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94 Cards in this Set

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What is glycogen, in general?
it is glucose in storage form.
Where is glycogen primarily stored?
predominantly in the liver and muscle cells.
What is glycogen's structure and main components?
It is a polymer of glucose residues linked by A,1-4 bonds that is branched by A,1-6 bonds every 8-12 links. (like cellulose, only different branch lengths.)
What percentages of the liver/muscle are glycogen by weight?
Liver = 5-6%
Muscle = 1-2%
How is glycogen actually "stored" in in the liver/muscle cells?
they are in the cytosol in the form of glycogen granules.
What else is stored with the glycogen in the cytosol?
the enzymes that catalyzed glycogenolysis, and glycogenesis, plus regulatory enzymes.
What is the main advantage of how glycogen in stored in the body?
It provides an efficient glucose storage system that is readily available for systemic glucose needs.
What is glycogenesis?
synthesis of new glycogen from glucose (anabolism)
IE - storing it.
What is glycogenolysis?
hyrdolysis of glycogen to glucose (catabolism)
IE - un-storing it.
How does Glycogenolysis occur?
glycogen <<---> glucose-1-phosphate <----> glucose -6-phosphate
How is a glycogen residue (one of them) removed from the chain and converted to G-1-P?
It is hydrolyzed at non-reducing end of the glycogen chain by the enzyme...
Glycogen phosphorylase
How is the phosphate incorporated on the glucose in G-1-P. In what process does this occur?
It is added during glycogenolysis by the glycogen phosphorylase
What happens in the glycogenolysis process when it encounters a branch?
It stops 4 glucose (or glycogen residues) away from the branch and another enzyme removes the branch then it continues. It is all part of glycogenolysis.
How do debranching enzymes work during glycogenolysis?
you just have to know this.. I can't put it in words.
how is the 1 final glucose thats left of a branch removed in glycogenolysis? What happens to it?
a-1-6-glucosidase releases it as a single glucose.
What is the net effect of the debranching enzymes?
it converts a branched structure to a linear one.
How is the G-1-P converted to G6P during glycogenolysis?
G1P ----> phosphoglucomutase ---> G6P
What is overall path that a glycogen residue will follow on it's way to the glycolysis pathway?
removed from the glycogen chain via hyrolysis by glycogen phosphorylase where a phosphate group is added making it G1P.

G1P is convereted to G6P by phosphoglucomutase after which it can enter into the main metabolic pathway.
What happens to G6P once it enters the main metabolic pathway?
In tissues that have glucose-6-phosphatase can generate free glucose (main goal afterall)
Which tissue types have G6phosphatase and why is it important?
It can convert G6P to free glucose.

The liver, kidneys, and intestines have this enzyme and free glucose can be translated into the blood stream.

The muscle, brain, and adipose tissue do not have these. glucose/g6p are effectively trapped into these type tissues where it's used to generate ATP.
How does G1P convert to UDP-Glucose in glycogenesis?
G1P<----- UDP-glucose pyrophophorylase -----> UPD-glucose = PPi

G1P plus a UTP combine making a U-4-P momentarily before losing 2P by rapid hydrolization to drive the reaction.

Leaving behind a glucose + UDP bound together on the #1 Carbon.

so UPD-Glucose.
How does UPD-glucose attach itself to the chain in glycogenesis?
UPD-glucose <---- glycogen synthase ---> glycogen

Enzyme transfers glucose of UDP-glucose to the non-reducing terminal residue of glycogen and forms an a-1,4 bond.
How are the branches created in glycogen?
branching enzyme forms a-1,6 linakges to create the branched polymers.
What are the two primary regulators in the glycogen metabolism process.
glycogen synthase and Glycogen phophorylase are reciprocally regulated.
Why is regulation in glycogen synthesis and breakdown important?
synthesis and breakdown fo glycogen are both spontaneous so if nothing regulates them they would work against each other in a futile cycle.
In glycogen metabolism how does allosteric regulation work using phorphoylase?
Phosphorylase acts in two forms.

Phosphorylase A - actives (normally)
Phorphorylase B - inactivates (normally)
In the muscle how is glycogen metabolism regulated?
glycogen breakdown is inhibited by ATP, and G6P in high concentrations.
In the liver how is glycogen regulated in the liver?
glycogen breakdown is inhibited by high glucose concentrations.
What does glycogen synthase do in the liver acting as a regulator?
it is allosterically activated by G6P

