Metabolism Flashcards
Which enzyme is responsible for trapping glucose in step 1 of glycolsis?
Hexokianse traps glucose in the cell by phosphorylating it to produce glucose-6-phosphate
In glycolysis, glyceraldehyde 3-P is oxidised and phosphorylated by the enzyme 3P dehydrogenase. What is the product of this reaction?
1,3- bisphosphoglycerate
In step 3 of glycolysis, fructose 6-phosphate is phosphorylated by phosphofructokinase to fructose 1,6 bisphosphate. What is this step inhibited by?
ATP, H+ ions and citrate (presecense of energy/associated products). The reaction is stimulated AMP, ADP and Fructose 2,6 Bisphosphate
why cant glucsoe 6 phosphate move out of its cell?
it is charged so cant diffuse out of the cell (this is how glucose gets trapped!)
glut 4 transporters
GLUT4 can alter Vmax by increasing the number of transporters, doesn’t affect km, located in msucle and adipocytes
Where abouts in the body can the GLUT2 transporter be found? A brain B skeletal muscle C liver D heart
Liver andβ-cells of pancreas. Has a high km and low affinity (good after meals)
> so rate of uptake is proportional to extracellular glucose concenctration
Which of these glucose transporters is located in the brain and nerve tissue? A GLUT 1 B GLUT 2 C GLUT 3 D GLUT 4
GLUT 3
What is the net yield of glycolysis?
2 pyruvates 2 ATP, 2 NAHD
DHAP needs to be converted into G 3-P otherwise a 3c fragment capable of generating ATP will be lost. What enzyme catalyses this reversible reaction?
Triose phosphate isomerase (TIM)
gluconeogenesis must bypass three reactions. In bypass 1, there is a conversion of pyruvate to oxaloacetate and then a decarboxylation and phosphorylation of oxaloacetate by phosphenol pyruvate carboxykinase.
There are two versions of this enzyme, which is used if precursor doesn’t produce NADH in cytosol?
cytosolic phosphophenol carboxylase
> aa or pyruvate as precursor (anything other than lactate). malate shuttle is uses to produce NADH which is used later on in the gluconeogeneis steps
which amino acids are not glucogenic amino acids? A tyrosine and tryptophan B lycine and leucine C serine and asparagine D glutamte and glutamine
OPTION B PLEASE
lycine and leucine - these are exclusively ketogenic aa which means their carbon skellytons are precursors to fatty acid synthesis pathways (acetyl coA)
where does beta oxidation of FA take place?
mitchondiral matrix
What cell receptor is used when mobilising TAG from adipose tissue?
A GCPR
B receptor tyrosine kinase
C intracellular receport
D ion gated channel recertpo
option A
G-protein linked receptors. this is what glucagon binds to and initates a signal cascde!
What enzyme is used for fatty acid activation? ATP synthase Hexokinase Acyl CoA synthetase Pyruvate kinase Protein phosphatase 1
Acyl CoA synthetase
>Acyl CoA as the fatty acid is linked to CoA before oxidation in the cytoplasm
What bond is formed in FA activation?
thioester bond
> this is done by acyl coA synthase which creates acyl-CoA in the cytosol!!
Which of the following is a characteristic of white adipocytes? Has many lipid vacuoles Has a low number of mitochondria Contains many organelles Has many mitochondria Has a double membrane
has low numbr of mitch (and other organelles) as it a FAT GLOBULE
Which of these statements is incorrect?
A Alpha oxidation occurs much less than beta oxidation.
B Omega oxidation happens when Beta oxidation is blocked.
C The order of reactions in omega oxidation is hydroxylation, oxidation, reduction
D Products from omega oxidation enter the Kreb Cycle
E Refsum’s disease is when you cant metabolise phytanic acid
OPTION C is incorrect
The order of reactions in omega oxidation is hydroxylation (remove toxicitiy), oxidation, oxidation (alcohol to aldehyde)
> products enter krebs
There are 4 reactions in oxidising fat ( Beta oxidation), what are these 4 reactions?
Oxidation, hydration, oxidation, lysis
Which of these statements is incorrect regarding break down of fats?
A Endocrine tissue stimulates breakdown of fats
B Using g-protein linked receptor, glucagon and epinephrine will stimulate the endocrine tissue
C G-protein linked receptors involve ATP. They activate protein kinase A.
D G-protein linked receptors involve GTP. They activate protein kinase A.
E In adipose tissue, PKA phosphorylates triacylerolases to break down TAG.
OPTION C
g-coupled receptors use gtp
gtp is on – activate PKA
What is the fate of the Alpha amino group after a protein is degredated?
A Transferred to a another Alpha amino group which yields glutamate and then ammonium ions.
