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MCP > Unit 6 Random Facts > Flashcards

Unit 6 Random Facts Flashcards

1
Q

Glycosidase specificities: List target glycosidic bond and enzyme type for:

a-amylase
glucoamylase
maltase
isomaltase
lactase
sucrase
A
  1. a-amylase Glu-a1,4-Glu (endoglycosidase)
  2. glucoamaylase Glu-a-1, 4-Glu (exoglycosidase)
  3. maltase Glu-a1,4,Glu (disaccharidase)
  4. isomaltase Glu-a1,6-Glu (disaccharidase)
  5. lactase Gal-b1,4-Glu (disaccharidase)
  6. sucrase Glu-a,1,2-Fru (disaccharidase)
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2
Q

What are the breakdown products of salivary & pancreatic amylase?

A
  • isomaltose
  • maltose
  • a-dextrins (mixtures of D-glucose linked by a1-4 or a1-6 bonds)
  • trisaccharides
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3
Q

What are the 3 reasons why breaking ATP bonds is energy rich?

A
  1. charge repulsion is relieved upon breaking the a-b or b-y bonds (the phosphoanhydride bonds)
  2. greater resonance stabilization of products, ADP + Pi or AMP + PPi
  3. more favorable interactions of products with water
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4
Q

List the 3 types of work that our cells can do to maintain living state. List 2 that we cannot do but other living things can.

A

We can perform these 3 work functions:

  • mechanical (solely ATP driven)
  • transport
  • biosynthesis

We cannot perform these 2 work functions:

  • gas expansion
  • bioilluminescence
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5
Q

Explain what it means that energy is a 3-tier system.

A

3-tier system:
immediate energy need is supplied by ATP
intermediate need is met by glycogen
long-term need is met by fats and proteins

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6
Q

List the 4 reasons why ATP is well suited for its role as energy carrier.

A
  1. has 2 Pi
  2. soluble & mobile
  3. high affinity binding to enzymes
  4. recognition handle
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7
Q

Why are ATP’s phosphoric acid anhydride bonds well suited for a role in energy transfer?

A

ATP is kinetically stable, at a local energy minima, that in the presence of a catalyst, can form ADP + Pi because it has a negative Gibbs free energy (-7.3). -7.3 is an intermediate thermodynamic value that is consistent with ATP’s role as an acceptor, as well as a donor of energy.

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8
Q

What is the common intermediate principle?

A

When exergonic and endergonic rxns are obligatorily coupled by E-P serving as a common intermediate with ATP acting as an acceptor and donor of energy.

X + E —> E-X + Pi –> E-P
ADP + E-P –> E + ATP

E-P has a lot of energy

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9
Q

The presence of which enzyme creates a central pool of energy?

A

Due to the presence of nucleoside diphosphate kinase (NDK), the various nucleotide triphosphate pools (ATP, CTP, GTP, UTP) can be interconverted and share available energy while avoiding rate-liminting steps.

ex:
GTP + ADP —> GDP + ATP

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10
Q

Explain how ATP, ADP, AMP regulate ATP-generating pathways and ATP-utilizing pathways.

A

ATP-generating pathways make ATP so the presence of high ATP will feedback inhibit these pathways while presence of ADP/AMP will stimulate these pathways

ATP-utilizing pathways use ATP so will be stimulated by high levels of ATP and inhibited by high levels of ADP/AMP.

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11
Q

Explain allosteric regulation of enzyme by ATP in ATP-generating pathway.

A

Enzyme has regulatory and catalytic sites. Binding of ATP at regulatory site decreases the affinity for substrate at catalytic site while the binding of AMP at regulatory site will increase the afifnity for substrate at catalytic site.

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12
Q

What are the three ways to maintain ATP levels in severe energy stress? These are temporary solutions to keeping cells alive for a couple more minutes.

