylated --> serotonin
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What is the amino acceptor group in the synthesis of:
1. Alanine 2. Aspartate 3. Asparagine 4. Glutamate 5. Glutamine |
1. pyruvate
2. oxaloacetate 3. oxaloacetate 4. alpha-keto-glutarate 5. alpha-keto-glutarate |
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Synthesis of glutamate:
1. what is combined with ammonium ion? and also dehydrated? 2. What does that form? 3. What do you do to that? 4. What is the product reduced with? 5. Enzyme involved with all o this? |
1. alpha keto glutarate
2. schiff base 3. protonate it 4. NADPH, to form glutamate. 5. Glutamate dehydrogenase |
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Pyruvate is a major metabolic precursor for which amino acids?
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Alanine
valine (ess) leucine (ess) |
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Alpha keto glutarate is a major precursor for which amino acids?
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glutamate
which gives rise to: glutamine proline arginine |
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3-phosphoglycerate is a major precursor for which amino acids?
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Serine
which gives rise to: Cysteine Glycine |
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Metabolic regulation: 5 types
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Allosteric modification
Covalent modification Enzyme amount Compartmentation Metabolic Specializations of Organs |
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Compartmentation:
What occurs in: 1. The cytoplasm 2. Inner mitochondrial membrane 3. Mitochondrial matrix 4. Interplay of both compartments |
1. Glycolysis
Pentose phosphate pathway fatty acid synthesis 2. Oxidative phosphorylation 3. Citric acid cycle Beta oxidation of fatty acids Ketone body formation 4. Gluconeogenesis Urea synthesis |
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What is the key enzyme in the regulation of glycolysis?
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Phosphofructokinase
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Phosphofructokinase:
1. What does it do 2. Activated by 3. Inhibited by |
1. Converts F-6-P to F-1,6-BP
2. F-2,6-BP AMP 3. ATP and Citrate |
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Pyruvate dehydrogenase complex:
1. What does it do 2. How is it regulated |
1. converts pyruvate into acetyl coA
2. by allosteric interactions. Only if ATP or two carbon fragments are required for the synthesis of lipids. |
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Pentose phosphate pathway
1. What does it do 2. How is it regulated 3. products 4. committed step |
1. Converts G6P to ribose-5-phosphate
2. controlled by the level of NADP+. 3. NADPH (X2) 4. dehydrogenation of g6p |
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Gluconeogenesis
1. What is it 2. What is the major entry point 3. What is an essential enzyme |
1. creation of glucose from non carbohydrate precursors
2. Pyruvate, converted to oxaloacetate and then phosphoenolpyruvate 3. fructose 1,6 bisphosphatase |
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fructose 1,6 bisphosphatase
1. What does it do 2. What activates it 3. What inhibits it |
1. Converts fructose 1,6 bisphosphate to fructose 6 phosphate
2. citrate 3. AMP, F-2,6-BP |
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Fatty acid synthesis
1. What is the key enzyme 2. What activates it 3. What inhibits it 4. what does this enzyme do to acetyl coA |
1. Acetyl CoA carboxylase
2. citrate 3. palmitoyl CoA 4. carboxylates it to form malonyl coA |
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Fatty acid stuff transportation:
1. How does acetyl coA get out of the mitochondria 2. How do fatty acids enter the mitochondria |
1. citrate malate shuttle
2. Carnitine |
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What inhibits carnitine acyltransferase?
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Malonyl coA
if you're trying to build up fatty acids, you synthesize malonyl CoA, and definately don't need to transport fatty acids inside the mitochondria to break them down |
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G-6-Phosphate
What happens to it if 1. g6p and atp are abundant 2. atp or carbon skeletons for biosynthesis are required 3. we need NADPH for reductive biosynthesis and ribose 5 for sythesis of nucleotides |
1. glycogen is formed
2. glycolytic pathway 3. pentose phosphate pathway |
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Pyruvate
1. role in allowing glycolysis to continue under anaerobic conditions 2. role in linking amino acid and carbohydrate metabolism 3. gluconeogenesis 4. glycolysis |
1. replenishes NAD+ supply by forming lactate
2. transamination of pyruvate forms alanine 3. can be carboxylated to form oxaloacetate, which then turns to phosphoenolpyruvate, bypassing checking system of glycolysis 4. decarboxylated to form acetyl CoA |
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Acetyl CoA
1. sources 2. role in citric acid cycle 3. role in fatty acid synthesis 4. 3-hydroxy-3-methylglutaryl CoA |
1.Decarboxylation of pyruvate
B-oxidation of fatty acids 2. turned into CO2 with a crank of the citric acid cycle, pumps out atp, nadh and fadh2 3. exported to cytoplasm in the form of citrate 4. formed from 3 molecules of acetyl CoA. precursor of cholesterol and ketone bodies, which are transport forms of acetyl CoA |
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What is the sole fuel source of brain during normal conditions?