B It is deaminated to produce ammonium ions
C It is hydrolysed into Nitrogen and carbon constituents which is used to make Acetyl CoA
D It is transferred to an Alpha ketogluterate which yields glutamate. This is deaminated to produce ammonium ions (urea).
OPTION D
>look at that lovely diagram
What is glutamate dehydrogenase’s function in the liver?
A It is used in the oxidative deamination of Glutamate to Alpha ketogluterate to produce ammonium ions via
NAD+ also producing a schiff base intemediate.
B It is used in the oxidative deamination of glutamate to Alpha ketogluterate to produce ammonia
C It is used in the production of NADH to produce a Glutamate.
OPTION A
It is used in the oxidative deamination of Glutamate to Alpha ketogluterate to produce ammonium ions via NAD+ also producing a schiff base intemediate.
> glutamate relases the ammonia and regenates alpha-k-g as a result!
What is the role of an aminotransferase?
Transfer the Alpha amino group to an alpha ketogluterate. It required the B6 vitamin.
Transfers the nitrogen constituents to a hyrogen to yield NH4+
Uses VitaminB6 to transfer the amino group to carbomoyl phosphate
Uses pyrodoxial phosphate to transfer the amino group too a ketoacid
OPTION A
What are the two parts to a 26S proteasome?
19S-Recognition
20S-The protease
20S-Recognition
19S-The proteasome
13S-Catalytic
15S-Holds the cayalytic domain together.
19S-Recognition
20S-The protease.
What is carbomoyl phosphate synthatase’s role?
It joins NH3 (NH4+ at pH) to bicarbonate to produce carbomoyl phosphate by the use of ATP.
What is ubiquitins role?
A It is used after the alpha keto group is oxidised, where it phosphorylates succinate.
B Targets proteins for degredation so that proteasomes can recycle peptides.
C A proteasome that degrades proteins so that they can be used as precursors for the citric acid cycle.
D Starts the urea cycle by isomerising the arbomoyl phosphate.
E A type of phosphatase that can break molecules apart.
Targets proteins for degredation so that proteasomes can recycle peptides.
> ubiquitin is added/tagged so proteins are RECOGNISED for degrading!
What can be the fate of fumerate after arginine is hydrolysed into ornithine?
A Fumerate can be targeted by a proteasome and broken down so its carbon skeleton can be used in the citric acid cycle.
B Fumerate can be converted into malate and then oxaloacetate and then produces glucose by gluconeogenesis.
C Fumerate can be phosphorylated and then sent directly in the citric acid cycle.
D Fumerate can be combined with ornithine again to make citruline.
OPTION B
>follows the gluconeogenic pathway
what is name of enzyme that ADDS phosphates?
kinase!
major storage organs of glycogen?
liver and muscle
where can gluconeogenesis take place?
liver and kidney….
products of beta oxidarion A ATP, acetyl coA, NADPH and FADH2 B acetyl coA, NADH and FADH2 C ATP, acetyl coA, NADH and FAD D acetyl coA, NADH and FAD
OPTION B
acetyl coA, NADH and FADH2
> beta oxidation doesnt MAKE atp, it USES atp
which enzyme in krebs forms a direct link with ETC? A beta ketothiolase B isocitrate dehydrogenase C succinate dehydrogenase D fumerase E pyruvake carboxyknase
succinate dehydrogenase
> complex 2 in ETC
what carries e- in the ECT from complex 3 to comlex 4? A Coenzyme Q B cytochrome C oxidase C FADh2 D Cytochrome C E flavin mononucleotide
OPTION D
complex 4 is called cytochrome C oxidase so cytochrome C transfers its e- to oxygen and therefore gets oxidised as it LOSES electron
> complex 3 is called CoQ-cytochromeC oxi-reduct
in catabolism, is Gibbs + or -?
catabolism you break down stuff, producing ATP so gibbs is NEGATIVE
> also generate NADH and FADH2 as reducing potential
What does it mean is Gibbs free energy is -ve?
A Reaction is endergonic and needs energy input
B Reaction is exergonic, energy is liberated and reaction is spontaneous
C Reaction neither releases energy or needs it
and rate is slow.
D Reaction at equilibrium
OPTION B
exergonic! yaaay
> only spontaneous in forward direction
> CATABOLISM
what is gibbs free energy
Amount of free energy in a system available to do work.
What are the main steps in the link reaction? (pyruvate to acetyl CoA)
Decarboxylation, Oxidation, Group transfer, ocidation.
Which one of the following is not a major precursor for gluconeogenesis? A Lactate B Leucine C Glycerol D Histidine
B
leucine is a ketogenic amino acid! NOT glucogenic aa as it doenst have the correct carbon skellyton
Which of the following pathways is catabolic? A Glycogenesis B Pyrimidine synthesis C Glycogenolysis D lipogenesis
option C
> CATABOLIC =breaking down/lysis
Lipogenesis is the metabolic process through which acetyl-CoA is converted to triglyceride for storage in fa
Free energy change is the amount of energy in a system available to do work. If free energy change is negative, is the reaction exergonic or endergonic?
exergonic!
negatvie gibbs, release energy/catabolic creates energy
Active transport can either be described as primary active transport or secondary active transport. Which is described as energy in the electrochemical gradient of one molecule is used to move another molcule against its electrochemical gradient?
