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Block 3 Week 9 > Integration of Metabolism II > Flashcards

Integration of Metabolism II Flashcards

1
Q

Where are the bulk of nutrients absorbed

A

ileum

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2
Q

Where does the absorptive process begin?

A

jejunum

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3
Q

How many grams of protein do you excrete in your stool?

A

5-20g

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4
Q

What activated F1,6BPase (i.e. step that converts F1,6bp to F6P for gluconeogenesis)

A

citrate :)

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5
Q

In the well fed state, what will you have a lot of?

A

citrate, acetyl CoA, ATP, Insulin, Glucose, Alanine

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6
Q

What is the point of the glucose-alanine cycle?

A

so you can use the breakdown products of glycolysis from other tissues and put them into the liver to make gluconeogenesis since it is the only organ that can do this

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7
Q

In the fasting, starving state what will you have a lot of?

A

AMP, ADP, cAMP, glucagon, cortisol

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8
Q

In most cases, (blank) act by changing the rate of transcription or by affecting the stability of the messenger RNA.

A

hormones

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9
Q

What kind of affectors are ATP, Alanina, and Citrate?

A

allosteric

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10
Q

What kind of affector is phosphate?

A

covalent

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11
Q

What kind of affector is ADP, F2,6 BP?

A

competitive

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12
Q

Most Potent Modulator: (blank) turns ON glycolysis and OFF gluconeogenesis (hormonally regulated).

A

F2,6bis-P

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13
Q

Why will your levels of ATP and acetyl CoA be high during fasting?

A

because you will be undergoing beta oxidation! What does this tell us…. IT tells us that we should stimulate gluconeogenesis :)

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14
Q

What does glucagon do to cAMP and why is this important?

A

stimulates it which makes for phophorylation and thus gluconeogenesis

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15
Q

What is the most important regulator of F16Bpase and PFK1?

A

F2,6BP

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16
Q

Liver gluconeogenesis is linked to (blank) in other tissues. Why?

A

glycolysis

so that gluconeogenesis can occur since it only occurs in the liver

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17
Q

What are the 2 cycles that link glycolysis to gluconeogenesis?

A

cori cycle

alanine cycle

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18
Q

How does the cori cycle work?

A

RBC break down glucose into lactate, lactate gets transferred to the liver where it is used in gluconeogenesis

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19
Q

How does the alanine cycle work?

A

muscles breakdown glucose-> make pyruvate-> alanine-> trasnferred to liver-> gluconeogenesis

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20
Q

What three things stimulate glycogen breakdown in the muscle?

A

epinephrine
calcium
AMP

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21
Q

Why cant the muscle undergo gluconeogenesis?

A

because it doesnt have glucose 6 phosphatase! this means that when it breaks down glycogen it will just go straight into the TCA cycle. SO you can think of its glycogen stores as just being part of glycolysis so that when you are thinking about allosteric effectors it will make more sense. I.e AMP, ADP will stimulate glycogen breakdown (glycolysis).

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22
Q

What is also an allosteric effector of the muscle that is somewhat confusing?

A

epinephrine, it will breakdown glycogen stores promote glycolysis in the muscle because epinephrine promotes gluconeogenesis which will only happen in the liver and since muscle can only make lactate to be transfered to the liver to undergo gluconeogenesis it will do just that

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23
Q

Will AMP from the muscle activate the less active form of glycogen phosphorylase or the more active form?

A

the less active form

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24
Q

What are the products of the PPP?

A

RIbose 5 phosphate and NADPH

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25
Q

What does transketolase do?
What does transaldolase do?
Which contains thiamin pyrophosphate?

A

transfers a 2 carbon unit (thiamin pyrophosphate bound)

transfers a 3 carbon unit

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26
Q

What is the rate limiting step of the PPP?

A

G6PD

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27
Q

What all can pyruvate turn into?

A

OAA, Alanine, Lactate, acetyl coA

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28
Q

What can make pyruvate?

A

G6P, alanina, lactate

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29
Q

What can OAA turn into?

A

G6P

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30
Q

What can acetyl coa turn into?

A

FA
CO2
Cholesterol
Ketones

31
Q

What are the 5 coenzymes of the pyruvate dehydrogenase?

What are the 3 enzymes of pyruvate dehydrogenase?

A 
The Five Needed Coenzymes L
TPP
FAD
NADH
CoA SH
Lipoate
E1, E2, E3
32
Q

What is defective in “classic galactosemia” (the worst one)?

A

uridyl transferase

33
Q

What causes essential fructosuria?

A

problem w/ fructokinase

34
Q

What causes fructose intolerance?

A

problem w/ fructose 1 phosphate aldolase

35
Q

What does triose kinase do?

A

bypasses PFK1 to make G3P from glyceraldehyde

36
Q

In fatty acid synthesis we convert acetyl CoA to malonyl CoA with acetyl CoA Carboxylase. Acetyl CoA Carboxylase is activated by (blank) and inhibited by (Blank).

A

citrate

palmitoyl CoA

37
Q

What inhibits CPT1?

A

malonyl CoA

38
Q

What causes Von Gierkes disease?