A

1) phosphagens using creatine kinase
phosphocreatine + ADP –> creatine + ATP
(in muscle)

2) adenylate kinase (ubiquitous)
2 ADP –> ATP + AMP

3) adenylate deaminase (liver & skeletal muscle)
AMP + H20 –> IMP + NH3
**by removing AMP in this rxn, it will stimulate adenylate kinase (#2).

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13
Q

What are 3 functions of citric acid cycle?

A
  1. converts a # of different fuels to a common mobile fuel (NADH)
  2. serves as a final meeting place of nearly all oxidizable substrates
  3. provides intermediates for biosynthesis
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14
Q

In liver, up to what percentage is devoted to the pentose phosphate shunt? Why is this shunt impt?

A

about 30% of glucose in liver is used for this shunt b/c it generates NADPH and ribose. Ribose is impt in biosynthesis of RNA/DNA, ATP and other nucleotides, NADH/FAD, CoA while NADPH is impt in detoxification as well as in biosynthesis.

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15
Q

Starting from pyruvate, where does gluconeogenesis begin? Why?

A

In the liver mitochondria b/c pyruvate carboxylase is only found in the mitochondrial matrix converting pyruvate into OAA.

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16
Q

Five types of Redox centers. List them and state how many e- can they donate/accept.

A

1) Flavins (Vit B2)
- FMN (NADH Dehydrogenase -Complex I)
- FAD (Succinate Dehydrogenase -Complex II)
* **2 e- donor/acceptor

2) Fe-S
- Complex I to Q to Complex III to cyto c
* **1 e- donor/acceptor

3) CoQ aka Cofactor Q or Ubiquinone
- embedded in membrane
- in 10x molar excess to act as e- buffer
* **2 e- donor/acceptor

4) Cytochrome
- different cytochromes have diff prosthetic groups
- only cytochrome a3 doesn’t have axial ligands b/c cytochrome a3 is what is bound to CuB and what binds O2
* **1 e- donor/acceptor

5) Cu Centers
- CuA in complex IV contains 2 coppers and receives e- from cytochrome c
- CuB along with cytochrome a3 forms O2 binding site.
* **1 e- donor/acceptor

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17
Q

Cytochrome oxidase (complex IV in the ETC). Explain the 4 redox centers found here.

A

cytochrome c (1 e- donor/acceptor) has to make 4 passes/trips to fully reduce cytochrome oxidase

  1. CuA
  2. cyt a
  3. cyt a3 (heme a3 maintains ferric state so needs to be reduced to ferrous state)
  4. CuB

therefore, need to have 4 e- to O2 to produce H20. if not, will form peroxides and superoxides.

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18
Q

What is “respiratory control?”

A

rate of respiration is controlled by availability of ADP in which endergonic synthesis of ATP is obligatorily coupld to exergonic redox rxns. Therefore, O2 consumption is coupled to ATP synthesis which is controlled by ADP availability

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19
Q

What is P/O ratio?

A

= ADP consumed/Oxygen consumed = ATP formed per pair e- from substrate to O2

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20
Q

Mithcell’s Chemiosmotic Theory (an ex. of Common Intermediate Princple)

  • membranes are impermeable to H+
  • there’s a delocalized electrochemical gradient, which is a required intermediate in coupling the exergonic redox rxns to endergonic synthesis of ATP
A

Mitchell’s Loops aka Q cycle b/c only applies to CoQ (2 e- donor/acceptor)

  • REQUIRES:
    1. alternate btw e- donors & H+ donor/acceptors
    2. alternate which side of the membrane it’s happening

Q is a H+ acceptor and is reduced on inside surface of IMM by e- donors from Fe-S & cytochrome bh. The 2 H+ are provided by matrix. Now reduced, Q must be oxidized so it moves to outside surface of the membrane. It transfers e- to 2 e- acceptors (Fe-S and cytochrome b) & 2 H+ will be transported out into intermembrane space. Since only 1 e- flows down to O2, the other is recycled via bl –> bh –> Q.

