Metabolism Review Dr. Tuohy Flashcards Preview

NBDE PART 1 BIOCHEM/PHYSIOLOGY > Metabolism Review Dr. Tuohy > Flashcards

Flashcards in Metabolism Review Dr. Tuohy Deck (99):
1

glucose synthesis and glucose degradation occur in the

cytosol = glycolysis and gluconeogenesis

2

fatty acid synthesis occurs in the

cytosol

3

the 3 pathways that occur in the cytosol are

glucose and fatty acid synthesis, and glycolysis

4

Oxidative phosphorylation occurs in the

mitochondria

5

fatty acid degradation (beta oxidation) occurs in the

mitochondria

6

TCA cycle occurs in the

mitochondria

7

3 things that happen in the mitochondria

TCA cycle
fatty acid degradation
Oxidative phosphorylation

8

allosteric modification is covalent or non covalent?

non covalent

9

covalent modification of enzymes are fast/slow processes

slow

10

speed of a reaction depends on

the amount of activation energy

11

Most enzyme-catalyzed reactions proceed from ___times faster than uncatalyzed reactions.

(10)^3 - 10^8 x faster

12

enzymes affected by

temperature pH and cofactors

13

Holoenzyme is an Enzyme with its

cofactor

14

Apoenzyme is the __ portion of the haloenzyme

protein

15

__is a tightly bound coenzyme that does not dissociate

prosthetic group

16

pyruvate dehydrogenase coenzyme is

thiamine pyrophosphate

17

monoamine oxidase coenzyme

flavin adenine nucleotide

18

lactate dehydrogenase coenzyme

nicotinamide adenine dinucleotide (NAD)

19

glycogen phosphorylase coenzyme

pyridoxal phosphate

20

acetyl coA carboxylase coenzyme

coenzyme A (coA)

21

pyruvate carboxylase coenzyme

Biotin

22

methylmalonyl mutase coenzyme

5'-Deoxyadenosyl cobalamin

23

thymidylate synthase coenzyme

tetra hydrofolate

24

carbonic anhydrase coenzyme

Zn2+

25

carboxypeptidase coenzyme

Zn2+

26

EcoRV coenzyme

Mg2+

27

Hexokinase coenzyme

Mg2+

28

Urease coenzyme

Ni2+

29

1. cofactors are not proteins
2. if the cofactor is organic, it is called more specifically a

1. not
2. coenzyme

30

in michaelis-menten kinetics what are the y and x axis

y = initial velocity
x = substrate concentration

31

in michaelis-menten kinetics the curve is what shape

hyperbolic shape

32

in michaelis-menten kinetics, how do you find Km

you find 1/2 Vmax and then go down to x axis

33

the top of the curve in michaelis-menten kinetics is the

Vmax

34

in the hyperbolic shape, the initial reaction velocity is first/zero order?

first order

35

in the hyperbolic shape, as we approach Vmax the reaction becomes _ order

zero order

36

if you increase the enzyme concentration in the reaction what will change? Vmax/Km

Vmax will change but not the Km

37

the rate of reaction is directly proportional to the enzyme/substrate concentration?

enzyme concentration at any substrate concentration

38

if enzyme concentration is halved then the initial velocity will be

also halved

39

covalent modification of enzymes vs allosteric modification of enzymes. Reversible inhibitors bind enzymes through _ bonds

non covalent

40

the 2 most common inhibition

competitive and non competitive

41

methotrexate used in cancer therapy is an example of what kind of inhibition

competitive. binds dihydrofolate reductase that is the enzyme needed to make tetrahydrofolate (THF). when it binds it wont the appropriate substrate in, so we don't make THF, so the cell cant make nucleotides, so the cell dies. Kills the cancer cells.

42

what are the axis of the lineweaver burk plot?

1/V is the y
1/[S] is x

43

lineweaver burk plot is a __ plot

double reciprocal plot

44

the vmax is more easily found on the lineweaver burk plot or the michaelis menten curve?

lineweaver burk plot

45

what is the vmax in the lineweaver burk plot

the intercept of the y axis is 1/vmax

46

on a lineweaver burk plot if your vmax has gone higher up on the y axis has your vmax increased or decreased?

decreased ==> bc reciprocal plot

47

the intercept on the x axis of the lineweaver burk plot is

-1/Km

48

lineweaver burk plot: as your x intercept approaches the origin, does your Km increase or decrease?

increase

49

covalent modification = irreversible inhibition
give examples of GI enzymes

proinsulin ==> insulin
adding phosphates, sugars, OH groups
pepsinogen ==> pepsin
trypsinogen===> trypsin

50

ibuprofen (Advil) binds reversibly or irreversibly to COX

reversibly = therefore not covalent modification

51

aspirin binds reversibly or irreversibly to COX

irreversibly = aspirin adds acetyl group to the COX enzyme = covalent modification

52

any non protein molecule that assists an enzyme is called a

cofactor

53

cofactors can be metal ions or organic molecules. if a cofactor is organic it is specifically called a

coenzyme

54

Which is true:
all cofactors are coenzymes or
all coenzymes are cofactors?

all coenzymes are cofactors

not all cofactors are coenzymes

55

Km is a constant/or will it change

same = constant no matter how much enzyme you have

56

Vmax is a constant?

no it is not a constant it can change depending on how much enzyme you have. if you have more enzyme your vmax will be higher

57

changing enzyme concentration will affect Vmax or Km?

