Metabolism Goodness (Basics to Glycogen Metabolism) Flashcards
What do NAD+ and FAD act as: oxidizing or reducing agents?
sexy electron strippers-oxidizing agents, stripping away electrons
Which electron taxi cab do we use in catabolism?
NAD+
Which taxi cab do we use in Anabolism?
NADP+
What are the 3 MAJOR membrane lipid families?
- GlyceroPhosphoLipids 2. SphingoLipids 3. Cholesterol
What are the four variable groups we talked about for GlyceroPhosphoLipids?
- EthanolAmide 2.Choline 3. Serine 4. In-O-Si-Tol
What are the four types of sphingolipids?
1.CER-AMIDE 2. sphingo-MYELIN 3. Glucosyl-Cerebro-side 4. Ganglio-Side
What is the most common sphinolipid in our cells? What is the ONLY sphingolipid AND phospholipid?
SphingoMyelin
What is the disease that arises from the inability to degrade gangliosides in the cell?
Tay-Sachs Disease (NERVOUS tissue most affected)
What is the disease that arises front he inability to degrade glucosyl-cerebro-sides?
Gaucher’s Disease
What happens in the Adenylate cyclase cAMP pathway? Namely: Type of GPCR; Name of Target Protein; the last two steps
GPCR: Beta-Adrenergic Receptor…..Target: Adenylate Cyclase. Next step: Adenylate cyclase converts ATP to cAMP. Last step: cAMP activates Protein Kinase A
What 2 things does the activated Protein Kinase A accomplish?
1.Phosphorylates Serine and Thyronine targets. 2. Stimulates transcription
What are the two items activated via the PhosphoLipase C pathway?
1.PKC and 2. Calmodulin
What are the new/main players in the NitricOxide pathway? What is the main function of the Nitric Oxide pathway?
1.Nitric Oxide 2.cGMP 3.ProteinKinaseG..Relaxation of Smooth Muscle!
What are the 3 positive AA’s?
HAL! Histidine, Arginine, Lysine
What are the 2 Negative AA’s?
GA! Glutamate, Aspartate
High Ka=?pKa?
High Ka=Low pKa (logarithmic relationship)
Low pKa=?pH?
Low pKa=Low pH (strong acid)
What is the Henderson-Hasselbalch Equation?
pH= pKa + log [ConjBase] / [Acid]
Where does aspirin (pKa=3.5) get absorbed? Stomach (pH=1.5) or S.I. (pH=6.5)
Stomach (pH 1.5). Here, the aspirin is very associated, so it is not charged, so it can pass the membrane.
What % dissociation occurs when you have a 1 pH unit above the pKa?
91% dissociation
What % dissociation occurs when you have a 1 pH unit below the pKa?
9.1% dissociation
BIG ONE!!! What are the polar and charged (+&-) AAs?
HAL (+) (Histidine, Arginine, Lysine), GA! (-) (Glutamate, Aspartate), and (Polar) St. AG Cystine chapel (Serine, Threonine, Asparagine Glutamine, Cystine)
If I have a substrate with a LARGE Km do I have a high or low affinity for that enzyme?
I have a LOW affinity.. Lots of fries to FINALLY reach the 1/2Vmax..
What does a SMALL Km tell me about the affinity of a substrate to an enzyme?
Small Km = HIGH affinity of the substrate for the enzyme
What effect does a COMPETITIVE inhibitor have on Vmax? Km?
No change in Vmax with an inhibitor. Inhibitors INCREASE Km. (Need to have more S to get the same 1/2Vmax)
What effect does a NONcompetitive inhibitor have on Vmax? Km?
DECREASES Vmax (Adding more S doesn’t do anything!). Km stays the same (S still binds to E).
What are the three CK (creatine kinase) Iso(en)zymes we discussed? Where can I find them?
BB in Brain, MB in Heart, MM in skeletal and heart muscle
What type of transporter gets glucose from the lumen of the small intestine into an enterocyte? What ion is involved?