Stoichiometry: 2 H+/e- so NADH = 2 e- = 4 H+

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21
Q

Is energy required to make ATP in catalytic site (F1) of ATP Synthase (F0F1)?

A

No, energy isn’t required to make ATP however energy is required to release ATP from catalytic site.

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22
Q

Do the 3 catalytic sites (F1) of ATP synthase interact with one another?

A

These sites are cooperative, meaning tight binding of substrate & product release occur simultaneously on separate but interacting sites.

23
Q

Describe the 3 shuttles we talked about in mitochondrial transport systems.

A

A. Shuttles reducing equivalents from glycolytic NADH
1. glycerol phosphate shuttle (2 ATP/2 e-), which doesn’t involve membrane transport since the enzyme is on the outer surface of inner membrane (intermembrane space)

  1. Malate/aspartate shuttle (3 ATP/2 e-) present in liver and heart, and does involve membrane transport

b. ADP/ATP & Pi translocases
3. Together, one turnover of the 2 translocases is equivalent to transport of one H+ down electrochemical gradient into matrix

ADP/ATP translocase = electrogenic transport of ADP-3 into matrix, and ATP-4 out of matrix

Pi translocases = electroneutral = 1 H+ into matrix and 1 Pi- out

24
Q

List the 7 things that the H+ transmembrane gradient play a role in.

A
  • ATP synthesis
  • transport of ADP & ATP
  • heat
  • rotation of bacterial flagella
  • acidification of endomembrane components
  • tx of Pi
  • antiports/symports
25
Q

What are the 3 reasons why metabolic energy is stored as fat?

A
  1. Carbons in triacylglyceride have lower oxidation state than carbons in carbohydrates or proteins. (Fat = 9 kcal/g, carbohydrate & protein = 4 kcal/g)
  2. TGs (water insoluble) can be stored without bound water. Carbs have twice their dry weight as bound to water. Therefore, fats provide 6x the metabolic energy per gram of tissue (wet weight)
  3. Fats don’t participate in cell’s osmotic balance so they can be stored to a large fraction of the cell volume
26
Q

FATP5 vs FATP1 transporters

A

FATP5 transporters are primarily found on brush border of intestinal mucosal cells facilitating uptake of fats by intestines where the fats are re-esterified and packaged in chylomicrons. FATP1 transporters are found in adipocytes responsible for adipocytes intake of fats for fatty acid synthesis and storage

27
Q

What is insulin’s effects in glut4 and fat1p transporters found on adipocytes?

A

Insulin is secreted when theres an increase in serum glucose. Insulin promotes translocation of GLUT4 and FAT1P transporters to plasma membrane allowing the adipocytes to store the excess glucose as energy

28
Q

Give the ranges of BMI for underweight, normal, overweight, grade 1 obese, grade 2 obese, grade 3 obese

A 
BMI < 18.5 underweight 
BMI = 18.5 - 24.9 normal 
BMI = 25 - 29.9 overweight 
BMI = 30 - 34.9 grade 1 obese 
BMI = 35 - 39.9 grade 2 obese
BMI > 40 grade 3 obese
29
Q

List the 6 enzymes that use glutamine as NH3 donor, and thus will be inhibited by azaserine (an analog of glutamine).

A
  1. CPSII (CO2 + NH4 + 2 ATP –> carbamoyl phosphate) in pyrimidine synthesis
  2. CTP synthetase (UTP + ATP –> CTP + ADP, requires glutamine)
  3. FGAR aminotransferase
  4. GMP synthase (IMP –> xanthosine-5-phosphate –> GMP)
  5. PRPP aminotransferase
  6. asparagine synthase (aspartate –> asparagine)
30
Q

What is the Friedewald formula?

A

TC = LDL-C + HDL-C + VLDL-C

VLDL-C = TG/5

31
Q

ACC/AHA 2013 Guidelines identified four groups of individuals that can benefit from statin therapies with a good margin of safety. What are these 4 groups?

