Exam 3 - Review Flashcards

1
Q

what is a by product of light reactions?

A

oxygen

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2
Q

what are dark reactions?

A

The Calvin Cycle - Uses ATP, NADPH, and CO2 to produce hexose carbohydrates

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3
Q

what are light reactions?

A

transform light energy into: ATP and NADPH (biosynthetic reducing power)

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4
Q

where does photosynthesis take place?

A

in chloroplasts

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5
Q

what enzyme breaks down glycogen?

A

glycogen phosphorylase

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6
Q

what induces glycogen degredation?

A

epinephrine and glucagon

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7
Q

what does phosphoglucomutase do?

A

it takes glucose 1-phosphate and makes glucose 6-phosphate

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8
Q

why does liver contain glucose 6 - phosphatase?

A

glucose 6-phosphatase generates free glucose from glucose 6-phosphate

absent from muscle

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9
Q

How is glycogen phosphorylase regulated in the liver and muscle?

A

activated when phospharylated

primarily phosphorylated a in active R state in the liver

primarily unphosphorylated b state in the muscle

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10
Q

what does glucose regulate?

A

phosphorylation state

binds and inhibits the allosteric site

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11
Q

what does AMP, ATP, and glucose 6-phosphate do to the liver enzyme? the muscle enzyme?

A

AMP - low energy, activates glycogen phosphorylase

ATP - high energy, inhibits glycogen phosphorylase

glucose 6-phosphate - high energy, inhibits glycogen phosphorylase

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12
Q

what type of regulators are AMP, ATP, and glucose 6 - phosphate?

A

isoforms

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13
Q

what does phosphorylation do to each enzyme?

A

exists in two forms

b is less active

a is more active (has a phosphorylated serine residue)

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14
Q

which phosphorylase state is more active?

A

R state

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15
Q

which phosphorylase state is less active?

A

T state

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16
Q

which phosphorylase state is usually found in muscle?

A

T state

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17
Q

what does glucagon do during fasting?

A

signals low glucose levels in the blood to start gluconeogenesis

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18
Q

what is UDP-Glucose?

A

higher level energy precursor for glucose to be synthesized

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19
Q

what does phosphorylation do to glycogen synthase activity?

A

inhibits it

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20
Q

what does glycogen synthase kinase (GSK) do?

A

it phosphorylates glycogen synthase

inhibiting it

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21
Q

what does insulin do to GSK?

A

inhibits GSK to turn on glycogen synthase

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22
Q

what effects do glucagon and epinephrine have on glycogen synthase?

A

inhibits synthesis

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23
Q

what does high glucose do to insulin?

A

high glucose instigates the release of insulin from the pancreas to store FAs as TAGs

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24
Q

what is the pentose phosphate pathway?

A

source of biosynthetic reducing power (electrons) and produces ribose phosphates for DNA/RNA synthesis, neurotransmitter synthesis, etc.

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25
Q

In the oxidative phase of the pentose phosphate pathway, what is being oxidized?

A

glucose - 6 - phosphate

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26
Q

In the oxidative phase of the pentose phosphate pathway, what is being reduced?

A

NADPH

27
Q

what is the oxidative phase of the pentose phosphate pathway?

A

Glucose - 6 - phosphate → 2 NADPH → Fatty Acid Synthesis, Cholesterol Synthesis, Nucleotide synthesis, Neurotransmitter synthesis

28
Q

what is the non-oxidative phase of the pentose phosphate pathway?

A

glucose - 6- phosphate → 2 NADPH + Ribose 5 - phosphate → Glycolytic intermediates →glucose - 6- phosphate

and

glucose - 6- phosphate → 2 NADPH + Ribose 5 - phosphate → DNA, RNA, ATP, NAD, FAD, CoA

29
Q

where are triacyclglycerols stored?

A

adipose tissue and muscle

30
Q

what hormones activate triacylglycerol breakdown?

A

epinephrine and glucagon

31
Q

what is the first step in the breakdown of fatty acids?

A

adding CoA to acyl group absorbed through intestines

32
Q

where does fatty acid oxidation occur and how does it get there?

A

mitochondrial matrix by carnitine shuttle

33
Q

what are the four steps in beta-oxidation?