Vmax only

58

proteins that go all the way through the plasma membrane are called

integral proteins

59

proteins that are attached to one side or the other of the plasma membrane are called

peripheral proteins

60

integral proteins/peripheral proteins needs a detergent to isolate?

integral only. the peripheral do not need a detergent bc they fall off the membrane

61

name the 3 types of lipids in the plasma membrane

glycerophospholipids, sphingolipids and cholesterol

62

(phospholipids)
aka glycerophospholipids are made up of

they have a glycerol backbone and 2 fatty acids,and a phosphate and an R group

63

the R groups differ in the glycerophospholipids what are the 5 phospholipids found in our membranes

phosphatidyl inositol
phosphatidylserine
phosphatidylcholine
phosphatidylethanolamine
phosphatidic acid

64

sphingolipids are made by?

sphingosine (hydrocarbon with an amino group) + Fatty acid ==> ceraminde ===> ceramide + sugar = glycosphingolipid

65

sphingosine + FA ==>

ceramide

66

sphingosine + FA + phosphocholine ==>

sphingomyelin

67

sphingosine + FA + glucose ==>

glucosylcerebroside

68

sphingosine + FA + oligosaccharide ==>

ganglioside

69

sphingomyelin found in many

nerve cell membranes

70

an inability to break down gangliosides give us what disease

Tay Sachs disease

71

1. Tay–Sachs disease is a rare autosomal recessive genetic disorder. it causes a progressive deterioration of nerve cells and of mental and physical abilities that begins around ___of age and usually results in death by the age of __.
2. The disease occurs when harmful quantities of cell membrane components known as gangliosides accumulate in the brain's nerve cells, eventually leading to the premature death of the cells.

six months
death = four years old

A ganglioside is a form of sphingolipid, which makes Tay–Sachs disease a member of the sphingolipidoses. There is no known cure or treatment.

72

cholesterol is important in maintaining the appropriate _ of the membrane

fluidity.
Fluidity, strength, thickness, permeability and curvature of membrane

73

cholesterol has how many carbons and how many rings

27 carbons, 4 rings

74

cholesterol's role is __ dependent

temperature and concentration dependent

75

the more UNSATURATED/SATURATED fatty acids you have in a membrane the more fluid?

unsaturated fatty acids = more fluidity

76

simple diffusion needs

only a concentration gradient, small non polar O2 CO2 -----water is not non polar!! so it does not do simple diffusion

77

facilitated diffusion needs

membrane helper and concentration gradient

78

glucose gets into cell by

glucose transported = facilitated diffusion

79

primary active transport

moving against gradient, need ATP to fuel it and you need a protein helper

80

secondary active transport

moving against gradient, but do need ATP to fuel it and you need a protein helper. you use an established gradient

81

Epinephrine glucagon and ACTH are all stimulatory/inhibitory hormones for signal transduction pathways.

stimulatory = bind receptor = activates the G protein (Gs) = binds adenylyl cyclase ==> makes cAMP ==> makes protein kinase A

82

PGE1 and Adenosine are stimulatory/inhibitory hormones for signal transduction pathways.

inhibitory: bind receptor = activates the inhibiotry G protein (Gi) = which binds adenylyl cyclase ==> does not make cAMP ==>does not make protein kinase A

83

adenosine in our brain is responsible for

lack of motivation, tired. its receptors are blocked by caffeine

84

when cyclic AMP binds protein kinase A where does it bind and what happens

cyclic AMP binds the 2 regulatory units of PKA, which makes it release the catalytic units = ACTIVE PKA

85

what does protein kinase A do?

it adds phosphates = remember all kinases add phosphates

86

what enzyme degrades cAMP

phosphodiesterase

87

what can block the receptor in signal transduction?

arrestin

88

insulin uses a __ receptor

a catalytic tyrosine kinase receptor (RTK = receptor tyrosine kinase). it is a dimer, it binds insulin and acts like an enzyme on the cytoplasmic side. DOES NOT USE G PROTEIN

89

thyroid hormones and steroid hormones bind their receptors

inside the cell.

90

Growth hormone activates a cascade that activates

protein kinase C
includes calcium

91

Ach uses?

neurotransmitter linked to ion channel. AcH binds receptor --> activates G protein which hits a potassium channel and opens it (directly activates the channel)

92

nitric oxide (gases) pathway uses

cGMP and protein kinase G

93

cGMP are broken down by

phosphodiesterases

94

Viagra inhibits

phosphodiesterase that breaks down cGMP so that there is more vasodilation

95

you have to have free glucose (monosaccharide) to pass into blood from intestinal cells: where is the low/high concentration- in the intestines or in the enterocyte cell?

enterocyte cell has higher glucose than inside the small intestine. Na+ is higher in the intestine than in the enterocyte, so sodium comes in down its gradient and glucose piggybacks in = Na+ glucose cotransporter

96

the Na+ glucose cotransporter is called __ and is __ transport

SGLT1 = Sodium Glucose Transporter 1, secondary transport, brings glucose that we ate into the intestinal cell.

97

glucose inside the enterocyte crosses into the blood using which transporter and is _ transport

GLUT2 transport protein = facilitated transport bc going down its concentration gradient

98

Na/K pump keeps

high potassium inside the cells and high sodium outside the cell. 3Na+ out, 2K+ in.

99

pancreas has _ receptors for glucose

GLUT 2 transporter