It is active when high blood glucose leads to elevated intracellular G6P.
What 2 hormones can activate G-protein coupled receptors that trigger cAMP cascades in glycogen metabolism?
glucagon, and epinephrine.
When are glucagon and epinephrine hormones produced?
low blood sugar conditions.
What does glucagon do specifically?
activates cAMP formation in the liver.
What does epinephrine do specifically?
activates cAMP formation in the muscle.
What does insulin do?
it atagonizes (reverses) the effects of glucagon/epinephrine.
Do you know and understand the steps involved with epinephrine/glucagon and how they can trigger phosphorylase A or B?
well do ya?
What causes glycogen storage diseases?
genetic enzyme deficiencies
What is associated with glycogen storage diseases?
excess glycogen storage in the cells.
What are the symptoms of glycogen storage disease in the liver?
hypoglycemia, relating to impaired mobilization of glucose for release during fasting.
What are the symptoms of glycogen storage disease in the muscle?
weakness and difficulty with exercise from the inability to increase glucose entry into glycolysis during exercise.
What causes Von Gierke's disease?

Andersen's?

McArdle's?

pfk defieciency
VG's = G6P deficient - hypoglycemia

Andersen's - no branching enzymes - liver disfunction and early death.

MA's GPhosphorylase - muscle craps with exercise.
pfk deficient leads to what?
an inability to exercise.
What is the TCA?
tricarboxylic acid cycle.. same damn thing as citric acid cycle with a newer, snazzier name.
How is pyruvate converted to Acetyl Co-A?
pyruvate --- pyruvate dihydrogenase ---> Acetyl Co-A + CO2
What is the enzyme, and 5 co-enzymes (grouped) for pyruvate/acetyl-co-a?

What is released from pyruvate/Acetyl Co-A during the reaction?
Pyruvate Dehydrogenase is the enzyme

CoA-SH
NAD+
TPP, lipaoate, and FAD

NADH is released during the reaction.
What regulates Pyruvate --> Acetyl Co-A reaction BESIDES PDC?
ATP, Acetyl Co-A, NADH, fatty acids DOWN regulate.

AMP, CoA, NAD+, Ca2+ UP regulate.
What is, and how does PDC regulate pyruvate --> Acetyl Co-A production?
Puruvate Dehydrogenase Complex is the enzyme that powers py --> acetyl co-A production.

If it is phosphorylated it turned off

unphosphorylated activates it.
What is the net reaction for Pyruvate ---> Acetyl Co-A?
2 Pyruvate + 2 CoA + 2 NAD+ -----> 2 AcetylCoA + 2 CO2 + 2 NADH.
what are the structural & storage forms for the TCA's general precursors.. and where are they located?
triglycerides, glycogen, and proteins.

They come from small carbon chains INSIDE the mitochondria.
What are the nutrient pool factors from the TCA general precursors and where are they found?
fatty acids, glucose, amino acids.

found in small carbon chains, and are in the mitochondria.
What are the 4 functions of TCA?
provides for oxidation of Acetyl-Co-A to CO2, and H20.

Generates reduced NAD+ and FAD for oxidative phophorylation to produce ATP.

provides key intermediates for synthetic reactions that can leave/enter the mitochondria.

TCA is the FINAL common pathway for fuel metabolism.
How many individual reactions make up the total coupled reaction of TCA?
8 different steps.. and you friggen better know them bitch.
What is the net reaction of the TCA?
Acetyl Co-A + 3 NAD+ + FAD + GDP + Pi + H2O -------> 2 CO2 + CoASH + 3 NADH + 3 H+ + FAD(2H) + GTP.
What are the four sites of electron transfer in the TCA that for NADH and FAD(2H)?
Rxn's - 3, 4, 6, and 8.
What happens at reactions 3,4, and 8 in the TCA that is important?

What is unique about 3 and 4 that is not in 8?
NADH is released.

3 and 4 also release CO2 while 8 does not.
Walk through TCA using the products.
Acetyl Co-A --> Citrate --> Isocitrate --> a-Ketoglutarate --> Succinyl-Co-A --> Succinate --> Fumarate --> Malate --> Oxaloacetate.
Regulation in the TCA. What effects which step and how?
step 3 (isocitrate)
ADP = up
NADH = down

Step 4 (a-ketoglutarate)
Succinyl-CoA & NAD = DOWN

Step 6 (Malate)
NADH = DOWN
Regulation for TCA also occurs at the citrate step. What, and how does this happen?
Large concentrations cause either inhibition or stimulation.