A
  1. Individuals with clinical ASCVD without NYHA class II-IV heart failure or receiving hemodialysis
  2. individuals with primary elevations of LDL-C >- 190 mg/dl
  3. individuals 40-75 years of age with diabetes, and LDL-C 70-189 mg/dl without clinical ASCVD
  4. Individuals without clinical ASCVD or diabeties, who are 40-75 years of age with LDL-C 70-189 mg/dl and have an estimated 10-year ASCVD risk of 7.5% or higher

ASCVD = acute coronary syndromes, or a h/o of MI, stable or unstable angina, coronary or other arterial revascularization, stroke, TIA, or peripheral arterial disease.

32
Q

ACC/AHA 2013 Guidelines no longer accepts “treat to target, lower is best” as an appropriate strategy. The new guideline recommends treat to level of ASCVD risk, based upon what?

A

estimated 10-year or lifetime risk of ASCVD (acute coronary syndromes, or a h/o of MI, stable or unstable angina, coronary or other arterial revascularization, stroke, TIA, or peripheral arterial disease).

33
Q

Do the ACC/AHA 2013 Guidelines provide recommendations for initiating or discontinuing statins in NYHA class II-IV ischemic systolic heart failure pts or those on maintenance hemodialysis?

A

NO

34
Q

What do ACC/AHA 2013 Guidelines advice on patients with LDL-C > 190 mg/dl?

A

should receive high-intensity or moderate-intensity statin therapy

35
Q

What do ACC/AHA 2013 Guidelines advice on diabetic patients?

A

diabetics with a 10-year ASCVD >- 7.5% should receive high-intensity statins; diabetics with a 10-yr ASCVD <- 7.5% receive moderate.

36
Q

What do ACC/AHA 2013 Guidelines advice on 40-75 y.o with a >- 7.5% 10-yr ASCVD risk

A

mod-to high statin intensity.

37
Q

How do the ACC/AHA 2013 Guidelines define high-intensity statin therapy and moderate intensity statin therapy.

A

High- intensity statin therapy is defined as a daily dose that lowers LDL-C by >- 50% and moderate intensity by 30%-50%.

38
Q

Are recommendations made by the ACC/AHA guidelines to inform treatment decisions in individuals not included in the 4 statin benefit groups?

A

No recommendations are made to inform treatment decisions in selected individuals who are not included in the four statin benefit groups.

39
Q

What is the Pooled Cohort Equations?

A

ACC/AHA 2013 Guidelines recommend use of the new Pooled Cohort Equations to estimate 10-yr ASCVD risk in both white and black men and women -> indicates groups that may benefit from statin treatments and those that don’t

40
Q

Which glycolytic molecule makes serine?

A

3-phosphoglycerate can be made into serine in 3 steps

41
Q

Disulfiram

A

Acetylaldehyde (ALDH) inhibitors
-used to deter ppl from drinking b/c will cause accumulation of acetylaldehyde, which is responsible for flushing, nausea, vomiting, and distaste for alcoholic beverages.

42
Q

What does a single a.a. substitution of glutamate to lysine in acetylaldehyde dehydrogenase (ALDH2) aka ALDH2*2 cause?

A

This variant will make the enzyme have less affinity for acetaldehyde. Thus, the person will not form acetate as fast. The accumulation of acetylaldehyde will cause symptoms such as flushing, nausea, vomiting, making these ppl less likely to drink

43
Q

LCFA –> Fatty acyl Coa (via acyl coa synthetase aka thiokinase)

acetate –> acetyl CoA (via acetyl CoA synthetase)
Explain the different acetyl CoA synthetase isoenzymes found in liver and other tissues.

A

-Liver
acetyl CoA synthetase I (ACSI) found in cytosol for fatty acid synthesis and cholesterol synthesis (regulated by insulin and cholesterol)

-Other tissues (muscles, heart)
acetyl CoA synthetase II (ACSII) found in mitochondria for TCA cycle

44
Q

Which cytochrome p450 enzyme is most active when ethanol is involved?