A sodium SYMporter
What type of transport protein gets the cell from the enterocyte to the blood? What type of transport is it?
A GLUT! (GLUcoseTransporter). FACILITATED diffusion
What is the saccaride that cements S. Mutans to teeth? What is the hard bond to break in this polysaccharide?
DexTRAN…Its oddball 1,3 alpha. So hard to break up the biofilm
Do GLUTs move glucose with or against its [ ] gradient?
With [ ] gradient
Where are GLUT1s mainly found?
Brain and RBCs
Where are GLUT2s mainly found? What is Dr. Ts analogy for GLUT2s?
Mainly found in liver, kidney, intestine and Beta Cells(pancreas)….They are the Ferrari of GLUTs
Where are GLUT3s mainly found?
nearly ALL cells!
Where are GLUT4s mainly found?
Muscle and Adipose (insulin dependent)
Where are GLUT5s mainly found?
Small Intestine (on arterial side of the epithelial cell)
What is the name of the Sodium/Glucose Symporter what moves glucose from the lumen of the intestine to the epithelial cell?
SGLT1
What is the first thing that happens when Glucose enters any cell? What enzyme is used?
HexoKinase phosphorylates the glucose to make it G-6-P!
How many NADH do I get out of Glycolysis? How much ATP? If you get these wrong, you need to go back to high school.
2 NADH, 2ATP
THIS IS BIG PEOPLE: What are the three Regulatory enzymes of Glycolysis? Why are they considered regulatory?
- HexoKinase 2. Pyruvate Kinase 3. PhosphoFructoKinase1 (PFK1)… They are “regulatory” because they catalyze steps that are irreversible (very energetically downhill)
Just more names to memorize: what is the isozyme of hexokinase in the LIVER?
GlucoKinase
High Insulin = _____ Fructose-2,6-Bisphosphonate = ______ glycolysis in LIVER
High Fructose-2,6-Bisphosphonate = INCREASED glycolysis in liver (to turn pyruvate to fat!)
High Glucagon = ______ Fructose-2,6-Bisphosphonate = _______ glycolysis in the liver.
Low Fructose-2,6-Bisphosphonate = Decreases glycolysis in liver (GNG to commense and feed body)
Phosphorylation of Glycogen Synthetase & Glycogen Phosphatase will favor glycogen synthesis or degradation?
glycogen degredation
DE-Phosphorylation of Glycogen Synthetase & Glycogen Phosphatase will favor glycogen synthesis or degradation?
glycogen synthesis
Which regulatory enzyme commits the cell to glycolysis? AKA the cross roads between glycolysis and gluconeogenisis…
PhosphoFructoKinase1 (PFK1)
What 4 molecules INCREASE PFK1 activity?
Molecules of Hunger: ADP, AMP, Fructose-6-Phosphate (Reactant), Fructose-2,6-BisPhosphate (mainly in liver)
What 2 molecules DECREASE PFK1 activity?
Molecules of Satiation: ATP, Citrate
What type of transport is Glucose into a cell?
Facilitated Diffusion
What are the three products of the pyruvate dehydrogenase reaction? Is this reaction REVERSIBLE??
- 1 CO2(per pyruvate) 2. 1 NADH (per pyruvate) and 3. 1 Acetyl-CoA (per pyruvate)….THIS RXN IS NOT REVERSIBLE (hence why we can’t turn FAT to GLUCOSE )
How many Cs get fed into the CAC? How many Cs come out?
2 in (acetyl-CoA) and 2 out (CO2)
How many NADH and FADH2 are made EACH TURN of CAC? How many CO2? Do we yield ATP out of CAC? BUTTTTTT Which high energy molecule do we get out of CAC?
3 NADH and 1 FADH2…2 CO2….No ATP!—BUT 1 GTP
HUGE concept! What are the 4 controls for PD & CAC? Which 3 are regulatory because of their EXERGONIC nature?