A

deficiency with G6Pase

39
Q

What is the cause of Pompe disease?

A

deficiency in alpha glucosidase (so you wont have breakdown of alpha 1,4 and alpha 1,6 bonds)

40
Q

What is the cause of cori disease or forbes disease?

A

have a problem with amylo 1,6 glucosidase (i.e you dont have your glycogen debranching enzyme)

41
Q

What is the cause of andersons disease?

A

dont have branching enzyme so you just have really long chains

42
Q

What is McArdles disease?

A

DOnt have muscle glycogen phosphorylase

I.e. you dont have muscle

43
Q

What is Hers disease?

A

Dont have liver glycogen phosphorylase

44
Q

What is Taruis disease?

A

dont have PFK1

45
Q

What dont you have in hereditary fructose intolerance?

A

aldolase B

46
Q

What dont you have in fructosuria?

A

hepatic fructokinase

47
Q

What dont you have in classic galactosemia (type 1)?

A

Uridyl transferease

48
Q

What dont you have in galactose epimerase (glactosemia III)

A

Galactose epimerase deficiency

49
Q

What dont you have in galactokinase deficiency (mild form type 2)?

A

galactokinase

50
Q

What is a rare disease that result in severe fat malabsorption and TAG accumulation in the intestinal mucosa and liver?

A

ABlipoproteinemia

51
Q

What causes aBlipoproteinemia?

A

deficiency in TAG transfer protein in the ER so you dont get ApoB lipoproteins assembled

52
Q

What disease is this:

Deposit cholesterol esters in reticuloendothelial cells, bone marrow and Schwann cells. Tonsils-”Orange”

A

Tangier Disease

53
Q

What causes Tangier disease?

A

absence of ABC1 protein so apoAs cant acquire lipid and mature HDLs dont form

54
Q

What disease is this:

Found in Amish and Ashkenazi Jewish populations. The polymorphism is found in 25% of centenarians.

A

Apo CIII deficiency

55
Q

What causes Apo CIII deficiency?

A

absence of APo CIII which inhibits LPL therefore decreased TAGs and LDL while increasing plasma HDLs

56
Q

What disease is this:

Benign condition. LDL is normal to low but HDL is elevated and CE get to the liver via HDL’s.

A

CETP deficiency

57
Q

What is the cause of CETP?

A

lack of ability to transfer cholesterol esters

58
Q

What disease is this:
deficiency in hexosaminidase resulting in ganglioside accumulation.
symptoms: mental retardation, blindness, red spots on macula, death b/w 2nd and 3rd year

A

Tay-Sachs disease

59
Q

What disease is this:
problem with glucocerebrosidase resulting in accumlation of glucocerebrosides and you get liver and spleen enlargement and erosin of bones, mental retardation in infants.

A

Gauchers disease

60
Q

What disease is this:
problem with galactosidase resulting in ceramid trihexoside accumulation and you get a skjn rash and kidney failure and pain in lower extremities.

A

Fabry disease

61
Q

What disease is this:
problem with sphingomyelinase resulting in accumulation of sphingomyelin and you get liver and spleen enlargement and mental retardation

A

Niemann-Pick disease

62
Q

What disease is this:
problem with galactocerebrosidase resulting in accumulation of galactocerebroside resulting in mental retardation and absence of myelin

A

Globoid leukodystrophy (Krabbe disease)

63
Q

What are the four acyl coA dehydrogenase deficiencies?

What kind of disorders are these?

A 
VLCAD-> very long chain
LCAD-> long chain
MCAD-> medium chain
SCAD-> short chain
mitochondrial beta oxidation disorders
64
Q

What are the 2 carnitien translocase deficiencies?

What kind of disorders are these?

A

CPT1
CPTII
mitochondrial beta oxidation disorders

65
Q

HOw do you stimulate the activity of glut transporters in the muscle?

A

via insulin, hypoxia, or diet

66
Q

What is the cellular location of Glut1,2,3,4?

What about Glut 5?

A

PM

sarcolemmal vesicles

67
Q

What glut receptor is found on the liver, pancreas, intestine and kidney?

A

glut 2

68
Q

What glut receptor is found on brain, kidney, placenta?

A

glut 3

69
Q

What glut receptor is found on adipose tissue, heart, skeletal muscle, and blastocyts?

A

glut 4

70
Q

What glut receptor is found on muscle and spermatozoa?

A

glut 5 (uses fructose)

71
Q

What three enzymes does insulin increase to upregulate fatty acid synthesis?

A 
increases
ATP citrate lyase (converts citrate into OAA and Acetyl COA for fatty acid synthesis)
Malic enzyme (converts malate from the TCA cycle into pyruvate for FA synthesis and makes NADPH)
72
Q

What are the 2 ways to make NADPH?

A

malic enzyme and PPP

73
Q

With epinephrine in the muscle, what will you be increasing that is counterintuitive>

A

glycolysis

74
Q

With cortisol in the liver, what will you be increasing that is counterintuitive?

A

glycogen synthesis

Block 3 Week 9 (6 decks)

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