It is secondary active transport. Primary active transport is transport directly couple to ATP hydrolysis. Its using ATP to drive things against its concentration gradient.
What precursor is used in bypass one when Mitochondrial PEP carboxykinase is used? Why?
Lactate
Used to yield NADH which is used in the reaction 1 3-bisphosphoglycerate -> Glyceraldehyde-3-phosphate further up the pathway
What is the Glyoxylate cycle?
A An anabolic pathway in plants and micro-organisms that centres on the conversion of Malate -> Glucose
B A catabolic pathway in plants and micro-organisms that centres on the conversion of fatty acids -> Glucose
C An anabolic pathway in humans that centres on the conversion of fatty acids -> Glucose
D An anabolic pathway in plants and micro-organisms that centres on the conversion of fatty acids -> Glucose
E A catabolic pathway in plants and micro-organisms that centres on the conversion of Malate -> Glucose
OPTION D
> not in human
> anabolic as you building!
What is the Cori cycle?
A metabolic pathway in which Lactate (Produced by anaerobic glycolysis in muscles) is transported to the liver and converted to glucose and hen returns to the muscle
> large animal has longer oxygen debt//low stamina
GLUCAGON binds to liver and fat cells via what kind of receptor? A GCPR B receptor tyrosine kinase C enzyme linked receptor D ion gated channel recertpo E nuclear receptor
gpcr
fatty acid oxdiation, getting TAG out of adipose
which secondary messenger is formed when glucagon binds? calcium inositol triphosphate cAMP diacylglycerold IP3
cAMP
MUTATION IN CPT1. what would you not expect (fatty acid oxidation) reduced blood glucose elevated insulin elavated ketones elevated carnitine elevated alanine aminotransferase
not expect the elevated ketones as ketoacidosis aint happening
> low glucose as we are in fasting mode, lots of carnitine as the shuttle (CAT antiporter) ain’t happening and lots of aminotransferase as we are trying to DO b-oxidation
what molecule is needed in adition to acetyl coA to make citrate? oxaloacetae isocitrate citrate alpha keto glutamte c02
OPTION A
> krebs?
where does alpha, beta and omega oxidation occur? a peroxisome, adipose, kidney ER b peroxisome, mitcoondria, liver ER c mitochondira, liver ER, perxoisme d mitcohndair, peroxisome, liver er e kidney ER, mitochindria, peroxisome
OPTOPN B
peroxisome - alpha
mitch - beta
liver er -omega
in fatty acid synthesis, how does acetylCOA carboxylase affect the regulation of FAmetabolsim?
as seen in mice, if this enzyme is knocked out, it prevents the build up of malonyl ACP
this decreased concentration means that CPT1 is NOT inhibited so FA oxidation increases
» mice have weight loss, reduced body fat
What is the order of the beta oxidation cycle steps?
A. Dehydrogenation, hydration, oxidation and thyolisis.
B. Hydration, dehydrogenation, oxidation and thyolisis.
C. Dehydrogenation, oxidation, thyolisis and hydration.
D. Hydration, dehydrogenation, thyolisis and oxidation
option A (oxidation, hydration ,oxidation, thiolysis) > REMOVAL Of a hydrogen = overall loss of electron > loss of electron = oxidation
What end products does each beta oxidation cycle yield?
A. One acyl-CoA, one NADH, water and one acetyl-CoA chain two carbons shorter.
B. One two-carbon acyl-CoA, one NADH, water and another acyl-CoA chain two carbons shorter.
C. One acyl-CoA, one FADH2, one NADH, water and one acetyl-CoA chain two carbons shorter.
D. One acetyl-CoA, one FADH2, one NADH, water and one acyl-CoA chain two carbons shorter.
D is correct. Each cycle of beta oxidation yields one (two-carbon) acetyl-CoA, one FADH2, one NADH, water and one acyl-CoA chain two carbons shorter.
FADH2, NADH and acetyl-CoA later enter the KREBS, which will yield ATP.
which parts of the body use ketone bodies?
the heart and brain use ketone bodies. they can cross the blood brain barrier = useful for FASTING!
in alpha oxidation, what FA can the alpha carbon be oxidised to?
phytanic acid –> pristanic acid which then can undergo perisome beta oxidation (yields no ATP though)
where does deamination of alanine occur? A brain B white adipos tissue C brown adipsoe tissue D liver E pancreas
liver!!
> look at that lovely diagram!