1.PD Reaction (most complex) 2. Citrate Synthase 3. Isocitrate Dehydrogenase 4.alpha-ketogluatate dehydrogenase… all the CACs (#s 2,3,4) (2,3,4 are all on R side of the cycle!!)
What are the 4 main allosteric INHIBITORS of PDHComplex? (Think high energy molecules)
- ATP/GTP 2. Acetyl-CoA 3.NADH 4. FAs (all “high energy” molecules)
What are the 4 allosteric ACTIVATORS of the PDHComplex? (Think of low energy molecules)
1.AMP 2.CoA (=low acetyl-CoA) 3.NAD+ 4.Ca2+ (ODD BALL) (All “low energy” molecules)
Is PDHComplex active when DEphosphorylated or phosphorylated?
PDHComplex is ACTIVE when DEPHOSPHORYLATED (ONLY TIME WE SEE GLUCAGON DOING A DEPHOSPHORYLATING EVENT!!!)
Which ETC protein does not move H+’s across the inner mitochondrial membrane?
II
Which ETC protein receives NADH?
I
Which ETC protein receives FADH2?
II
Which two ETC proteins surround the Q pool?
II and III
Where do e’s get dropped off after going through the iron clusters in NADH-Q Oxidoreductase?
Ubiquinone (Coenzyme Q) (Q pool)
What are the names for coenzyme Q when it is reduced and when it is not reduced?
Reduced: UbiqunOL (Its all fat happy and DRUNK with protons!!) Not reduced:Ubiquinone (both considered “coenzyme Q”)
What is the enzyme that protects or tissues from free oxygen radicals? THANK YOU! What is the metal in our superman enzyme that saves us from peroxide?
SUPERMAN! (SuperOxide Dismutaste)..Mn (Manganese)
What are the two molecules that save us from H2O2?
Catalase and Glutathione Peroxidase
Which step is blocked by CYANIDE and CO?
CytoChrome Oxidase (IV), blocks electron transport
Which shuttle moves NADH into the Matrix?
Malate Shuttle
Which shuttle system exchanges and FADH2 for an NADH?
Glycerol-3-Phosphate Shuttle
What are the four starting materials/precursors for MAKING GLUCOSE?
- Lactate 2.Pyruvate 3. Glycerol 4. Amino Acids (18 out of 20)
Is GNG simply a reversal of Glycolysis? What atet the 3 bypasses?
Nope, there are 3 irreversible steps that we will have to bypass! 1. Pyruvate–>PEP (Pyruvate Carboxylase) 2. Fructose-1,6-BisPhosphatase 3. Glucose-6-Phospatase
SAY WHATTT? Where does each of the four starting materials enter GNG?
1.Lactate-Enters by being converted to Pyruvate before the first step 2. Amino Acids-a.some are converted to pyruvate b. some are converted to Oxaloacitate for step 2 3. Pyruvate-first step of GNG 4. Glycerol-enters late, in part 2 go GNG
What is the first step in the MAJOR pathway for Pyuvate to PEP? What Enzyme is used? Where does it happen? Is there ATP used? What is it controlled by?
1st step: Pyruvate–>Oxaloacetate Enzyme: Pyruvate Carboxylase. Occurs in the mitochondrial matrix. 1 ATP used.Controlled by HIGH Acetyl-CoA…BTW-after all of this we are just going to end up converting
Pyruvate carboxylase is the only gluconeogenic enzyme that has a _________ location.
mitochondrial
Which AA can we use to make pyruvate and then intimate GNG?
AL-a-neeeeen (Alanine)
____________ is not present in brain and muscle and so GLUCOSE CANNOT BE FORMED by these organs.
Glucose 6 phosphatase (Glucose-6-Phosphate—>Glucose)…so opposite of Hexokinase
What are the two regulators of GNG?
Pyruvate Carboxylase & PFK1/Fructose-1,6-BisPhospatase
What is the enzyme that helps us break down glycogen?
Glycogen Phosphorylase