A
  • Oxidation (FAD)
  • Hydration (H2O)
  • Oxidation (NAD+)
  • Thiolysis (CoA)
34
Q

are there meaningful intermediates in the reactions of beta-oxidation of fatty acids?

A

yes, the reduced forms NAD and FAD

35
Q

unsaturated fatty acids with odd numbers of double bonds need what enzymes?

A

only isomerase

36
Q

unsaturated fatty acids with even numbers of double bonds need what enzymes?

A

isomerase and reductase

37
Q

beta-oxidation of fatty acids with odd numbers of carbons generate what intermediates?

A

Propynol CoA (3 carbon chain)

becomes succinyl CoA

38
Q

where does the intermediate of beta - oxidation end up?

A

Succinyl CoA → TCA Cycle

39
Q

where does ketone body formation take place?

A

made from Acyl CoA

related to glucose levels

primarily in the liver

40
Q

what organs normally use ketone bodies?

A

kidney and heart

41
Q

what conditions generate abnormally high levels of ketone bodies?

A

diabetes → no insulin

chronic alcohol use

42
Q

where does fatty acid synthesis occur in the cell?

A

cytosol

43
Q

what are the three stages of fatty acid synthesis?

A
  1. Acyl CoA moves out of the mitochondria to Cytosol by citrate shuttle
  2. activate CoA to malonyl CoA
  3. addition of 2 carbon units to get to C16
44
Q

what does the enzyme, acetyl CoA carboxylase do?

A

converts Acetyl CoA to malonyl CoA; regulatory enzyme

45
Q

what do the following do to the activity of acetyl CoA carboxylase?

citrate, insulin, glucagon, epinephrine, ATP

A

citrate - partially activates acetyl CoA

insulin - activates acetyl CoA carboxylase

glucagon - inhibits acetyl CoA carboxylase

epinephrine - inhibits acetyl CoA carboxylase

ATP - downregulates (inhibits) acetyl CoA carboxylase

46
Q

what enzyme phosphorylates CoA carboxylase and what does phosphorylation do to this enzyme?

A

AMP activated protein kinase

phosphorylation inhibits

47
Q

what is the most detrimental intermediate in excessive alcohol use?

A

high levels of reduced NAD

glycolysis and FA breakdown

48
Q

what is LDL?

A

bad cholesterol

distributes cholesterol throughout the body

49
Q

what is HDL?

A

good cholesterol

less fatty acids and more good proteins

takes cholesterol back to the liver

50
Q

The regulation of cholesterol synthesis is dependent on the activity of?

A

HMG CoA Reductase

51
Q

cholesterol is a precursor for what hormones?

A

sex hormones (proestrogen, androgen, and estrogen)

glucocortisoids

mineralcorticoids

52
Q

Vitamin D deficiency results in what condition?

A

rickets

53
Q

what function does the glucose - alanine cycle serve?

A

way of getting rid of amino groups from branched amino acids

used in the urea cycle

54
Q

what does the urea cycle do? where does it occur?

A

Urea Cycle gets rid of ammonia from the body

occurs in the liver cells (according to google)

55
Q

what are glucogenic amino acids?

A

amino acids that can enter glucose synthesis pathways to create glucose

56
Q

what are ketogenic amino acids?

A

only enter at acetyl CoA site

can’t make glucose

Leucine and Lysine

57
Q

which amino acids are only ketogenic?`

A

leucine

lysine

58
Q

how do we obtain nitrogen for the synthesis of biomolecules?

A

dietary sources → nitrogen fixing bacteria

needs to be fixed to ammonia

59
Q

what is the difference between the de novo pathway of nucleotide synthesis and the salvage pathway?

A

de novo pathway - build from from scratch out of nucleotides

salvage pathway - nucleotides “gathered” and reused after cell is broken down

60
Q

how are purines in the de novo pathway built?

A

purines are made on the ribose and then the ring is added

61
Q

how are pyrimidines in the de novo pathway built?

A

pyrimidines connect to the ring then the ribose

62
Q

what does the enzyme, ribonucleotide reductase do and how is it regulated?

A

takes ribose and reduces to get deoxy from reduced nucleotides

63
Q

how is TMP synthesized?

A

de novo from dUMP

adds methyl group form methyl donor