UP =ADP

DOWN = NADH, succinyl-CoA, citrate, and ATP
What are the three most important things about TCA to understand?
1. Provides oxidation for acetyl CoA to CO2 and H2O

2. Generates reduced NAD+ and FAD for oxidative phosphorylation to produce ATP.

3. Provides key intermediates for synthetic reactions.
IE - conversion of an amino acid to glucose via gluconeogenesis.
What is ETS?
electron transport system.
what is cellular respiration?
It is the whole shebang.. glycolysis, TCA, and ETS.
What are the three stages of cellular respiration, and their purpose?
1. acetyl-CoA production from glucose, fatty acids, and amino acids. (glycolysis)

2. Acetyl-CoA oxidation (TCA)

3. Electron transfer and oxidative phosphorylation.
Where do all fuel oxidation pathways, except for glycolysis occuer?
in the mitochondrial matrix.
Where do protons accumulate during ETS?
the intermembrane space of the mitochondria.
What do the first three steps of ETS do?
provide electrochemical gradient "driving force of ETS"
What is Complex 1 in ets?
NADH
What is complex 2 in eTS?
succinate to fumarate & coenzyme Q, ubiquinone, UQ.
What is complex 3 in ETS?
cytochrome C
What is complex 4 in ETS?
cytochrome C1, and C3.
How does ETS electron flow work?
it emplys integral membrane proteins (the 4 complexes) having prosthetic groups that can carry 1 or 2 electrons.

These electrons are passed laterally through the 4 complexes with two mobile carriers along the way (Q and cytochrome)

electron transfer is mirrored by H+ transfer from the matrix to the intermembrane space.
What are the two mobile carriers in ETS?
Q and cytochrome c
What is the source of H+ for electron flow in ETS?
NADH + H+
How does ETS Proton Flow work?
in concert with electron transfer is H+ transfer from the matrix to the intermembrane space.
What does increasing the H+ concentration in the intermembrane space do to further the reaction in ETS?
It lowers the pH of the intermembrane below than the pH of the matrix. This drives the "rotation" of ATP synthase via 3 different conformations causing the bonding/phosphorylation of 3 ADP+ + P-.
What type of nucleotides do NAD+ and NADP+ use?
pyridine nucleotides.
FMN and FAD use what type of nucleotides in ETS?
flavin.
What carrier can accept 1 or 2 electrons is small, hydrophobic and freely diffusible in the lipid bilayer?
Ubiquinone... Q
What is Q and what can it do ETS?
Ubiquinone, it can couple electron flow to proton movement in ETS.
What do the cytochromes do in ETS and how many are there?
3, A-b-c. They can carry single electrons in their noncovalently bound (except cyt c) heme prosthetic groupos.
Where, and what does cytochrome c do ETS?
it is found on the outer surface of the outer surface of the inner membrane. it's peripheral. It helps couple the movement of protons to the electrons.
What do Fe-S proteins do in ETS?
It is a prosthetic group and can carry 1 electron using Fe++ coordinated to inorganic S and/or sulhydryl groups of the protein.
What is the chemiosmotic theory from eTS?
for the overall transfer of 2 E- from NADH to O2 (H2O).
explain chemiosmotic theory...
10 H+ are pumped out.

This creates a pH and electrical gradient by repiration and serves as the driving force for H+ uptake.
What does H+ do in ETS according to chemiosmotic theory?
It drives the rotation of ATP synthase via 3 conformations.
How does ATP Synthase create ATP?
by phophorylating ADP.
What are, and how does the 3 conformations of ATP synthase occur?
The first H+ causes the first conformation which binds substrates ADP + Pi

second H+ causes conformation change to move ADP + PI within bonding distance.

Third H+ causes conformation change that promotes bond formation producing ATP.

ATP is then released due to poor binding).
What does adenine nucleotide translocase do during ETS?
serves as a ADP/ATP carrier. ti's an antiporter that catalyzes the exchange of ADP for ATP.
How does phosphate re enter the matrix with H+ by an electroneutral symport?
Pi entry is driven by, and uses up the pH gradient that was created earlier.
What regulates ETS/Oxidative phosphororylation?
Primarily it depends on the availability of ADP.

Increased ADP in mitochondrial matrix causes H+ channel to open, H= moves through creating the pH gradient causing respiration to increase to compensate for the decline in pH.
When ADP is low what happens to ETS?
it stops until the pH gradient builds upa nd o2 use diminishes... in other words.. it stops until there is a need.
What serves as inhibitors to the 4 complexes in oxidative phosphorylation in ETS?
Complex 1 inhibited by Rotenone
2 by Carboxin
3 by antimycin A
4 by cyanide, azide, carbon monoxide.
What inhibites ATP synthase?

ATP-ADP translocase?
Oligomycin = Oligomycin

Atractylose = ATP-ADP translocase.
What are uncouplers?
DNP suttles H_ across the inner membrane dissipating the gradient.. stopping ETS.
Dinitrophenol is one of these because it causes a proton leak.
What does CaCL2 stimulate?
oxidative phosphorylation and ATP production.
What is the net reaction for the complete oxidation of glucose?
2 pyruvate + 5 o2 + 30 ADP + 30 Pi ==== 6 Co2 + 30 ATP = 34 H2o.