9/18 Intro to Matabolism Flashcards

1
Q

what are the three sources of energy for the body?

A

Fats, Carbs, or Proteins

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2
Q

what is the common product of all metabolites?

A

Acetyl CoA

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3
Q

what is the basic structure of Acetyl CoA?

A

A two carbon Acetyl group bound to vitamin B5-derived cofactor, coenzyme A.

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4
Q

basic metabolic roadmap

A

Fat/Carb/Protein/ to Acetyl CoA to TCA cycle (donate two carbons). To the electron transport chain; to ATP pump.

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5
Q

where does TCA cycle electron transport and ATP pump occur?

A

the mitochondria.

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6
Q

what is the high engergy link in Acetyl CoA?

A

the Carbon-Sulfer linkage where the OH group would have been in acetic acid.

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7
Q

what is the purpose of the energy stored in the high energy S-C bond in Acetyl CoA

A

to give energy to synthesize new covalent linkages or even ATP/GTP synthesis. Gives energy for the transfer of the acetyl group.

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8
Q

How many reactions and catalyzes are in the Krebs cycle

A

eight, resulting in fully oxidizing two carbons from acetyl part of AcetylCoA.

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9
Q

What does a kinase do? (gluco Kinase, Hexo Kinase?)

A

they phosphorilate molecules (the ones in name wll be phosphoed)

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10
Q

complex four of the e-transport is what in the TCA?

A

cytochrome C oxidase.

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11
Q

Describe the TCA cycle is brief

A

first step makes a six carbon citrate from four carbon oxaloacetate, then fully oxidize two carbons to carbon dioxide and transfer electrons to vitamin-derived cofactors NAD, and FAD.

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12
Q

how many NADH are produced in the TCA cycle?

A

Three.

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13
Q

How many FADH2 are produced in the TCA cycle?

A

one (though it takes two electrons.

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14
Q

what type of enzyme adds an electron to NAD/FAD to make the reduced form of the molecule?

A

dehydrogenase.

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15
Q

What is the dehydrogenase that does both the double reduction of FAD and part of complex two of electron transport?

A

Succinate dehydrogenase.

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16
Q

what can slow down the overall catabolism of ATP? (most common physiological ones)

A

lack of oxygen and lack of ADP, lack of Acetyl CoA

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17
Q

what could inhibit the elecctron transport chain?

A

carbon-monoxide; oligomyosin; cyonide, lack of oxygen,

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18
Q

where does the CO2 come from that we exhale?

A

the two completely reduced carbons of actly coa that are made in the TCA cycle.

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19
Q

how does 2,4 dinitrophenol lead to weight loss?

A

it can pick up protons, and move across the membrane and lose the protons, and then distribute the charge and not be polar, and still move back through the membrane and pick up more protons. This basically increases uncoupling.

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20
Q

what are the products of TCA cycle?

A

oxidize 2 carbon units to produce 2 molecules of CO2; 1 molecule of ATP or GTP and 5 high energy electrons in the form of 3 NADH, and one FADH2

21
Q

how will an increase in input of Acetyl CoA change the cylce?

A

It does not cause any net increase in the levels of oxalozcetate or other cycle intermediates sicne the carbons are lost as CO2!

22
Q

What is the vitamin that is used to make NAD?

A

Niacin, or vitamin B3

23
Q

what vitamin is used to make FAD?

A

Riboflavin, or vitamin B2

24
Q

why must we cadtabolize amin acids when fasting or starving?

A

we can’t synthesize glucose from fatty acids, and the Acetyl CoA adds no net carbons to the TCA cycle.

25
Q

How do we keep the TCA ccyle full of its required intermediates/

A

use Amin acid catabolize.

26
Q

what viatamin is needed in the active sit of alpha-ketoglutarate dehydrogenase?

A

Thiamine, or B1

27
Q

what are the results of Thiamine insufficiency?

A

Cardiac and neural malfunctions from the lack of TCA cycle products and lack of ATP

28
Q

what sub population has problems with thiamine defficiency?

A

alcoholics, as alcohol seems to prevent thiamin absorption.

29
Q

what is Wernicke encephalopathy/ Korsakoff’s syndrom?

A

due to alcohol consumption leading to thiamine defficiency leading to poor memory, confusion, ataxia, irritability, sleep problems, bilaterl, symmetrical lower extremiety tingling or burning sensation and muscle cramps. high output heart failure, tachycardia orthopnea and chest pain.

30
Q

regulation of the carbon flux through the TCA cycle?

A

citrate synthase inhibited if up citrate, if up NADH/NAD then dehydrogenase reactions down. Isocitrate dehydrogenase activated by ADP.

31
Q

what is another name for the electron transport chain?

A

the respiratory chain (this is were we use most of our oxygen)

32
Q

what do the electrons from NADH and FADH get used for?

A

the first four complexes of the E-transport chain use them to pump protons t teh inner mitrochondrial membrane space.

33
Q

what is the function of the fifth protein complex in the e-transport chain?

A

the fifth is ATP synthase, and uses the proton gradient to create ATP!

34
Q

Oxidative Phosphorilation?

A

the formation of ATP from ADP + Pi

35
Q

how do we get the product of metabolism out and more ADP/P in?

A

ATP/ADP anti-porter, and a Pi/H+ symporter.

36
Q

what do the genes in the mitochondial genome code for?

A

components of the repiratory chain proteins.

37
Q

Iron Suffer clusters?

A

required by complexes I,II,III, IV, and cytorchome c in the chain

38
Q

availablilty of what molecule contrls the flux of electrons through the tranport chain?

A

ADP

39
Q

How does ADP control the E-transport and the TCA cycle

A

less ADP, the proton gradient only gets so large, then slow the transport chain, then slow use of NADH then slow the TCA cycle. therefore fewer calories burned!

40
Q

what controls the metabolic rates overall?

A

amount of ADP produced within the cells of our bodies

41
Q

what if hypoxia or anoxia?

A

repiratory chain backs up, and proton gradient falls too low to make ATP, cells eventually die.

42
Q

what are some common toxins for the E-chain and where do they act?

A

carbon monoxide and cyanide, both act on complex IV.

43
Q

what would a mutation in Mitochondrial DNA cause?

A

diseases affecting the repiratory chain and oxidative phoshporylation; central nervous system problems, and/or myopathy — elevated blood lactate!!!

44
Q

what is Uncoupling of the electron transport and ADP phosphorylation?

A

protons re-enter the mitochondrial matrix by pahts other than through ATP synthase.

45
Q

what does uncoupling lead to?

A

increases NADH oxidation and oxygen consumption, large amounts of fuel are consumed producing heat.

46
Q

what tissue is known to have high uncoupling?

A

brown adipose tissue.

47
Q

how does brown adipose differ in thin/obese

A

more in thin! and in infants!

48
Q

what if we eat more calories than needed for the TCA cycle?

A

the acetyl coA as citrate gets shuttled out of the mitohondria tinto the cytosol for fat synthesis.