A

CYP2E1

45
Q

Which has higher affinity for ethanol: alcohol dehydrogenase or CYP2E1?

A

alcohol dehydrogenase, which is why CYPE21 and other cytochrome enzymes in liver’s microsomal alcohol oxidizing system (MEOS) are not activated unless there’s a huge quantity of ethanol.

46
Q

What is the effect of chronic alcohol consumption on CYP2E1 activity?

A

its expression is induced 5-10 fold leading to increased production of reactive oxygen species. This induction of CYP2E1 allows for increased ethanol clearance from blood, but produces acetaldehyde faster than it can be metabolized by acetylaldehyde dehydrogenase causing damage to liver and other tissues.

47
Q

what are acute effects of alcohol on lipid metabolism in liver?

A
  1. inhibits beta-oxidation of fatty acids (due to high NADH/NAD+ ratio)
  2. stimulation of TG synthesis = fatty liver
  3. ketoacidosis or lactic acidosis causing hypo or hyperglycemia depending on dietary state
    * lactic acidosis b/c so much NADH will want to drive (pyruvate + NADH –> lactate + NAD+ rxn forward)
48
Q

Why will drinking alcohol during fasting lead to hypoglycemia?

A

Ethanol –> – > acetate will form 2 NADH (NADH/NAD+ higher than normal)

pyruvate + NADH –> lactate + NAD+ will be favored so pyruvate cannot be used for gluconeogenesis

49
Q

Explain how drinking alcohol with meal can lead to transient hyperglycemia.

A

b/c high NADH/NAD+ ratio will inhibit GAP dehydrogenase (GAP –> 1,3 bisphosophoglycerate, acyl thioester, oxidation)

50
Q

List 4 general chronic effects of alcoholism

A
  • alcohol induced hepatitis (liver inflammation & necrotic cell death)
  • damage to hepatocytes –> cirrhosis (fibrosis)
  • altered blood flow
  • loss of liver function (decrease hepatic protein synthesis = decrease clotting factors; decrease secretions leading to accumulation of proteins in liver cells –> swelling –> portal HTN)
51
Q

Fibrosis –> Sclerosis –> Cirrhosis

A

Cirrhosis is irreversible. Initially, liver is enlarged, full of fat & crossed with collagen (fibrosis) & have nodules of ballooning hepatocytes. As liver function is lost, the liver will shrink. Loss of metabolic functions include problems w/ protein synthesis and secretion, detoxification, ability to incorporate amino groups into urea = hyperammonemia, conjugation & secretion of bilirubin = jaundice)

52
Q

List the vitamins and minerals that have antioxidant activity

A

ACESC

Vit a
Vit c
Vit e 
Selenium
Copper
53
Q

Long term use of antibiotics can cause which vitamin deficiency? What about long term use of TB drugs? Long term use of which 3 drugs can cause vit c deficiency?

A

Long term use of antibiotics can cause vitamin k deficiency. Tb drugs can cause vit b6 def and vit c deficiency can be caused by long term use of aspirin, oral contraceptives and corticosteroids

54
Q

UCP1 is an uncoupler protein that is ubiquitous in brown fat. It can dissipate energy by allowing H+ entry into the mitochondrial matrix. What are 5 stimulators of UCP-1?

A
  1. In response to cold or overfeeding, the sympathetic neurons in Brown adipose tissue release norepinephrine which will activate b3 adrenergic receptors on the cell surface increasing lipolysis and releases fatty acids which activate ucp1
  2. B3 adrenergic receptor activation can directly increase tx of ucp1
  3. PPARy and RXR (nuclear receptors) can activate ucp1
  4. Thyroid hormone receptor can also activate ucp1
  5. Exercise can cause browning of fat

MCP (2 decks)

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