What can also be a source during starvation? |
glucose
ketone bodies and glucose |
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How much of the bodies glycogen is stored in muscle.
What is the heart's main source of fuel? What is the major source of fuel of resting skeletal muscle |
3/4
fatty acids but sometime ketone bodies too fatty acids |
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Ways muscle and liver interact
1. during vigorous exercise 2. how it uses branched chain amino acids, how it gets rid of urea 3. what the liver does after step 2 |
1. glycolysis occurs much faster than citric acid cycle. Excess pyruvate converted to lactate, transported to liver, converted to glucose
2. muscle transaminates amino acids to use carbon skeleton for fuel. Muscle cannot form urea, so it transports ammonia in form of alanine to liver. 3. liver absorbs alanine, disposes of nitrogen, processes pyruvate to glucose or fatty acids |
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Why do adipose cells need glucose for th synthesis of triacylglycerols?
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Because glucose provides an intermediate, glycerol 3 phosphate, the backbone to which fatty acids attach. This comes from the reduction of the glycolytic intermedate, dihydroxyacetone phosphate.
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If glucose levels are low inside adipose tissue, what happens to fatty acids?
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They are released into the blood because they do not have the glycerol 3 phosphate backbone to attach to.
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Can the liver remove nitrogen from branched chain amino acids, leucine, isoleucine, and valine?
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No. Transamination of these takes place in the muscle.
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How does the liver form glycogen after a meal, faster than muscle can?
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It possess glucokinase, a special kind of hexokinase that has a very high Km. This means that it would take a substantial increase in blood glucose for it to be stored away as glycogen. Muscle and brain must use first.
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How does glucose change the glycogen system from a degradative to a synthetic mode?
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Glucose acts as an allosteric modifier of glycogen phosphatase a, turning it to phosphatase B which is inactive.
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Insulin
1. Promotes entry of 2. Stimulates the synthesis of 3. Entry of glucose into adipose tissue provides 4. promotes uptake of what kind of amino acids? 5. Stimulates protein synthesis or degradation? 6. Inhibits what process involved with proteins? |
1. glucose into muscle and adipose tissue
2. glycogen, by muscle and liver 3. glycerol 3 phosphate for triacylglyercol production 4. branched chain amino acids 5. Protein synthesis 6. protein degradation |
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Glucagon
1. Stimulates 2. inhibits |
1. glycogen breakdown by triggering cyclic AMP cascade leading to phosphorylation and activation of phosphorylase. also stimulates gluconeogenesis
2. Glycogen synthase by phosphorylating it via signal transduction cascade. Inhibits fatty acid synthesis by diminishing the production of pyruvate and lowering activity of acetyl CoA carboxylase by maintaining it in a phosphorylated state. |
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What is the structural relationship between glycogen phosphorylase and glycogen synthase?
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Glycogen phosphorylase has a phosphatase attached to it. In the presence of glucose, it will allosterically change to release this phosphatase. The phosphatase will cleave off the phosphate from glycogen synthase, activating it. Thus glycogen is made when there is plenty of glucose.
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Can fatty acids be converted into glucose?
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NO
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What is the first priority of metabolism in starvation?
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Provide sufficient glucose to the brain.
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What is the second priority of metabolism in starvation?
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To preserve protein. Accomplished by shifting the fuel being used from glucose to fatty acids and ketone bodies.
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Does muscle use glucose during starvation?
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No, it only uses fatty acids. It cannot take in glucose due to low insulin levels, but fatty acids enter freely.
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Diabetes causes a fuel shift from
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Carbohydrates to fatty acids and ketone bodies
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The excessive level of glucagon relative to that of insulin leads to a decrease in the amount of
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F-2,6-BP.
Glycolysis is inhibited and gluconeogenesis is stimulated |
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What is the fuel source for a 100 meter sprint?
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Stored ATP, creatine phosphate, and the anaerobic glycolysis of muscle glycogen
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What is the fuel choice for a 1000 meter run?
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ATP from oxidative phosphorylation
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What is the fuel choice for a marathon?
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Glycogen and fatty acids.
A high glucagon/insulin ratio, which mobilizes fatty acids from adipose tissue. Fatty acids make acetyl CoA, which inhibit pyruvate dehydrogenase, funneling glucose away from citric acid cycle so that it may be used in the end of the race. |
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Ethanol metabolism
1. reaction 2. produces excess 3. What does #2 do? it inhibits something.. 4. Inhibits something else |
1. ethanol --> acetaldehyde (enzyme = alcohol dehydrogenase)
acetaldehyde --> Acetate (enzyme = alcohol dehydrogenase) 2. NADH X2 3. gluconeogenesis. Prevents oxidation of lactate to pyruvate. 4. fatty acid oxidation. excess NADH signals that conditions are right for fatty acid synthesis. Leads to condition known as 'fatty liver.' |
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GLUT 4
1. In muscle 2. In Adipocytes |
1. stimulates glucose uptake from circulation when insulin is released. Provides a major source for glucose storage as glycogen for future use
2. Active w/ insulin. Brings glucose into adipocytes, which is needed for triacylglycerol synthesis. Adipocytes generate glycerol 3 phosphate from reduction of glycolytic DHAP. There is no other source of g3p. |
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Glucose 6 phosphatase:
1. Present in muscle? 2. Under stress, does the muscle maintain a constant supply of glucose for several minutes? |
1. NO
2. Yes |
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PFK-2
1. Is this sensitive to phosphorylation by pka in the muscle? 2. Is this sensitive to phosphorylation by pka in the liver? |
1. No. So under stress, epinephrine triggers an increased intracellular concentration of cAMP, leads to glycogen degradation, inhibits glycogen synthesis,does not affect glycolysis
2. Yes. Converted to fructose-2,6-bisphosphatase. Inhibits synthesis of F-2,6-bisP, and breaks it down. Inhibits glycolysis, stimulates gluconeogenesis. |
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Glycerol Kinase
1. Present in liver? 2. What does it make? 3. Present in adipocytes? What is the effect? |
1. Yes
2. glycerol 3 phosphate 3. No. Adipocytes will favor fatty acid release |
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Glucokinase:
1. Location 2. High or Low Km? 3. Inhibited by its product? |
1. Liver
2. High Km. ONly active at high concentrations of glucose. Lets muscle and fat cells take up glucose 3. Nope. Continuous activity. |
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What is the preferred fuel of resting skeletal muscle?
What is the fuel store of resting skeletal muscle? |
Fatty acids
Glycogen |
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Three tissues that have no fuel store
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Brain
Heart Active Muscle |
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What is the preferred fuel of active skeletal muscle?
What fuel sources are exported? |
Glucose
Lactate, alanine |
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What is the fuel store of adipose tissue?
What is the preferred fuel? |
triacylglyerols
fatty acids |
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What effect does insulin have (increase or decrease) on:
1. Cell permeability to glucose 2. glycolysis 3. Glycogen synthesis 4. Triacylglycerol synthesis 5. Gluconeogenesis 6. Lipolysis 7. Protein degradation 8. Protein, DNA, and RNA synthesis 9. Blood glucose level 10. Fuel storage 11. Cell growth and differentiation |
1. UP
2. UP 3. UP 4. UP 5. DOWN 6. DOWN 7. DOWN 8. UP 9. DOWN 10. UP 11. UP |
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Glucagon
1. cAMP level in liver and adipose tissue 2. Glycogenolysis 3. Glycogen synthesis 4. Triacylglyerol Hydrolysis 5. Gluconeogenesis 6. Glycolysis 7. Glucose release from liver 8. Blood glucose level |
1. UP
2. UP 3. DOWN 4. UP 5. UP 6. DOWN |
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Epinephrine
1. cAMP level in muscle 2. Triacylglycerol mobilization 3. Glycogenolysis 4 Glycogen synthesis 5. glucose release from liver 6. glucose use by muscle 7. blood glucose level |
1. UP
2. UP 3. UP 4. DOWN 5. UP 6. UP 7. UP |
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1. What is leptin and what does it do?
2. What part of the brain is responsive to it? 3. Mice lacking leptin will become... 4. Mice lacking perilipin protein that coats lipid droplets...(that also has a leptin deficiency) |
1. Fatty acid derived protein that controls hunger
2. hypothalamus 3. Obese 4. Almost as skinny as normal mouse |
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Type II diabetes
1. what is it 2. 2 treatments |
1. insulin resistance
2. sulfonylureas (increases insulin) diet and exercise |
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In type one diabetes, why is high blood sugar so dangerous?
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It causes protein glycation. A common one is hemoglobin A1C.
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